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Hoeveel DNA het mense?

Hoeveel DNA het mense?


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'n Normale menslike liggaam het ongeveer 3 miljard basispare. Gegewe dat mense 10 triljoen selle het, hoe is die aantal basispare DNA minder as die aantal selle? Dit kan net gebeur as die meeste van hierdie selle nie DNA het nie, of het ek die onderwerp verkeerd verstaan?

Kan jy 'n uiteensetting gee van hoekom die aantal selle die aantal DNS-basispare aansienlik oorskry? Is dit nie logies om meer DNS-basispare as die aantal selle te hê nie?


Antwoord op die vraag

Hoeveel DNA is daar in ons selkerne?

By mense is daar ongeveer 6 biljoen basispare in die kern van elke sel. Hoekom 6 miljard en nie 3 nie? Daar is 3 biljoen basispare per haploïede genoom (sien ploïdie) en dus 6 biljoen basispare vir die hele genoom. Hierdie getal kan eintlik verder verdubbel tydens spesifieke fases van die selsiklus. Elke enkele sel bevat 'n kopie van die hele genoom (met 'n paar uitsonderings soos byvoorbeeld rooibloedselle).

Dus is die totale aantal basispare in 'n 10 triljoen selle individue ongeveer $6cdot 10^9 cdot 10^{13} = 6cdot 10^{22}$ basis pare.

Verdere inligting vir pret

Hoeveel DNA in ons selle buite kerne

Nou, in selle is daar DNA buite kerne. By diere (insluitend mense) het ons DNA ook in mitochondria. daar is van die orde van 104104 basispare per mitochondria (16 569 plekke om akkuraat te wees) en daar is van die orde van 104104 mitochondria per sel, dit is 108108 basispare totaal per sel wat slegs een orde van grootte onder die aantal basisse is pare in die kern per sel.

Daar is dus 'n ekstra $3cdot 10^8 cdot 10^{13} = 3cdot 10^{21}$ basispare in selle buite die kern.

Hoeveel DNA in bakterieë wat in die menslike liggaam leef?

Let daarop dat ek deur "in die menslike liggaam" ook "in die ingewande" insluit, alhoewel die binnekant van die ingewande tipies as die buitekant van ons liggaam beskou word.

Daar is ongeveer 100 triljoene bakterieë in elkeen van ons (hierdie getal is 'n vae benadering; sien wiki > Menslike mikrobiota). Ja, meeste van die selle wat in ons woon is nie ons selle nie maar is bakteriële selle!

Bakteriële genoom verskil baie, maar as 'n growwe en byna beledigende benadering, kom ons oorweeg dat die gemiddelde bakteriese genoom van ons mikrobioom 'n genoomgrootte van $10^6$ basispare (let daarop dat bakterieë nie kerne of mitochondria het nie).

Dit beteken dat ons in ons liggaam by die bogenoemde getalle moet byvoeg $10^6 cdot 10^{14} = 10^{20}$ basispare (wat slegs 'n honderdste van $10^{22}$).

Hoeveel DNA in die virusse in ons liggaam?

Laat ons nie ons virome vergeet nie. Ongelukkig kon ek nie ramings vind van die aantal virusse (en viroïede) in ons liggaam nie.

Hoeveel DNA is buite selle en virusse in ons liggaam?

Natuurlik is daar baie DNA in ons liggaam. Daar is DNS in alles wat ons eet en hierdie DNS beland in ons bloedstroom en in ons selle. Ek kon nie 'n skatting vind van hoeveel DNA dit verteenwoordig nie.


Die virale inhoud van menslike genome is meer veranderlik as wat ons gedink het

Dele van menslike DNA is van virale oorsprong: baie van hulle is miljoene jare gelede in die oergenetiese materiaal van ons voorouers ingevoeg en is sedertdien deur opeenvolgende generasies geërf. Daar word dus nie gedink dat hulle veel verskil in die genome van moderne mense nie. Menslike endogene retrovirusse (HERV) is verreweg die mees algemene virus-afgeleide volgordes in ons genoom. Nuwe navorsing gepubliseer in Mobile DNA toon 'n meganisme wat meer inter-individuele variasie in HERV-inhoud tussen mense ingebring het as wat voorheen waardeer is.

