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Eukariotiese lewensiklusse - Biologie

Eukariotiese lewensiklusse - Biologie


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1. Beskrywing van eukariotiese lewensiklusse

In Biologie beskryf 'n lewensiklus (of lewensgeskiedenis) die verloop van ontwikkeling van 'n organisme. 'N Lewenssiklus is die hele geskiedenis van 'n organisme, gewoonlik deur 'n reeks ontwikkelingsfases wat die veranderinge wat 'n spesie ondergaan, uitbeeld vanaf die begin van 'n gegewe ontwikkelingsfase tot die aanvang van dieselfde ontwikkelingsfase in die volgende generasie. .

Die belangrikste verskille tussen eukariotiese lewensiklusse is die hoeveelheid tyd wat spandeer word in haploïede vs. diploïede fases en die meiotiese produkte (spore vs. gamete) wat geproduseer word. Onthou dat haploïede selle slegs een stel chromosome bevat (n). Diploïede selle bevat twee stelle chromosome (2n). Meiose is die proses waardeur diploïede selle twee keer in 'n ry verdeel nadat hulle hul chromosome slegs een keer herhaal het. Die gevolg is dat elke finale dogtersel haploïed is en slegs een kopie van elke chromosoom bevat. Dit verskil van mitose, wanneer selle verdeel maar die aantal chromosoomstelle dieselfde bly. In mitose verdeel haploïede selle om haploïede selle te vorm en diploïede selle verdeel om diploïede selle te vorm.

Diploïede selle bevat 2 kopieë van hul genoom, hulle tipies:

1. Verskaf genetiese oortolligheid wat weerstand teen DNA-skade kan verhoog (daar is 'n "rugsteun" kopie van DNA in die geval dat 'n mens beskadig word).
2. Vind voordeel uit genetiese uitruiling met ander individue, wat moontlik meer genetiese diversiteit kan verskaf en dus 'n groter potensiaal vir oorlewing in 'n veranderende omgewing bied.
3. Het stadiger groei omdat hulle 'n langer selsiklus het as gevolg van 'n groter hoeveelheid DNA wat met elke seldeling gerepliseer moet word.

Aangesien haploïede selle slegs een kopie van hul genoom het, is dit tipies:

1. Meer kwesbaar vir genetiese skade (geen "rugsteun" kopie van DNA nie).
2. In staat om vinniger te groei, aangesien hulle nie soveel DNA het om met elke selsiklus te herhaal nie.
3. In staat om te kombineer met ander haploïede selle via bevrugting.

Benewens seldeling, is bevrugting, of die samesmelting van twee selle, 'n ander belangrike stadium in elke lewensiklus, wat lei tot die vorming van 'n diploïede sel, die sigoot.

Ons sal nou die drie hooftipes Eukaryotiese lewensiklusse (spories, sigoties en gameties) in meer besonderhede hersien.

Gametiese lewensiklus

Die gametiese lewensiklus is die voortplantingsiklus wat by diere en sommige protistane voorkom. Die term gameties verwys na die feit dat gamete die resultaat van meiose is.

Gedurende die gametiese lewensiklus produseer 'n voortplantingsel haploïede gamete (geslagselle soos eier en sperms) wat saam 'n sigoot produseer. Die sigoot groei deur seldeling en selverlenging om 'n meersellige diploïede individu te produseer. In die gametiese lewensiklus is die gamete die enigste haploïede stadium wat in die lewensiklus gevind word. Die gamete (eier en sperms) is die enigste haploïede selle wat geproduseer word.

Figuur ( PageIndex {1} ). (CC BY-NC-SA)

Sigotiese lewensiklus

Die sigotiese lewensiklus is die eenvoudigste seksuele lewensiklus, algemeen onder swamme en protiste. Hierdie organismes is haploïed gedurende die grootste deel van hul lewensiklus.

In die sigotiese lewensiklus is die sigoot die enigste diploïede fase. Na bevrugting ondergaan die sigoot meiose om haploïede selle te produseer. Die selle ondergaan mitose om óf in getal toe te neem óf tot 'n haploïede meersellige organisme te groei. Sommige haploïede selle ontwikkel in gamete deur mitose.

Figuur ( PageIndex {2} ). (CC BY-NC-SA)

Sporiese Lewensiklus

Die sporiese lewensiklus is gewone alge en plante. Die term spories verwys na die feit dat spore die gevolg is van meiose.

Die sporiese lewensiklus is die gevolg van 'n afwisseling tussen 'n haploïede en 'n diploïede organisme. As gevolg hiervan word daar soms na hierdie siklus verwys as die "afwisseling van geslagte". Die diploïede sigoot word eers deur 'n reeks mitotiese afdelings herhaal om 'n meersellige diploïede organisme te vorm, bekend as 'n sporofiet. Die sporofiet ondergaan meiose en produseer haploïede spore. Hierdie spore ontkiem en differensieer in haploïede meersellige individue wat bekend staan ​​as gametofiete. Die gametofiet produseer eiers en sperm deur mitose. Die sigoot wat voortspruit uit syngamie van die gamete groei deur herhaalde mitotiese afdelings in die sporofiet en die siklus gaan voort.

Figuur ( PageIndex {3} ). (CC BY-NC-SA)


Eukaryotic Life Cycles Tutorial deur dr. Katherine Harris is gelisensieer onder 'n Creative Commons Erkenning-Nie-Kommersieel-Deel Soos 3.0 Ongedraagde lisensie.

Befonds deur die Amerikaanse Departement van Onderwys, Ontwikkeling van Hispanic Serving Institutions Program, #P031S090007.


Het meiose ontwikkel voor seks en die evolusie van eukariotiese lewensiklusse?

Bioloë het lank teoretiseer oor die evolusie van lewensiklusse, meiose en seksuele voortplanting. Ons kyk weer na hierdie onderwerpe en stel voor dat die fundamentele verskil tussen lewensiklusse is waar en wanneer multicellulariteit tot uiting kom. Ons ontwikkel 'n scenario om die evolusionêre oorgang van die lewensiklus van 'n eensellige organisme na een waarin meerselligheid uitgedruk word in óf die haploïede óf diploïede fase, of albei, te verduidelik. Ons stel verder voor dat meiose moontlik ontwikkel het as 'n meganisme om reg te stel vir spontane duplisering van die hele genoom (outo-poliplooidie) en dus voor die evolusie van seksuele voortplanting sensu stricto (dit wil sê die vorming van 'n diploïde sigoot via die samesmelting van haploïede gamete) in die belangrikste eukariotiese klades. Daarbenewens stel ons voor, net soos ander, dat seksuele voortplanting, wat in alle eukariotiese groepe voorkom, baie verskillende voordele inhou, onder meer dat dit wisselvalligheid tussen die nageslag veroorsaak en sodoende die mededinging tussen broers en susters verminder.

Sleutelwoorde: alge afwisseling van generasies outo-polyploïdie chiasmata embryofiete meiose syngamie.


Inhoud

Die studie van voortplanting en ontwikkeling by organismes is deur baie plantkundiges en dierkundiges uitgevoer.

Wilhelm Hofmeister het gedemonstreer dat afwisseling van generasies 'n kenmerk is wat plante verenig, en het hierdie resultaat in 1851 gepubliseer (sien plantseksualiteit).

Sommige terme (haplobiont en diplobiont) wat gebruik word vir die beskrywing van lewensiklusse, is aanvanklik deur Nils Svedelius vir alge voorgestel, en is toe vir ander organismes gebruik. [4] [5] Ander terme (outogamie en gamontogamie) wat in protistiese lewensiklusse gebruik word, is deur Karl Gottlieb Grell bekendgestel. [6] Die beskrywing van die komplekse lewensiklusse van verskillende organismes het bygedra tot die afweer van die idees van spontane generasie in die 1840's en 1850's. [7]

'n Sigotiese meiose is 'n meiose van 'n sigoot onmiddellik na karyogamie, wat die samesmelting van twee selkerne is. Op hierdie manier eindig die organisme sy diploïede fase en produseer verskeie haploïede selle. Hierdie selle verdeel mitoties om groter, meersellige individue of meer haploïede selle te vorm. Twee teenoorgestelde tipes gamete (bv. Manlik en vroulik) van hierdie individue of selle versmelt om 'n sigoot te word.

In die hele siklus is sigote die enigste diploïede sel mitose wat slegs in die haploïede fase voorkom.