Daar is dele van menslike DNA wat van virale oorsprong is: baie van hulle is miljoene jare gelede in die oergenetiese materiaal van ons voorouers ingevoeg en is sedertdien deur opeenvolgende generasies geërf. Menslike endogene retrovirusse (HERV) is verreweg die mees algemene virus-afgeleide volgordes in ons genoom. Die meeste HERV-volgordes is lank reeds geassimileer en word dus deur alle individue in die menslike bevolking gedeel, maar nie almal is nie en 'n paar is bekend dat hulle slegs in 'n subset van individue gevind word. Dit is bekend dat die meeste van hierdie ongefixeerde HERV-elemente afkomstig is van relatief onlangse invoegingsgebeure wat steeds in die menslike bevolking segregeer. Maar nuwe navorsing wat onlangs gepubliseer is in Mobiele DNA toon dat 'n ander meganisme meer inter-individuele variasie in HERV-inhoud tussen mense ingebring het as wat voorheen waardeer is. Hoe kan dit wees?

Eerstens is dit belangrik om na te dink oor die strukturele kenmerke van HERV's. Om in die gasheerchromosoom geïntegreer te word, moet hierdie reekse vollengte-elemente wees wat provirusse genoem word. Elke provirus is georganiseer rondom 'n sentrale kern wat die virale koderende gene bevat wat tussen lang nie-koderende rye wat aan elke kant herhaal word, genoem lang terminale herhalings (LTR's) bevat (sien Figuur 1). Na integrasie herkombineer die twee LTR's van 'n provirus, wat identies is ten tyde van invoeging, gereeld om te vorm wat na verwys word as 'n solo LTR. Die rekombinasieproses elimineer interne virale gene saam met een van die twee LTR's, wat 'n enkele LTR agterlaat. Daar is voorheen beraam dat 90% van alle HERV's in die menslike genoom solo LTR's is, en slegs 10% bly in hul provirale vorm. Maar wat as sommige van hierdie provirale elemente steeds die oorgang ondergaan om solo-LTR's te word? Navorsers aan die Universiteit van Utah en aan die Cornell Universiteit het opgestel om hierdie vraag te ondersoek en te bepaal in watter mate die proses van LTR-rekombinasie HERV-variasie onder mense kan genereer.

Dr. Jainy Thomas het 'n nuwe berekeningsbenadering ontwikkel wat hulle in staat sal stel om 'n groot hoeveelheid DNS-volgordes van uiteenlopende menslike bevolkings te skerm om te vind wat vermoedelik seldsame LTR-rekombinasiegebeurtenisse sou wees. Gegewe die groot hoeveelheid HERV-volgordes in menslike genome, was die taak soortgelyk aan die vind van naalde in 'n hooiberg. ’n Publiek beskikbare datastel, ondersteun deur die Simons-stigting, van heelgenoomvolgordes wat 130 verskillende genetiese populasies verteenwoordig, is gesoek vir variante van drie verskillende retrovirale families: HERV-K(HML2), HERV-W en HERV-H. Die pyplyn wat sy ontwikkel het, het dr Thomas in staat gestel om die meeste van die HERV-variante wat voorheen gekatalogiseer is, te herwin en baie meer te ontdek (Figuur 2). Miskien nie verbasend nie, was die meeste van die nuut ontdekte variante blykbaar skaars, aangesien hulle in net een of 'n paar individue gevind is. Maar hulle was ook onverwags, aangesien baie van hierdie HERV's lank gelede in die DNA van ons voorouers ingevoeg is en sommige selfs met ons groot aap-familielede gedeel is, en dus vermoedelik in die menslike bevolking gevestig is. Dr. Thomas was nietemin in staat om eksperimenteel te bevestig dat verskeie van hierdie variante wel in die menslike bevolking skei, en sodoende die doeltreffendheid van haar berekeningsbenadering bevestig.


Hierdie bevolkingskaart sal jou vertel of jy antieke Denisovan- of Neanderdal-DNS in jou genoom het

Antieke mense wat met 'n naverwante maar nou uitgestorwe spesie genaamd Denisovans gekruis het, het moontlik hul eie genepoel besoedel met sekere genetiese eienskappe wat verantwoordelik is vir manlike onvrugbaarheid. Volgens ’n nuwe studie in die joernaal Current Biology is dieselfde defekte waarskynlik ook opgetel as gevolg van mense wat met Neanderdalmense gepaar het, hoewel die navorsers interessant genoeg ontdek het dat sommige moderne menslike bevolkings eintlik meer van hul DNS van Denisovans erf as van Neanderdalmense.

As hominiede het Denisovans aan dieselfde familie behoort as Homo sapiens, met beide spesies wat van 'n gemeenskaplike voorouer afstam. Neanderdalmense behoort ook tot hierdie familie, en hoewel 'n genetiese spoor van hul kruising met mense gevind kan word in die meerderheid mense wat vandag leef, is gedink dat Denisovan-afkoms baie minder prominent in moderne mense is.

Deur die volledige genome van 257 individue van 120 nie-Afrika-bevolkings te ontleed, het navorsers egter ontdek dat sommige hedendaagse mense eintlik 'n groter deel van hul voorgeslagte van Denisovans as van Neanderdalmense aflei. Dit is veral waar van sekere groepe wat in Oseanië woon, waar fragmente van Denisovan-DNS 5 persent van die genetiese konstitusie van moderne individue uitmaak, terwyl Neanderdal-gene net 2 persent hiervan uitmaak.

Dit word algemeen beskou dat die inbring van beide tipes argaïese gene in die menslike genepoel 'n nadelige uitwerking op oorlewingskanse gehad het, wat daartoe gelei het dat hierdie voorgeslag mettertyd al hoe meer verdun word as gevolg van natuurlike seleksie. Daarom het die feit dat sulke hoë proporsies van Denisovan-genetiese materiaal steeds voortduur, die navorsers tot die gevolgtrekking laat kom dat dit baie later aan die menslike genoom bekendgestel moes gewees het as Neanderdal-DNS. Op grond hiervan bereken hulle dat mense ongeveer 100 generasies nadat hulle met Neanderdalmense met Denisovans gepaar het.

Kaart toon proporsie genoom wat van Denisovans in verskillende wêreldbevolkings geërf is. Rooi dui op die hoogste persentasie van Denisovan-afkoms. Sankararaman et al./Current Biology 2016

Sommige van die allele – of geenvariante – afkomstig van Denisovans word beskou as ten minste gedeeltelik verantwoordelik vir sekere moderne menslike eienskappe. Byvoorbeeld, daar word vermoed dat inboorlinge van Papoea-Nieu-Guinee sekere gene geërf het wat bydra tot 'n verbeterde reuksintuig, terwyl ander Denisovan-gene kan bydra tot die hoë hoogte-aanpassings van moderne Tibetane.

Teling met Denisovans kan egter ook gelei het tot 'n toename in menslike manlike onvrugbaarheid. Om dit te bepaal, het die navorsers gesoek na Denisovan-gene wat hoofsaaklik op die X-chromosoom uitgedruk word, en gevind dat dit geneig was om meer verdun te word in moderne mense as Denisovan-gene wat op ander chromosome voorkom.

Daar is gevind dat ander basterspesies gene vir manlike onvrugbaarheid op die X-chromosoom dra, en die uitputting van hierdie Denisovan-gene dui daarop dat hulle waarskynlik ook hierdie fenotipe geproduseer het en dus nie so suksesvol soos ander argaïese gene oorgedra is nie.

Hierdie teorie wil blykbaar bevestig word deur die feit dat gevind is dat Denisovan-gene wat hoofsaaklik in die testes uitgedruk word, ook in 'n baie groter mate uitgefaseer is as dié wat elders op die genoom uitgedruk word. Die uitputting van gene wat in die testes uitgedruk word, is nog 'n bekende eienskap van hibriede manlike onvrugbaarheid.

Op grond van hierdie bevindinge, het studie mede-outeur David Reich verduidelik dat “males wat toevallig Denisovan- of Neanderdal-DNS in hierdie afdelings gedra het, nie so suksesvol was in terme van die voortbring van nageslag soos ander nie, en daarom is daardie afdelings verwyder in daardie eerste handvol generasies nadat die mengsel plaasgevind het.”

Gevolglik is hierdie genetiese eienskappe in so 'n mate uitgefaseer dat daar nie gedink word dat hulle manlike onvrugbaarheid by moderne mense produseer nie, selfs in bevolkings met hoë proporsies van Denisovan-afkoms.


Harvard-wetenskaplikes het die DNA van wit mense bestudeer en iets werklik verrassend gevind

Soos dit blyk, is baie wit mense dalk tog nie so "wit" nie.

Trouens, miljoene Amerikaners wat hulself as wit beskou, het eintlik gemengde rasse wortels. 'n Studie bied nog meer bewyse dat ras niks meer as 'n sosiale konstruk is nie.

Ons "verborge" Afrikaanse voorgeslagte. Bevolkingsgenetika-wetenskaplikes van instellings, insluitend die Harvard-universiteit, het DNS ontleed van duisende Amerikaners wat hulself beskryf het as deel van 'n enkele rassegroep. Die resultate, gepubliseer in die American Journal of Human Genetics, het aan die lig gebring dat byna 4% van deelnemers wat as wit identifiseer, 'verborge' Afrika-afkoms het.