Die individue of selle as gevolg van mitose is haplonts, daarom word hierdie lewensiklus ook haplontiese lewensiklus genoem. Haplonte is:

  • By archaeplastidans: 'n paar groen alge (bv. Chlamydomonas, Zygnema, Chara) [8]
  • In stramenopiele: 'n paar goue alge [8]
  • In alveolate: baie dinoflagellate, bv. Ceratium, Gymnodinium, sommige apicomplexans (bv. Plasmodium) [9]
  • In rhizariërs: sommige eugliewe, [10]ascetospore
  • In opgrawings: sommige parabasaliede [11]
  • In amoebozoans: Dictyostelium[8]
  • In opisthokonts: die meeste swamme (sommige chytrids, zygomycetes, sommige ascomycetes, basidiomycetes) [8] [12]: 15

In gametiese meiose, in plaas van onmiddellik te verdeel meioties om haploïede selle te produseer, verdeel die sigoot mitoties om 'n meersellige diploïede individu of 'n groep meer eensellige diploïede selle te produseer. Selle van die diploïede individue ondergaan dan meiose om haploïede selle of gamete te produseer. Haploïede selle kan weer verdeel (deur mitose) om meer haploïede selle te vorm, soos in baie giste, maar die haploïede fase is nie die oorheersende lewensiklusfase nie. In die meeste diplonte kom mitose slegs in die diploïede fase voor, dit wil sê gamete vorm gewoonlik vinnig en versmelt om diploïede sigote te produseer.

In die hele siklus is gamete gewoonlik die enigste haploïede selle, en mitose kom gewoonlik slegs in die diploïede fase voor.

Die diploïede meersellige individu is 'n diplont, daarom word 'n gametiese meiose ook 'n diplontiese lewensiklus genoem. Diplome is:

  • By archaeplastidans: 'n paar groen alge (bv. Cladophora glomerata, [13]Acetabularia[8] )
  • By stramenopile: sommige bruin alge (die Fucales kan egter hul lewensiklus ook geïnterpreteer word as sterk heteromorfies-diplohaplonties, met 'n hoogs verminderde gametofietfase, soos in die blomplante), [12] : 207 sommige xantofiete (bv. Vaucheria), [12] : 124 meeste diatome, [11] sommige oomysete (bv. Saprolegnia, Plasmopara viticola), [8] opaliene, [11] 'n paar "heliozoans" (bv. Actinophrys, Actinosphaerium) [11][14]
  • In alveolate: siliate[11]
  • In opgrawings: sommige parabasaliede [11]
  • By opisthokonts: diere, sommige swamme (bv. Sommige ascomycetes) [8]

By sporiese meiose (ook algemeen bekend as tussenganger meiose) verdeel die sigoot mitoties om 'n meersellige diploïede sporofiet te produseer. Die sporofiet skep spore via meiose wat ook verdeel dan mitoties-produserende haploïede individue wat gametofiete genoem word. Die gametofiete produseer gamete via mitose. In sommige plante is die gametofiet nie net klein nie, maar ook kortstondig in ander plante en baie alge, die gametofiet is die "dominante" stadium van die lewensiklus.

  • By archaeplastidans: rooi alge (wat twee sporofiete het), sommige groen alge (bv. Ulva), landplante [8]
  • In stramenopiele: die meeste bruin alge [8]
  • By rhizarians: baie foraminiferane, [11] plasmodiophoromycetes [8]
  • In amoebozoa: myxogastrids
  • By opisthokonts: sommige swamme (sommige chytrids, sommige ascomycetes soos die brouersgis) [8]
  • Ander eukariote: haptofiete[11]

Sommige diere het 'n geslagsbepalingsisteem genaamd haplodiploïed, maar dit hou nie verband met die haplodiplontiese lewensiklus nie.

Sommige rooi alge (soos Bonnemaisonia [15] en Lemanea) en groen alge (soos Prasiola) het vegetatiewe meiose, ook genoem somatiese meiose, wat 'n seldsame verskynsel is. [12]: 82 Vegetatiewe meiose kan voorkom in haplodiplontiese en ook in diplontiese lewensiklusse. Die gametofiete bly geheg aan en deel van die sporofiet. Vegetatiewe (nie-reproduktiewe) diploïede selle ondergaan meiose, wat vegetatiewe haploïede selle genereer. Dit ondergaan baie mitose en produseer gamete.

'n Ander verskynsel, genaamd vegetatiewe diploïdisering, 'n tipe apomixis, kom by sommige bruin alge voor (bv. Elachista stellaris). [16] Selle in 'n haploïede deel van die plant dupliseer spontaan hul chromosome om diploïede weefsel te produseer.

Parasiete is afhanklik van die uitbuiting van een of meer gashere. Diegene wat meer as een gasheerspesie moet besmet om hul lewensiklus te voltooi, word gesê dat hulle komplekse of indirekte lewensiklusse het. Dirofilaria immitis, of die hartwurm, het byvoorbeeld 'n indirekte lewensiklus. Die mikrofilariae moet eers deur 'n wyfie muskiet ingeneem word, waar dit in die infektiewe larfstadium ontwikkel. Die muskiet byt dan 'n dier en dra die aansteeklike larwes in die dier oor, waar hulle na die longslagaar migreer en volwasse word. [17]

Daardie parasiete wat 'n enkele spesie besmet, het direkte lewensiklusse. 'n Voorbeeld van 'n parasiet met 'n direkte lewensiklus is Ancylostoma caninum, of die hondehaakwurm. Hulle ontwikkel tot die infektiewe larwestadium in die omgewing, dring dan die vel van die hond direk binne en word volwasse na volwassenes in die dunderm. [18]

As 'n parasiet 'n gegewe gasheer moet besmet om sy lewensiklus te voltooi, word daar gesê dat dit soms 'n verpligte parasiet van die gasheer is; infeksie is fakultatief - die parasiet kan oorleef en sy lewensiklus voltooi sonder om die spesifieke gasheersoort te besmet . Parasiete besmet soms leërskare waarin hulle nie hul lewensiklusse kan voltooi nie, dit is toevallige gashere.

'N Gasheer waarin parasiete seksueel voortplant, staan ​​bekend as die definitiewe, finale of primêre gasheer. By tussengashere plant parasiete óf nie voort nie óf doen dit ongeslagtelik, maar die parasiet ontwikkel altyd tot 'n nuwe stadium in hierdie tipe gasheer. In sommige gevalle sal 'n parasiet 'n gasheer besmet, maar geen ontwikkeling ondergaan nie; hierdie gashere staan ​​bekend as paratenic [19] of transportgashere. Die parateniese gasheer kan nuttig wees om die kans te verhoog dat die parasiet na die definitiewe gasheer oorgedra sal word. Byvoorbeeld, die kat longwurm (Aelurostrongylus abstrusus) gebruik 'n slak of slak as 'n tussengasheer die eerste stadium larwe gaan die weekdier binne en ontwikkel tot die derde stadium larwe, wat aansteeklik is vir die definitiewe gasheer - die kat. As 'n muis die slak vreet, sal die derde stadiumlarwe die weefsel van die muis binnedring, maar geen ontwikkeling ondergaan nie.

Die primitiewe tipe lewensiklus het waarskynlik haploïede individue met ongeslagtelike voortplanting gehad. [11] Bakterieë en archaea vertoon 'n lewensiklus soos hierdie, en sommige eukariote blykbaar ook (bv. Cryptophyta, Choanoflagellata, baie Euglenozoa, baie Amoebozoa, 'n paar rooi alge, 'n paar groen alge, die onvolmaakte swamme, sommige rotifers en baie ander groepe) , nie noodwendig haploïed nie). [20] Hierdie eukariote is egter waarskynlik nie primitief aseksueel nie, maar het hul seksuele voortplanting verloor, of dit is nog net nie waargeneem nie. [21] [22] Baie eukariote (insluitend diere en plante) vertoon ongeslagtelike voortplanting, wat fakultatief of verpligtend in die lewensiklus kan wees, met seksuele voortplanting wat meer of minder gereeld voorkom. [23]

Individuele organismes wat aan 'n biologiese lewensiklus deelneem, verouder en sterf gewoonlik, terwyl selle van hierdie organismes wat opeenvolgende lewensiklusgenerasies verbind (kiemlynselle en hul afstammelinge) potensieel onsterflik is. Die basis vir hierdie verskil is 'n fundamentele probleem in die biologie. Die Russiese bioloog en historikus Zhores A. Medvedev [24] het gemeen dat die akkuraatheid van genoomrepliserende en ander sintetiese stelsels alleen nie die onsterflikheid van kiemlyne kan verklaar nie. Medvedev het eerder gedink dat bekende kenmerke van die biochemie en genetika van seksuele voortplanting dui op die teenwoordigheid van unieke inligtingsonderhouds- en herstelprosesse in die gametogenese -stadium van die biologiese lewensiklus. In die besonder, Medwedef van mening dat die belangrikste geleenthede vir inligting instandhouding van kiemselle geskep word deur rekombinasie tydens meiose en DNA herstel hy het dit gesien as prosesse binne die kiem lyn selle wat in staat was om die integriteit van DNA en chromosome te herstel van die tipes skade wat onomkeerbare veroudering veroorsaak in selle wat nie kiem is nie, bv somatiese selle.

Die afkoms van elke hedendaagse sel spoor vermoedelik terug in 'n onafgebroke afstamming vir meer as 3 miljard jaar na die oorsprong van lewe. Dit is eintlik nie selle wat onsterflik is nie, maar multi-generasie sellyne. [25] Die onsterflikheid van 'n sellyn hang af van die handhawing van seldelingpotensiaal. Hierdie potensiaal kan verlore gaan in 'n spesifieke geslag as gevolg van selskade, terminale differensiasie soos in senuweeselle, of geprogrammeerde seldood (apoptose) tydens ontwikkeling. Instandhouding van seldelingspotensiaal van die biologiese lewensiklus oor opeenvolgende generasies hang af van die vermyding en die akkurate herstel van sellulêre skade, veral DNA-skade. By seksuele organismes hang die kontinuïteit van die kiemlyn oor opeenvolgende selsiklusgenerasies af van die doeltreffendheid van prosesse om DNA -skade te vermy en die DNA -skade wat wel voorkom, te herstel. Seksuele prosesse in eukariote, sowel as in prokariote, bied 'n geleentheid vir effektiewe herstel van DNA -skade in die kiemlyn deur homoloë rekombinasie. [25] [26]


Eukariotiese sel (met diagram)

'N Eukariote -sel is die een met 'n georganiseerde kern en verskeie membraanbedekte selorganelle. Behalwe monera, het die selle van alle ander koninkryke eukariotiese organisasie. Selwand is teenwoordig in selle van plante, swamme en sommige protiste.

Dit is afwesig in diereselle en sommige protiste. Muur minder selle is oor die algemeen onreëlmatig. Anders is die interne struktuur van alle selle ietwat soortgelyk. 'N Sel is 'n georganiseerde massa protoplasma omring deur 'n beskermende en selektief deurlaatbare membraan. Protoplasma van 'n sel word protoplast genoem.

Dit bestaan ​​uit sitoplasma, kern en vakuole. Aanvanklik is gedink dat sitoplasma 'n eenvoudige organisasie het. Elektronmikroskoop het getoon dat sitoplasma 'n komplekse organisasie het wat bestaan ​​uit sitoplasmatiese matriks en selorganelle. Daar is sitoskeletale strukture wat nie net beweging na sitoplasma bied nie, maar ook ander lokomotiewe aktiwiteite.

Genetiese materiaal of DNA is georganiseer in chromosome en chromatien. Plantselle beskik oor selwand, plastiede en groot sentrale vakuool. Hulle is afwesig in diereselle. Diereselle beskik oor sentriole wat afwesig is in plantselle.

'N Plantsel bestaan ​​uit selwand en protoplast. Die selwand is afwesig in diereselle. Protoplast dui die hele protoplasma aan wat in 'n sel voorkom.

Dit word gedifferensieer in plasmamembraan (= plasma lemma of selmembraan), sitoplasma, kern en vakuole. Sito&shiplasma is onderskeibaar in sitoplasmiese matriks en organelle. Sitoplasmatiese matriks word ook hyaloplasma genoem. Dit is 'n polifase kolloïdale stelsel wat bestaan ​​in twee toestande, sol en gel.

Die gelvorm kom gewoonlik naby die plasmamembraan voor. Hierdie gebied word soms ectoplast genoem in teenstelling met die sol -gebied wat bekend staan ​​as endoplast. Ectoplast is stewiger. Dit is redelik opvallend aan die vrye kante van die selle. By protosoë is ektoplas aan alle kante prominent.

Sitoplasmiese matriks is oor die algemeen in ewigdurende beweging. Die verskynsel word siklose, sitoplasmiese of protoplasmiese stroming genoem. Sitoplasmiese matriks beslaan die volume van die selle. Dit is die belangrikste arena van sellulêre aktiwiteite wat 'n sel in die lewende toestand hou.

In die sitoplasmiese matriks is 'n groot aantal selorganelle of georganiseerde protoplasmiese subeenhede ingebed met spesifieke funksies.

Dit is endoplasmiese retikulum, plastiede, mitochondria, ribosome, Golgi -liggame, sentriole (sentrale apparaat, sentrosoom), lysos en shyome, sfeerosome, peroksisome, glyoksisome, vakuole, mikrotubules, mikrofilamente, ens. Sommige van hulle het membraanbedekking terwyl ander sonder dieselfde is .

Verdubbeling van membraanbedekking vind plaas rondom plastiede en mitochondria. Enkelmembraanbedekking word oor endoplasmiese retikulum, Golgi-apparaat, lisosome, sferosome, peroksisome, glioksisome en vakuool gevind.

Organelle sonder 'n membraanbedekking is ribosome, mikro­tubules, mikrofilamente en sentrosome of sentriole (in dierselle). Ribosome kom in beide prokariote en eukariote voor. In eukariote -selle kom dit voor in sitoplasmatiese matriks, oor ruwe endoplasmiese retikulum, binne -in plastiede (slegs in plante en sommige protiste en mitochondria aangetref).

Selinsluitings sluit in styselkorrels, glikogeenkorrels, vetdruppels, aleuronkorrels, uitskeidings- of afskeidingsprodukte en kristalle. Kern is ook ingebed in die sitoplasmatiese matriks. Dit word omring deur 'n dubbele membraanomhulsel en bevat nukleoplasma, een of meer nukleoli en chromatien met DNA. DNA is die genetiese materiaal.


Inhoud

Die studie van voortplanting en ontwikkeling by organismes is deur baie plantkundiges en dierkundiges uitgevoer.

Wilhelm Hofmeister het getoon dat afwisseling van geslagte 'n kenmerk is wat plante verenig, en publiseer hierdie resultaat in 1851 (sien plantseksualiteit).

Sommige terme (haplobiont en diplobiont) wat gebruik word vir die beskrywing van lewensiklusse, is aanvanklik deur Nils Svedelius vir alge voorgestel, en is toe vir ander organismes gebruik. [4] [5] Ander terme (outogamie en gamontogamie) wat in protistiese lewensiklusse gebruik word, is deur Karl Gottlieb Grell bekendgestel. [6] Die beskrywing van die komplekse lewensiklusse van verskillende organismes het bygedra tot die afweer van die idees van spontane generasie in die 1840's en 1850's. [7]

'n Sigotiese meiose is 'n meiose van 'n sigoot onmiddellik na karyogamie, wat die samesmelting van twee selkerne is. Op hierdie manier beëindig die organisme sy diploïede fase en produseer verskeie haploïede selle. Hierdie selle verdeel mitoties om groter, meersellige individue of meer haploïede selle te vorm. Twee teenoorgestelde tipes gamete (bv. Manlik en vroulik) van hierdie individue of selle versmelt om 'n sigoot te word.

In die hele siklus is sigote die enigste diploïede sel mitose wat slegs in die haploïede fase voorkom.

Die individue of selle as gevolg van mitose is haplonts, daarom word hierdie lewensiklus ook haplontiese lewensiklus genoem. Haplonts is:

  • In archaeplastidans: sommige groen alge (bv. Chlamydomonas, Zygnema, Chara) [8]
  • In stramenopiele: 'n paar goue alge [8]
  • In alveolate: baie dinoflagellate, bv. Ceratium, Gymnodinium, sommige apicomplexans (bv. Plasmodium) [9]
  • In rhizariërs: sommige eugliewe, [10]ascetospore
  • In opgrawings: 'n paar parabasalyde[11]
  • In amoebosië: Dictyostelium[8]
  • In opisthokonts: die meeste swamme (sommige chytrids, zygomycetes, sommige ascomycetes, basidiomycetes) [8] [12]: 15

In gametiese meiose, in plaas van onmiddellik te verdeel meioties Die sigoot verdeel om haploïede selle te produseer mitoties om 'n meersellige diploïede individu of 'n groep meer eensellige diploïede selle te produseer. Selle van die diploïede individue ondergaan dan meiose om haploïede selle of gamete te produseer. Haploïede selle kan weer verdeel (deur mitose) om meer haploïede selle te vorm, soos in baie giste, maar die haploïede fase is nie die oorheersende lewensiklusfase nie. In die meeste diplonte kom mitose slegs in die diploïede fase voor, dit wil sê gamete vorm gewoonlik vinnig en versmelt om diploïede sigote te produseer.

In die hele siklus is gamete gewoonlik die enigste haploïede selle, en mitose kom gewoonlik slegs in die diploïede fase voor.