" Vir 'n generasie het historici boeke geskryf oor hoe ras kultureel saamgestel word," het Claudio Saunt, 'n historikus van die Universiteit van Georgia, kommentaar gelewer op die studie. "Hierdie artikel gebruik 'n ander hulpmiddel, DNS-analise, om by dieselfde vraag uit te kom."

Die studeerkamer: Duisende kliënte van 23andMe, ’n genotiperingsmaatskappy, het speekselmonsters vir DNS-ontleding ingedien en vraelyste oor hul rasse- en etniese identifikasie beantwoord. Een vraelys het deelnemers gevra oor geografiese voorvaderlike oorsprong terwyl 'n ander oor rasverwantskap gevra het. Slegs kliënte wat gesê het hulle identifiseer met 'n enkele ras- of etniese groep is ingesluit.

Die studie het 150 000 wit deelnemers en etlike duisende Latino's en Afro-Amerikaners ingesluit. Hulle kom gesamentlik uit 48 state. Navorsers het deelnemers se DNS-monsters gebruik om hul genetiese profiele weer te gee en die resultate met hul self-gerapporteerde voorgeslagte vergelyk.

Daar is 'n verband tussen rasse-identiteit en geografie. Die frekwensie waarmee self-geïdentifiseerde wit deelnemers Afrika-afkoms gehad het, het aansienlik gewissel volgens streek. En voorgeslagpatrone het blykbaar groot bevolkingsverskuiwings weerspieël wat verband hou met historiese gebeure in die Amerikaanse geskiedenis.

Navorsers het byvoorbeeld wit mense met Afrika-afkoms teen baie hoër pryse in suidelike state gevind. Soveel as 12% van selfbeskryfde Europese Amerikaners van Suid-Carolina en Louisiana het Afrika-afkoms gehad. En in ander dele van die Suide was dit ongeveer 1 uit 10. Navorsers het beraam dat hierdie interrasvermenging, wat genetici 'quotadmixture' noem, ongeveer ses generasies gelede (ongeveer 180 jaar) begin het - voordat Afro-Amerikaners na die noordelike state gemigreer het.

Oklahoma, het die studie aan die lig gebring, het die hoogste persentasie self-geïdentifiseerde Afro-Amerikaners met inheemse Amerikaanse gene. Oklahoma is toevallig ook waar inheemse Amerikaners en Afro-Amerikaners hul paaie so te sê die eerste keer gekruis het toe inheemse Amerikaners in die 1830's die Traneroete gestap het nadat hulle uit die Suide gedwing is.

Hoe mense hulself beskryf, blyk dit toenemend, het minder te doen met genetiese samestelling as die invloed van sosiale norme.

"Baie Amerikaners maak aanspraak op afkoms wat hulle nie het nie, of maak nie aanspraak op afkoms wat hulle het nie," het Saunt gesê. "In my eie staat Georgia, byvoorbeeld, waar ek inheemse Amerikaanse geskiedenis onderrig, vertel talle studente vir my dat hulle Cherokee-afkoms het, maar in werklikheid het blankes van Georgia minder inheemse afkoms as blankes van omtrent enige ander staat."

Die studie is nie sonder omstredenheid nie: Persoonlike genotiperingsmaatskappye soos 23andMe het onder skoot gekom omdat hulle die gene wat hulle ontleed (miljoene uit miljarde) vir deelnemers se DNS-profiele uitgesoek het. Maar 23andMe kodeer vir gene wat redelik goed gevestig is in die opsporing van voorgeslagte, volgens 'n maatskappyverteenwoordiger.

En hoewel daar potensieel vooroordeel is om slegs 23andMe-kliënte te bestudeer, het beide studie-outeurs en ander kundiges in die veld gesê dit sal moeilik wees vir 'n enkele navorsingsinstelling, of selfs 'n regeringsagentskap, om 'n studie van hierdie omvang en kompleksiteit uit te voer.

"Ons het baie, baie mense nodig gehad," het hoofstudieskrywer Kasia Bryc gesê, "so dit was nie net 'n kort tydjie gelede moontlik nie. 23andMe was die eerste bron wat hierdie soort data kon bied."

Oor die algemeen, en miskien die belangrikste, spreek die bevindinge van die netelige verhouding tussen biologie en identiteit.

"Individue wat hulself as wit identifiseer, sal op verskillende maniere reageer op genetiese toetse wat wys dat hulle onlangse Afrika-afkoms het," het Saunt gesê. "Sommige sal die bevindings omhels, en ander sal dit ontken, selfs in die lig van die getuienis. Die aandrang op rassuiwerheid is deel van 'n lang Amerikaanse tradisie. Selfs voor DNS-ontleding het families familielede wat hulle geweet het hulle s'n was, geweier. Daardie tradisie is besig om te kwyn, maar dit is ongelukkig nog lank nie uitgedoof nie."