Die diploïede meersellige individu is 'n diplont, dus word 'n gametiese meiose ook 'n diplontiese lewensiklus genoem. Diplome is:

  • In archaeplastidans: sommige groen alge (bv. Cladophora glomerata, [13]Acetabularia[8] )
  • By stramenopiele: sommige bruin alge (die Fucales, hul lewensiklus kan egter ook as sterk heteromorf-diplohaplonties geïnterpreteer word, met 'n sterk verminderde gametofietfase, soos in die blomplante), [12]: 207 sommige xantofiete (bv. Vaucheria), [12]: 124 meeste diatomee, [11] 'n paar oomycetes (bv. Saprolegnia, Plasmopara viticola), [8] opaliene, [11] 'n paar "heliozoans" (bv. Actinophrys, Actinosphaerium) [11][14]
  • In alveolate: ciliates [11]
  • In opgrawings: sommige parabasaliede [11]
  • By opisthokonts: diere, sommige swamme (bv. Sommige ascomycetes) [8]

By sporiese meiose (ook algemeen bekend as tussenganger meiose) verdeel die sigoot mitoties om 'n meersellige diploïede sporofiet te produseer. Die sporofiet skep spore via meiose wat ook verdeel dan mitoties-produserende haploïede individue wat gametofiete genoem word. Die gametofiete produseer gamete via mitose. By sommige plante is die gametofiet nie net klein nie, maar ook van korte duur in ander plante en baie alge, die gametofiet is die 'dominante' stadium van die lewensiklus.

  • By archaeplastidans: rooi alge (wat twee sporofiete het), sommige groen alge (bv. Ulva), landplante [8]
  • In stramenopile: meeste bruin alge[8]
  • By rhizarians: baie foraminiferane, [11] plasmodiophoromycetes [8]
  • In amoebozoa: myxogastrids
  • In opisthokonte: sommige swamme (sommige chytriede, sommige askomycete soos die brouersgis) [8]
  • Ander eukariote: haptofiete [11]

Sommige diere het 'n geslagsbepalingsisteem genaamd haplodiploïed, maar dit hou nie verband met die haplodiplontiese lewensiklus nie.

Sommige rooi alge (soos Bonnemaisonia [15] en Lemanea) en groen alge (soos Prasiola) het vegetatiewe meiose, ook genoem somatiese meiose, wat 'n seldsame verskynsel is. [12]: 82 Vegetatiewe meiose kan voorkom in haplodiplontiese en ook in diplontiese lewensiklusse. Die gametofiete bly geheg aan en deel van die sporofiet. Vegetatiewe (nie-reproduktiewe) diploïede selle ondergaan meiose, wat vegetatiewe haploïede selle genereer. Dit ondergaan baie mitose en produseer gamete.

'n Ander verskynsel, genaamd vegetatiewe diploïdisering, 'n tipe apomixis, kom by sommige bruin alge voor (bv. Elachista stellaris). [16] Selle in 'n haploïede deel van die plant dupliseer spontaan hul chromosome om diploïede weefsel te produseer.

Parasiete is afhanklik van die uitbuiting van een of meer gashere. Diegene wat meer as een gasheerspesie moet besmet om hul lewensiklus te voltooi, word gesê dat hulle komplekse of indirekte lewensiklusse het. Dirofilaria immitis, of die hartwurm, het byvoorbeeld 'n indirekte lewensiklus. Die mikrofilariae moet eers deur 'n wyfie muskiet ingeneem word, waar dit in die infektiewe larfstadium ontwikkel. Die muskiet byt dan 'n dier en dra die aansteeklike larwes in die dier oor, waar hulle na die longslagaar migreer en volwasse word. [17]

Daardie parasiete wat 'n enkele spesie besmet, het direkte lewensiklusse. 'N Voorbeeld van 'n parasiet met 'n direkte lewensiklus is Ancylostoma caninum, of die hondehaakwurm. Hulle ontwikkel tot die infektiewe larwestadium in die omgewing, dring dan die vel van die hond direk binne en word volwasse na volwassenes in die dunderm. [18]

As 'n parasiet 'n gegewe gasheer moet besmet om sy lewensiklus te voltooi, word daar gesê dat dit soms 'n verpligte parasiet van die gasheer is; infeksie is fakultatief - die parasiet kan oorleef en sy lewensiklus voltooi sonder om die spesifieke gasheersoort te besmet . Parasiete besmet soms leërskare waarin hulle nie hul lewensiklusse kan voltooi nie, dit is toevallige gashere.

'n Gasheer waarin parasiete seksueel voortplant, staan ​​bekend as die definitiewe, finale of primêre gasheer. By intermediêre gashere reproduseer parasiete óf nie, óf aseksueel, maar die parasiet ontwikkel altyd na 'n nuwe stadium in hierdie tipe gasheer. In sommige gevalle sal 'n parasiet 'n gasheer besmet, maar geen ontwikkeling ondergaan nie, hierdie gashere staan ​​bekend as parateniese [19] of vervoergashere. Die parateniese gasheer kan nuttig wees om die kans te verhoog dat die parasiet na die definitiewe gasheer oorgedra sal word. Byvoorbeeld, die kat longwurm (Aelurostrongylus abstrusus) gebruik 'n slak of slak as 'n tussengasheer die eerste stadium larwe gaan die weekdier binne en ontwikkel tot die derde stadium larwe, wat aansteeklik is vir die definitiewe gasheer - die kat. As 'n muis die slak vreet, sal die derde stadiumlarwe die weefsel van die muis binnedring, maar geen ontwikkeling ondergaan nie.

Die primitiewe tipe lewensiklus het waarskynlik haploïede individue met ongeslagtelike voortplanting gehad. [11] Bakterieë en archaea vertoon 'n lewensiklus soos hierdie, en sommige eukariote blykbaar ook (bv. Cryptophyta, Choanoflagellata, baie Euglenozoa, baie Amoebozoa, 'n paar rooi alge, 'n paar groen alge, die onvolmaakte swamme, sommige rotifers en baie ander groepe) , nie noodwendig haploïed nie). [20] Hierdie eukariote is egter waarskynlik nie primitief aseksueel nie, maar het hul seksuele voortplanting verloor, of dit is nog net nie waargeneem nie. [21] [22] Baie eukariote (insluitend diere en plante) vertoon ongeslagtelike voortplanting, wat fakultatief of verplig kan wees in die lewensiklus, met seksuele voortplanting wat meer of minder gereeld voorkom. [23]

Individuele organismes wat aan 'n biologiese lewensiklus deelneem, verouder gewoonlik en sterf, terwyl selle van hierdie organismes wat opeenvolgende lewensiklusgenerasies (kiemslynselle en hul afstammelinge) verbind, moontlik onsterflik is. Die basis vir hierdie verskil is 'n fundamentele probleem in die biologie. Die Russiese bioloog en historikus Zhores A. Medvedev [24] het gemeen dat die akkuraatheid van genoomrepliserende en ander sintetiese stelsels alleen nie die onsterflikheid van kiemlyne kan verklaar nie. Medvedev het eerder gedink dat bekende kenmerke van die biochemie en genetika van seksuele voortplanting dui op die teenwoordigheid van unieke inligtingsonderhouds- en herstelprosesse in die gametogenese -stadium van die biologiese lewensiklus. Medvedev was veral van mening dat die belangrikste geleenthede vir inligtingonderhoud van kiemselle geskep word deur rekombinasie tydens meiose en DNA -herstel, en hy beskou dit as prosesse binne die kielslynselle wat die integriteit van DNA en chromosome van die tipes skade wat onomkeerbare veroudering in nie-kiemlyn selle veroorsaak, bv somatiese selle.

Die afkoms van elke hedendaagse sel spoor vermoedelik terug in 'n onafgebroke afstamming vir meer as 3 miljard jaar na die oorsprong van lewe. Dit is nie eintlik selle wat onsterflik is nie, maar multi-generasie sel afstammelinge. [25] Die onsterflikheid van 'n sellyn hang af van die handhawing van seldelingpotensiaal. Hierdie potensiaal kan verlore gaan in 'n spesifieke geslag as gevolg van selskade, terminale differensiasie soos in senuweeselle, of geprogrammeerde seldood (apoptose) tydens ontwikkeling. Die handhawing van die seldelingspotensiaal van die biologiese lewensiklus oor opeenvolgende generasies hang af van die vermyding en akkurate herstel van sellulêre skade, veral DNA -skade. By seksuele organismes hang die kontinuïteit van die kiemlyn oor opeenvolgende selsiklusgenerasies af van die doeltreffendheid van prosesse om DNA -skade te vermy en die DNA -skade wat wel voorkom, te herstel. Seksuele prosesse in eukariote, sowel as in prokariote, bied 'n geleentheid vir effektiewe herstel van DNA-skade in die kiemlyn deur homoloë rekombinasie. [25] [26]


Swam diversiteit

Die koninkryk Fungi bevat vier groot afdelings wat volgens hul manier van seksuele voortplanting tot stand gekom het. Polifiletiese, onverwante swamme wat voortplant sonder 'n seksuele siklus, word gerieflikheidshalwe in 'n vyfde afdeling geplaas, en 'n sesde groot swamgroep wat nie goed by enige van die vorige vyf pas nie, is onlangs beskryf. Nie alle mikoloë stem saam met hierdie skema nie. Vinnige vooruitgang in molekulêre biologie en die opeenvolging van 18S rRNA ('n komponent van ribosome) onthul steeds nuwe en verskillende verwantskappe tussen die verskillende kategorieë swamme.

Die tradisionele afdelings van Swamme is die Chytridiomycota (chytrids), die Zygomycota (gekonjugeerde swamme), die Ascomycota (sak swamme) en die Basidiomycota (klub swamme). 'N Ouer klassifikasieskema het swamme gegroepeer wat ongeslagtelike voortplanting streng gebruik in Deuteromycota, 'n groep wat nie meer gebruik word nie. Die Glomeromycota behoort aan 'n nuut beskryfde groep ([Figuur 5]).

Figuur 5: Afdelings van swamme sluit in (a) chytrids, (b) gekonjugeerde swamme, (c) sak swamme, en (d) klub swamme. (krediet a: wysiging van werk deur USDA APHIS PPQ krediet c: wysiging van werk deur “icelight ”/Flickr krediet d: wysiging van werk deur Cory Zanker.)


Gesoek: loriciferans, dood of lewendig

Die huidige debat moet nie net die rente fokus op die ou dooie of lewende kwessie van die Wilde Weste nie, maar ook op die ryk biologie in hierdie habitats en die belangrikheid van die verkryging van nuwe monsters uit die betrokke sedimente en soortgelyke habitats. Daar is inderdaad geen debat oor die vermoë van eensellige eukariote om in die anoksiese pekel te oorleef nie, en daar is ook geen debat oor diere wat op die rand van die anoksiese sone [3] leef nie. Die probleem is die vermoë van metazoane (meersellige eukariote) om in die streng anaeorbiese sone te oorleef. Ideaal gesproke sou 'n mens bewyse wil sien vir aktief getranskribeerde gene in loriciferane uit hierdie habitats. Dit sal ons ook baie vertel oor hoe hulle groei met betrekking tot kernkoolstof- en energiemetabolisme. In die besonder wil u weet of hierdie diere die gene bevat wat protiste gebruik om in anaërobiese omgewings te oorleef, soos [FeFe] -hidrogenase, pyruvat: ferredoksienoksidoreduktase, bifunksionele alkoholdehidrogenase E (ADHE), asetiel- CoA synthase (ADP forming), and the like [4], or whether they have some other means of surviving without oxygen. It is perhaps more likely that they use strategies more similar to those found in the anaerobic mitochondria of parasitic animals, for example, malate dismutation with the involvement of rhodoquinone [4].

As a long shot alternative, if the animals are alive, it is even imaginable that they have acquired genes via lateral gene transfer (LGT) for a new strategy to survive anoxia. Indeed, some camps argue that all eukaryotes are ancestrally strict aerobes and that the ability of eukaryotes to survive anoxia is always the result of lateral gene transfer [9]. We do not agree with that view, mainly for three reasons. First, the eukaryotic anaerobes studied so far always have the same basic carbon and energy metabolic backbone [4] and if LGT was behind eukaryote anaerobiosis, then eukaryotic anaerobes should be as physiologically diverse as prokaryotic anaerobes, which is definitely not the case energy metabolism based on sulfate reduction [10], which is lacking in eukaryotes, is a strong case in point. Second, the Earth sciences tell us that anaerobic habitats are ancient and that aerobic habitats are recent [8]. So, if anything, we should be seeing LGT as a means of improving mitochondrial function in aerobic habitats. For example, aerobic methane oxidation is a very widespread form of energy metabolism in prokaryotes but we don’t see eukaryotes that have acquired genes to do that rather, eukaryotes possess one ancestrally present stock of enzymes [4]. Third, it is often proposed that one lineage of eukaryotes acquires one or the other anaerobic enzyme via LGT from prokaryotes and then passes it around via eukaryote to eukaryote LGT in order to account for the monophyly of the eukaryote enzymes involved. That idea has been specifically tested at the whole-genome level, and rejected, whereby the “patchy gene distributions” that are often seen as the hallmark of LGT are actually better explained by differential loss than they are by LGT [11].

Of course it might also turn out that the loriciferans from the habitats in question do not show vital signs of gene expression. It might be that they are dead, not alive. There is only one way to find out: biologists will have to go back out to those deep environments and get new samples.


TCA cycle signalling and the evolution of eukaryotes

A major question remaining in the field of evolutionary biology is how prokaryotic organisms made the leap to complex eukaryotic life. The prevailing theory depicts the origin of eukaryotic cell complexity as emerging from the symbiosis between an α-proteobacterium, the ancestor of present-day mitochondria, and an archaeal host (endosymbiont theory). A primary contribution of mitochondria to eukaryogenesis has been attributed to the mitochondrial genome, which enabled the successful internalisation of bioenergetic membranes and facilitated remarkable genome expansion. It has also been postulated that a key contribution of the archaeal host during eukaryogenesis was in providing 'archaeal histones' that would enable compaction and regulation of an expanded genome. Yet, how the communication between the host and the symbiont evolved is unclear. Here, we propose an evolutionary concept in which mitochondrial TCA cycle signalling was also a crucial player during eukaryogenesis enabling the dynamic control of an expanded genome via regulation of DNA and histone modifications. Furthermore, we discuss how TCA cycle remodelling is a common evolutionary strategy invoked by eukaryotic organisms to coordinate stress responses and gene expression programmes, with a particular focus on the TCA cycle-derived metabolite itaconate.

Copyright © 2020 Elsevier Ltd. All rights reserved.

Syfers

Overview of all 8 chemical reactions of the TCA cycle…

Figure 2. The endosymbiont and entangle-engulf-endogenize (E3)…

Figure 2. The endosymbiont and entangle-engulf-endogenize (E3) hypothesis

Overview of the endosymbiont/E3 hypothesis. (A) Lokiarchaeon…

Figure 3. The acquisition of mitochondria supported…

Figure 3. The acquisition of mitochondria supported the emergence of multicellularity

Heterotrophic prokaryotes with low…

Figure 4. An evolutionary timeline of eukaryotic…

Figure 4. An evolutionary timeline of eukaryotic cell development

In our proposed timeline, the TCA…

Figure 5. How TCA cycle signalling may…

Figure 5. How TCA cycle signalling may have contributed to eukaryogenesis by acting as a…


Inhoud

The eukaryotic cell cycle consists of four distinct phases: G1 phase, S phase (synthesis), G2 phase (collectively known as interphase) and M phase (mitosis and cytokinesis). M phase is itself composed of two tightly coupled processes: mitosis, in which the cell's nucleus divides, and cytokinesis, in which the cell's cytoplasm divides forming two daughter cells. Activation of each phase is dependent on the proper progression and completion of the previous one. Cells that have temporarily or reversibly stopped dividing are said to have entered a state of quiescence called G0 fase.

Staat Fase Afkorting Beskrywing
Resting Gap 0 G0 A phase where the cell has left the cycle and has stopped dividing.
Interfase Gap 1 G1 Cells increase in size in Gap 1. The G1 kontrolepunt control mechanism ensures that everything is ready for DNA synthesis.
Sintese S DNA replication occurs during this phase.
Gap 2 G2 During the gap between DNA synthesis and mitosis, the cell will continue to grow. Die G2 kontrolepunt control mechanism ensures that everything is ready to enter the M (mitosis) phase and divide.
Seldeling Mitose M. Cell growth stops at this stage and cellular energy is focused on the orderly division into two daughter cells. A checkpoint in the middle of mitosis (Metaphase Checkpoint) ensures that the cell is ready to complete cell division.

Na seldeling begin elk van die dogterselle die interfase van 'n nuwe siklus. Although the various stages of interphase are not usually morphologically distinguishable, each phase of the cell cycle has a distinct set of specialized biochemical processes that prepare the cell for initiation of cell division.

G0 phase (quiescence) Edit

G0 is a resting phase where the cell has left the cycle and has stopped dividing. The cell cycle starts with this phase. Non-proliferative (non-dividing) cells in multicellular eukaryotes generally enter the quiescent G0 state from G1 and may remain quiescent for long periods of time, possibly indefinitely (as is often the case for neurons). This is very common for cells that are fully differentiated. Some cells enter the G0 phase semi-permanently and are considered post-mitotic, e.g., some liver, kidney, and stomach cells. Many cells do not enter G0 and continue to divide throughout an organism's life, e.g., epithelial cells.

The word "post-mitotic" is sometimes used to refer to both quiescent and senescent cells. Cellular senescence occurs in response to DNA damage and external stress and usually constitutes an arrest in G1. Cellular senescence may make a cell's progeny nonviable it is often a biochemical alternative to the self-destruction of such a damaged cell by apoptosis.

Interphase Edit

Interphase is a series of changes that takes place in a newly formed cell and its nucleus before it becomes capable of division again. It is also called preparatory phase or intermitosis. Typically interphase lasts for at least 91% of the total time required for the cell cycle.

Interphase proceeds in three stages, G1, S en G.2, followed by the cycle of mitosis and cytokinesis. The cell's nuclear DNA contents are duplicated during S phase.

G1 phase (First growth phase or Post mitotic gap phase) Edit

The first phase within interphase, from the end of the previous M phase until the beginning of DNA synthesis, is called G1 (G indicating gaping). It is also called the growth phase. During this phase, the biosynthetic activities of the cell, which are considerably slowed down during M phase, resume at a high rate. The duration of G1 is highly variable, even among different cells of the same species. [3] In this phase, the cell increases its supply of proteins, increases the number of organelles (such as mitochondria, ribosomes), and grows in size. In G1 phase, a cell has three options.

  • To continue cell cycle and enter S phase
  • Stop cell cycle and enter G0 phase for undergoing differentiation.
  • Become arrested in G1 phase hence it may enter G0 phase or re-enter cell cycle.

The deciding point is called check point (Restriction point). This check point is called the restriction point or START and is regulated by G1/S cyclins, which cause transition from G1 to S phase. Passage through the G1 check point commits the cell to division.

S phase (DNA replication) Edit

The ensuing S phase starts when DNA synthesis commences when it is complete, all of the chromosomes have been replicated, i.e., each chromosome consists of two sister chromatids. Thus, during this phase, the amount of DNA in the cell has doubled, though the ploidy and number of chromosomes are unchanged. Rates of RNA transcription and protein synthesis are very low during this phase. An exception to this is histone production, most of which occurs during the S phase. [4] [5] [6]

G2 phase (growth) Edit

G2 phase occurs after DNA replication and is a period of protein synthesis and rapid cell growth to prepare the cell for mitosis. During this phase microtubules begin to reorganize to form a spindle (preprophase). Before proceeding to mitotic phase, cells must be checked at the G2 checkpoint for any DNA damage within the chromosomes. Die G.2 checkpoint is mainly regulated by the tumor protein p53. If the DNA is damaged, p53 will either repair the DNA or trigger the apoptosis of the cell. If p53 is dysfunctional or mutated, cells with damaged DNA may continue through the cell cycle, leading to the development of cancer.

Mitotic phase (chromosome separation) Edit

The relatively brief M phase consists of nuclear division (karyokinesis). It is a relatively short period of the cell cycle. M phase is complex and highly regulated. The sequence of events is divided into phases, corresponding to the completion of one set of activities and the start of the next. These phases are sequentially known as:

Mitosis is the process by which a eukaryotic cell separates the chromosomes in its cell nucleus into two identical sets in two nuclei. [7] During the process of mitosis the pairs of chromosomes condense and attach to microtubules that pull the sister chromatids to opposite sides of the cell. [8]

Mitosis occurs exclusively in eukaryotic cells, but occurs in different ways in different species. For example, animal cells undergo an "open" mitosis, where the nuclear envelope breaks down before the chromosomes separate, while fungi such as Aspergillus nidulans en Saccharomyces cerevisiae (yeast) undergo a "closed" mitosis, where chromosomes divide within an intact cell nucleus. [9]

Cytokinesis phase (separation of all cell components) Edit

Mitosis is immediately followed by cytokinesis, which divides the nuclei, cytoplasm, organelles and cell membrane into two cells containing roughly equal shares of these cellular components. Mitosis and cytokinesis together define the division of the mother cell into two daughter cells, genetically identical to each other and to their parent cell. This accounts for approximately 10% of the cell cycle.

Because cytokinesis usually occurs in conjunction with mitosis, "mitosis" is often used interchangeably with "M phase". However, there are many cells where mitosis and cytokinesis occur separately, forming single cells with multiple nuclei in a process called endoreplication. This occurs most notably among the fungi and slime molds, but is found in various groups. Even in animals, cytokinesis and mitosis may occur independently, for instance during certain stages of fruit fly embryonic development. [10] Errors in mitosis can result in cell death through apoptosis or cause mutations that may lead to cancer.

Regulation of the cell cycle involves processes crucial to the survival of a cell, including the detection and repair of genetic damage as well as the prevention of uncontrolled cell division. The molecular events that control the cell cycle are ordered and directional that is, each process occurs in a sequential fashion and it is impossible to "reverse" the cycle.

Role of cyclins and CDKs Edit

Two key classes of regulatory molecules, cyclins and cyclin-dependent kinases (CDKs), determine a cell's progress through the cell cycle. [11] Leland H. Hartwell, R. Timothy Hunt, and Paul M. Nurse won the 2001 Nobel Prize in Physiology or Medicine for their discovery of these central molecules. [12] Many of the genes encoding cyclins and CDKs are conserved among all eukaryotes, but in general, more complex organisms have more elaborate cell cycle control systems that incorporate more individual components. Many of the relevant genes were first identified by studying yeast, especially Saccharomyces cerevisiae [13] genetic nomenclature in yeast dubs many of these genes cdc (for "cell division cycle") followed by an identifying number, e.g. cdc25 of cdc20.

Cyclins form the regulatory subunits and CDKs the catalytic subunits of an activated heterodimer cyclins have no catalytic activity and CDKs are inactive in the absence of a partner cyclin. When activated by a bound cyclin, CDKs perform a common biochemical reaction called phosphorylation that activates or inactivates target proteins to orchestrate coordinated entry into the next phase of the cell cycle. Different cyclin-CDK combinations determine the downstream proteins targeted. CDKs are constitutively expressed in cells whereas cyclins are synthesised at specific stages of the cell cycle, in response to various molecular signals. [14]

General mechanism of cyclin-CDK interaction Edit

Upon receiving a pro-mitotic extracellular signal, G1 cyclin-CDK complexes become active to prepare the cell for S phase, promoting the expression of transcription factors that in turn promote the expression of S cyclins and of enzymes required for DNA replication. Die G.1 cyclin-CDK complexes also promote the degradation of molecules that function as S phase inhibitors by targeting them for ubiquitination. Once a protein has been ubiquitinated, it is targeted for proteolytic degradation by the proteasome. However, results from a recent study of E2F transcriptional dynamics at the single-cell level argue that the role of G1 cyclin-CDK activities, in particular cyclin D-CDK4/6, is to tune the timing rather than the commitment of cell cycle entry. [15]

Active S cyclin-CDK complexes phosphorylate proteins that make up the pre-replication complexes assembled during G1 phase on DNA replication origins. The phosphorylation serves two purposes: to activate each already-assembled pre-replication complex, and to prevent new complexes from forming. This ensures that every portion of the cell's genome will be replicated once and only once. The reason for prevention of gaps in replication is fairly clear, because daughter cells that are missing all or part of crucial genes will die. However, for reasons related to gene copy number effects, possession of extra copies of certain genes is also deleterious to the daughter cells.

Mitotic cyclin-CDK complexes, which are synthesized but inactivated during S and G2 phases, promote the initiation of mitosis by stimulating downstream proteins involved in chromosome condensation and mitotic spindle assembly. A critical complex activated during this process is a ubiquitin ligase known as the anaphase-promoting complex (APC), which promotes degradation of structural proteins associated with the chromosomal kinetochore. APC also targets the mitotic cyclins for degradation, ensuring that telophase and cytokinesis can proceed. [16]

Specific action of cyclin-CDK complexes Edit

Cyclin D is the first cyclin produced in the cells that enter the cell cycle, in response to extracellular signals (e.g. growth factors). Cyclin D levels stay low in resting cells that are not proliferating. Additionally, CDK4/6 and CDK2 are also inactive because CDK4/6 are bound by INK4 family members (e.g., p16), limiting kinase activity. Meanwhile, CDK2 complexes are inhibited by the CIP/KIP proteins such as p21 and p27, [17] When it is time for a cell to enter the cell cycle, which is triggered by a mitogenic stimuli, levels of cyclin D increase. In response to this trigger, cyclin D binds to existing CDK4/6, forming the active cyclin D-CDK4/6 complex. Cyclin D-CDK4/6 complexes in turn mono-phosphorylates the retinoblastoma susceptibility protein (Rb) to pRb. The un-phosphorylated Rb tumour suppressor functions in inducing cell cycle exit and maintaining G0 arrest (senescence). [18]

In the last few decades, a model has been widely accepted whereby pRB proteins are inactivated by cyclin D-Cdk4/6-mediated phosphorylation. Rb has 14+ potential phosphorylation sites. Cyclin D-Cdk 4/6 progressively phosphorylates Rb to hyperphosphorylated state, which triggers dissociation of pRB–E2F complexes, thereby inducing G1/S cell cycle gene expression and progression into S phase. [19]

However, scientific observations from a recent study show that Rb is present in three types of isoforms: (1) un-phosphorylated Rb in G0 state (2) mono-phosphorylated Rb, also referred to as "hypo-phosphorylated' or 'partially' phosphorylated Rb in early G1 state and (3) inactive hyper-phosphorylated Rb in late G1 state. [20] [21] [22] In early G1 cells, mono-phosphorylated Rb exits as 14 different isoforms, one of each has distinct E2F binding affinity. [22] Rb has been found to associate with hundreds of different proteins [23] and the idea that different mono-phosphorylated Rb isoforms have different protein partners was very appealing. [24] A recent report confirmed that mono-phosphorylation controls Rb's association with other proteins and generates functional distinct forms of Rb. [25] All different mono-phosphorylated Rb isoforms inhibit E2F transcriptional program and are able to arrest cells in G1-phase. Importantly, different mono-phosphorylated forms of RB have distinct trans criptional outputs that are extended beyond E2F regulation. [25]

In general, the binding of pRb to E2F inhibits the E2F target gene expression of certain G1/S and S transition genes including E-type cyclins. The partial phosphorylation of RB de-represses the Rb-mediated suppression of E2F target gene expression, begins the expression of cyclin E. The molecular mechanism that causes the cell switched to cyclin E activation is currently not known, but as cyclin E levels rise, the active cyclin E-CDK2 complex is formed, bringing Rb to be inactivated by hyper-phosphorylation. [22] Hyperphosphorylated Rb is completely dissociated from E2F, enabling further expression of a wide range of E2F target genes are required for driving cells to proceed into S phase [1]. Recently, it has been identified that cyclin D-Cdk4/6 binds to a C-terminal alpha-helix region of Rb that is only distinguishable to cyclin D rather than other cyclins, cyclin E, A and B. [26] This observation based on the structural analysis of Rb phosphorylation supports that Rb is phosphorylated in a different level through multiple Cyclin-Cdk complexes. This also makes feasible the current model of a simultaneous switch-like inactivation of all mono-phosphorylated Rb isoforms through one type of Rb hyper-phosphorylation mechanism. In addition, mutational analysis of the cyclin D- Cdk 4/6 specific Rb C-terminal helix shows that disruptions of cyclin D-Cdk 4/6 binding to Rb prevents Rb phosphorylation, arrests cells in G1, and bolsters Rb's functions in tumor suppressor. [26] This cyclin-Cdk driven cell cycle transitional mechanism governs a cell committed to the cell cycle that allows cell proliferation. A cancerous cell growth often accompanies with deregulation of Cyclin D-Cdk 4/6 activity.

The hyperphosphorylated Rb dissociates from the E2F/DP1/Rb complex (which was bound to the E2F responsive genes, effectively "blocking" them from transcription), activating E2F. Activation of E2F results in transcription of various genes like cyclin E, cyclin A, DNA polymerase, thymidine kinase, etc. Cyclin E thus produced binds to CDK2, forming the cyclin E-CDK2 complex, which pushes the cell from G1 to S phase (G1/S, which initiates the G2/M transition). [27] Cyclin B-cdk1 complex activation causes breakdown of nuclear envelope and initiation of prophase, and subsequently, its deactivation causes the cell to exit mitosis. [14] A quantitative study of E2F transcriptional dynamics at the single-cell level by using engineered fluorescent reporter cells provided a quantitative framework for understanding the control logic of cell cycle entry, challenging the canonical textbook model. Genes that regulate the amplitude of E2F accumulation, such as Myc, determine the commitment in cell cycle and S phase entry. G1 cyclin-CDK activities are not the driver of cell cycle entry. Instead, they primarily tune the timing of E2F increase, thereby modulating the pace of cell cycle progression. [15]

Inhibitors Edit

Endogenous Edit

Two families of genes, the cip/kip (CDK interacting protein/Kinase inhibitory protein) family and the INK4a/ARF (Inhibitor of Kinase 4/Alternative Reading Frame) family, prevent the progression of the cell cycle. Because these genes are instrumental in prevention of tumor formation, they are known as tumor suppressors.

Die cip/kip gesin includes the genes p21, p27 and p57. They halt the cell cycle in G1 phase by binding to and inactivating cyclin-CDK complexes. p21 is activated by p53 (which, in turn, is triggered by DNA damage e.g. due to radiation). p27 is activated by Transforming Growth Factor β (TGF β), a growth inhibitor.

Die INK4a/ARF family includes p16 INK4a , which binds to CDK4 and arrests the cell cycle in G1 phase, and p14 ARF which prevents p53 degradation.

Synthetic Edit

Synthetic inhibitors of Cdc25 could also be useful for the arrest of cell cycle and therefore be useful as antineoplastic and anticancer agents. [28]

Many human cancers possess the hyper-activated Cdk 4/6 activities. [29] Given the observations of cyclin D-Cdk 4/6 functions, inhibition of Cdk 4/6 should result in preventing a malignant tumor from proliferating. Consequently, scientists have tried to invent the synthetic Cdk4/6 inhibitor as Cdk4/6 has been characterized to be a therapeutic target for anti-tumor effectiveness. Three Cdk4/6 inhibitors - palbociclib, ribociclib, and abemaciclib - currently received FDA approval for clinical use to treat advanced-stage or metastatic, hormone-receptor-positive (HR-positive, HR+), HER2-negative (HER2-) breast cancer. [30] [31] For example, palbociclib is an orally active CDK4/6 inhibitor which has demonstrated improved outcomes for ER-positive/HER2-negative advanced breast cancer. The main side effect is neutropenia which can be managed by dose reduction. [32]

Cdk4/6 targeted therapy will only treat cancer types where Rb is expressed. Cancer cells with loss of Rb have primary resistance to Cdk4/6 inhibitors.

Transcriptional regulatory network Edit

Current evidence suggests that a semi-autonomous transcriptional network acts in concert with the CDK-cyclin machinery to regulate the cell cycle. Several gene expression studies in Saccharomyces cerevisiae have identified 800–1200 genes that change expression over the course of the cell cycle. [13] [33] [34] They are transcribed at high levels at specific points in the cell cycle, and remain at lower levels throughout the rest of the cycle. While the set of identified genes differs between studies due to the computational methods and criteria used to identify them, each study indicates that a large portion of yeast genes are temporally regulated. [35]

Many periodically expressed genes are driven by transcription factors that are also periodically expressed. One screen of single-gene knockouts identified 48 transcription factors (about 20% of all non-essential transcription factors) that show cell cycle progression defects. [36] Genome-wide studies using high throughput technologies have identified the transcription factors that bind to the promoters of yeast genes, and correlating these findings with temporal expression patterns have allowed the identification of transcription factors that drive phase-specific gene expression. [33] [37] The expression profiles of these transcription factors are driven by the transcription factors that peak in the prior phase, and computational models have shown that a CDK-autonomous network of these transcription factors is sufficient to produce steady-state oscillations in gene expression). [34] [38]

Experimental evidence also suggests that gene expression can oscillate with the period seen in dividing wild-type cells independently of the CDK machinery. Orlando et al. used microarrays to measure the expression of a set of 1,271 genes that they identified as periodic in both wild type cells and cells lacking all S-phase and mitotic cyclins (clb1,2,3,4,5,6). Of the 1,271 genes assayed, 882 continued to be expressed in the cyclin-deficient cells at the same time as in the wild type cells, despite the fact that the cyclin-deficient cells arrest at the border between G1 and S phase. However, 833 of the genes assayed changed behavior between the wild type and mutant cells, indicating that these genes are likely directly or indirectly regulated by the CDK-cyclin machinery. Some genes that continued to be expressed on time in the mutant cells were also expressed at different levels in the mutant and wild type cells. These findings suggest that while the transcriptional network may oscillate independently of the CDK-cyclin oscillator, they are coupled in a manner that requires both to ensure the proper timing of cell cycle events. [34] Other work indicates that phosphorylation, a post-translational modification, of cell cycle transcription factors by Cdk1 may alter the localization or activity of the transcription factors in order to tightly control timing of target genes. [36] [39] [40]

While oscillatory transcription plays a key role in the progression of the yeast cell cycle, the CDK-cyclin machinery operates independently in the early embryonic cell cycle. Before the midblastula transition, zygotic transcription does not occur and all needed proteins, such as the B-type cyclins, are translated from maternally loaded mRNA. [41]

DNA replication and DNA replication origin activity Edit

Analyses of synchronized cultures of Saccharomyces cerevisiae under conditions that prevent DNA replication initiation without delaying cell cycle progression showed that origin licensing decreases the expression of genes with origins near their 3' ends, revealing that downstream origins can regulate the expression of upstream genes. [42] This confirms previous predictions from mathematical modeling of a global causal coordination between DNA replication origin activity and mRNA expression, [43] [44] [45] and shows that mathematical modeling of DNA microarray data can be used to correctly predict previously unknown biological modes of regulation.

Cell cycle checkpoints are used by the cell to monitor and regulate the progress of the cell cycle. [46] Checkpoints prevent cell cycle progression at specific points, allowing verification of necessary phase processes and repair of DNA damage. The cell cannot proceed to the next phase until checkpoint requirements have been met. Checkpoints typically consist of a network of regulatory proteins that monitor and dictate the progression of the cell through the different stages of the cell cycle.

It is estimated that in normal human cells about 1% of single-strand DNA damages are converted to about 50 endogenous DNA double-strand breaks per cell per cell cycle. [47] Although such double-strand breaks are usually repaired with high fidelity, errors in their repair are considered to contribute significantly to the rate of cancer in humans. [47]

There are several checkpoints to ensure that damaged or incomplete DNA is not passed on to daughter cells. Three main checkpoints exist: the G1/S checkpoint, the G2/M checkpoint and the metaphase (mitotic) checkpoint. Another checkpoint is the Go checkpoint, in which the cells are checked for maturity. If the cells fail to pass this checkpoint by not being ready yet, they will be discarded from dividing.

G1/S transition is a rate-limiting step in the cell cycle and is also known as restriction point. [14] This is where the cell checks whether it has enough raw materials to fully replicate its DNA (nucleotide bases, DNA synthase, chromatin, etc.). An unhealthy or malnourished cell will get stuck at this checkpoint.

Die G.2/M checkpoint is where the cell ensures that it has enough cytoplasm and phospholipids for two daughter cells. But sometimes more importantly, it checks to see if it is the right time to replicate. There are some situations where many cells need to all replicate simultaneously (for example, a growing embryo should have a symmetric cell distribution until it reaches the mid-blastula transition). This is done by controlling the G2/M checkpoint.

The metaphase checkpoint is a fairly minor checkpoint, in that once a cell is in metaphase, it has committed to undergoing mitosis. However that's not to say it isn't important. In this checkpoint, the cell checks to ensure that the spindle has formed and that all of the chromosomes are aligned at the spindle equator before anaphase begins. [48]

While these are the three "main" checkpoints, not all cells have to pass through each of these checkpoints in this order to replicate. Many types of cancer are caused by mutations that allow the cells to speed through the various checkpoints or even skip them altogether. Going from S to M to S phase almost consecutively. Because these cells have lost their checkpoints, any DNA mutations that may have occurred are disregarded and passed on to the daughter cells. This is one reason why cancer cells have a tendency to exponentially accrue mutations. Aside from cancer cells, many fully differentiated cell types no longer replicate so they leave the cell cycle and stay in G0 until their death. Thus removing the need for cellular checkpoints. An alternative model of the cell cycle response to DNA damage has also been proposed, known as the postreplication checkpoint.

Checkpoint regulation plays an important role in an organism's development. In sexual reproduction, when egg fertilization occurs, when the sperm binds to the egg, it releases signalling factors that notify the egg that it has been fertilized. Among other things, this induces the now fertilized oocyte to return from its previously dormant, G0, state back into the cell cycle and on to mitotic replication and division.

p53 plays an important role in triggering the control mechanisms at both G1/S and G2/M checkpoints. In addition to p53, checkpoint regulators are being heavily researched for their roles in cancer growth and proliferation.

Pioneering work by Atsushi Miyawaki and coworkers developed the fluorescent ubiquitination-based cell cycle indicator (FUCCI), which enables fluorescence imaging of the cell cycle. Originally, a green fluorescent protein, mAG, was fused to hGem(1/110) and an orange fluorescent protein (mKO2) was fused to hCdt1(30/120). Note, these fusions are fragments that contain a nuclear localization signal and ubiquitination sites for degradation, but are not functional proteins. The green fluorescent protein is made during the S, G2, or M phase and degraded during the G0 of G.1 phase, while the orange fluorescent protein is made during the G0 of G.1 phase and destroyed during the S, G2, or M phase. [49] A far-red and near-infrared FUCCI was developed using a cyanobacteria-derived fluorescent protein (smURFP) and a bacteriophytochrome-derived fluorescent protein (movie found at this link). [50]

A disregulation of the cell cycle components may lead to tumor formation. [51] As mentioned above, when some genes like the cell cycle inhibitors, RB, p53 etc. mutate, they may cause the cell to multiply uncontrollably, forming a tumor. Although the duration of cell cycle in tumor cells is equal to or longer than that of normal cell cycle, the proportion of cells that are in active cell division (versus quiescent cells in G0 phase) in tumors is much higher than that in normal tissue. [ aanhaling nodig ] Thus there is a net increase in cell number as the number of cells that die by apoptosis or senescence remains the same.

The cells which are actively undergoing cell cycle are targeted in cancer therapy as the DNA is relatively exposed during cell division and hence susceptible to damage by drugs or radiation. This fact is made use of in cancer treatment by a process known as debulking, a significant mass of the tumor is removed which pushes a significant number of the remaining tumor cells from G0 to G1 phase (due to increased availability of nutrients, oxygen, growth factors etc.). Radiation or chemotherapy following the debulking procedure kills these cells which have newly entered the cell cycle. [14]

The fastest cycling mammalian cells in culture, crypt cells in the intestinal epithelium, have a cycle time as short as 9 to 10 hours. Stem cells in resting mouse skin may have a cycle time of more than 200 hours. Most of this difference is due to the varying length of G1, the most variable phase of the cycle. M and S do not vary much.

In general, cells are most radiosensitive in late M and G2 phases and most resistant in late S phase.

For cells with a longer cell cycle time and a significantly long G1 phase, there is a second peak of resistance late in G1.

The pattern of resistance and sensitivity correlates with the level of sulfhydryl compounds in the cell. Sulfhydryls are natural substances that protect cells from radiation damage and tend to be at their highest levels in S and at their lowest near mitosis.

Homologous recombination (HR) is an accurate process for repairing DNA double-strand breaks. HR is nearly absent in G1 phase, is most active in S phase, and declines in G2/M. [52] Non-homologous end joining, a less accurate and more mutagenic process for repairing double strand breaks, is active throughout the cell cycle.


Coupling of S Phase to M Phase

Die G.2 checkpoint prevents the initiation of mitosis prior to the completion of S phase, thereby ensuring that incompletely replicated DNA is not distributed to daughter cells. It is equally important to ensure that the genome is replicated only once per cell cycle. Thus, once DNA has been replicated, control mechanisms must exist to prevent initiation of a new S phase prior to mitosis. These controls prevent cells in G2 from reentering S phase and block the initiation of another round of DNA replication until after mitosis, at which point the cell has entered the G1 phase of the next cell cycle.

Initial insights into this dependence of S phase on M phase came from cell fusion experiments of Potu Rao and Robert Johnson in 1970 (Figure 14.10). These investigators isolated cells in different phases of the cycle and then fused these cells to each other to form cell hybrids. When G1 cells were fused with S phase cells, the G1 nucleus immediately began to synthesize DNA. Thus, the cytoplasm of S phase cells contained factors that initiated DNA synthesis in the G1 kern. Fusing G2 cells with S phase cells, however, yielded a quite different result: The G2 nucleus was unable to initiate DNA synthesis even in the presence of an S phase cytoplasm. It thus appeared that DNA synthesis in the G2 nucleus was prevented by a mechanism that blocked rereplication of the genome until after mitosis had taken place.

Figure 14.10

Cell fusion experiments demonstrating the dependence of S phase on M phase. Cells in S phase were fused either to cells in G1 or to cells in G2. When G1 cells were fused with S phase cells, the G1 nucleus immediately began to replicate DNA. In contrast, (more. )

The molecular mechanism that restricts DNA replication to once per cell cycle involves the action of a family of proteins (called MCM proteins) that bind to replication origins together with the origin replication complex (ORC) proteins (see Figure 5.17). The MCM proteins act as “licensing factors” that allow replication to initiate (Figure 14.11). Their binding to DNA is regulated during the cell cycle such that the MCM proteins are only able to bind to replication origins during G1, allowing DNA replication to initiate when the cell enters S phase. Once initiation has occurred, however, the MCM proteins are displaced from the origin, so replication cannot initiate again until the cell passes through mitosis and enters G1 phase of the next cell cycle.

Figure 14.11

Restriction of DNA replication. DNA replication is restricted to once per cell cycle by MCM proteins that bind to origins of replication together with ORC (origin replication complex) proteins and are required for the initiation of DNA replication. MCM (more. )

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