Realiteit van DNA en genoomooreenkoms

Kom ons hersien 'n paar basiese beginsels om 'n meer akkurate beeld van genome te kry. Menslike, plant- en dier-DNS word in aparte pakkette verpak wat chromosome genoem word. Elkeen bevat miljoene van die vier verskillende DNS-basisse (T, A, C, G), gestapel soos sporte op 'n leer. Hul spesifieke volgorde vorm 'n komplekse stel instruksies wat die "genetiese kode" genoem word. Mense het twee kopieë van elke chromosoom: een stel van 23 van die moeder en een stel van 23 van die vader. Elke chromosoomstel bevat meer as 3 miljard basispare. Die inligting wat hulle kodeer bou hele organismes uit enkele eierselle en onderhou elke skepsel sy lewe lank. Ons 46 chromosome het 'n totaal van 6 biljoen DNS-basisse. Byna elke sel in ons liggaam het almal van hulle. Wanneer wetenskaplikes oor 'n wese se genoom praat, verwys hulle na een stel chromosome. Die verwysingsgenoom by mense is dus die somtotaal van een volledige stel van 23 chromosome.

Die "aanvanklike konsep" van DNS-volgordes in die menslike genoom is in 2001 gepubliseer. In 2004 het wetenskaplikes 'n meer volledige weergawe gepubliseer, maar daar was nog klein dele wat nog gerangskik moes word, so navorsers het die menslike genoom as DNS-volgordebepalingstegnologie bly bywerk. verbeter en meer data is verkry. Die menslike genoom is nou een van die volledigste van alle bekende genoomvolgordes – meestal omdat aansienlik meer navorsingsgeld daaraan bestee is in vergelyking met ander lewensvorme.

Om 3 biljoen basisse te organiseer, gebruik navorsers unieke DNS-volgordes as verwysingsmerkers. Dan bepaal hulle waar hierdie kort rye op elke chromosoom geleë is. Hulle het aanvaar dat die vergelyking van rye tussen verwante wesens sou help om hulle op te spoor. Wetenskaplikes het aanvanklik sjimpansees as die naaste wese aan mense gekies omdat hulle geweet het dat hul proteïene en DNS-fragmente soortgelyke biochemiese eienskappe het.[xvi] Sommige nuuskierige navorsers het egter gorillas en orangoetangs gekies vir vergelyking. ’n Onlangse navorsingsartikel het die bewering gemaak dat orangoetangs se DNA's meer soortgelyk is aan mense se DNA in struktuur en voorkoms as sjimpansee, en daarom moet orangoetangs as ons naaste voorouer beskou word. Evolusionêre wetenskaplikes verontagsaam dit om 'n konsensus te handhaaf dat sjimpansees die naaste aan mense is op die hipotetiese evolusionêre boom. Om hierdie rede neem die meeste genetiese studies hierdie verwantskap aan voordat hulle selfs DNS begin ontleed.

In die vroeë dae van DNS-volgordebepaling, in die 1970's, kon wetenskaplikes slegs baie kort segmente van DNS volgorde. Om hierdie rede het hulle gefokus op DNS-segmente wat hulle geweet het baie soortgelyk tussen diere sou wees, soos bloedglobienproteïene en mitochondriale DNS (DNS wat van die moeder geërf word). Hulle het soortgelyke streke vir vergelyking gekies, want jy kan geen sinvolle vergelykings tussen twee DNS-volgordes wat net in die een en nie die ander bestaan ​​nie, optel. Navorsers het ontdek dat baie van die kort stukke DNA-genetiese volgordes wat vir algemene proteïene kodeer, nie net baie soortgelyk was in baie soorte diere nie, maar dat hulle byna identies was tussen sekere wesens, insluitend mense en ape.[xvii]

'n Basiese begrip van wat DNA-volgordebepaling eintlik behels, help ons om die mens- en sjimpansegenoomakkuraatheid te verstaan. Terwyl die basiese DNS-volgordebepalingstegnieke nie veel verander het sedert hulle ontwikkel is nie, stel die gebruik van kleinskaalse robotika en outomatisering navorsers nou in staat om groot hoeveelhede klein DNS-fragmente te volgorde. Die DNS van 'n hele organisme is te lank om alles op een slag te volgorde, dus volg hulle miljoene stukke, elk honderde basisse lank. Werkers gebruik dan rekenaars om die klein individuele stukke digitaal saam te stel in groter fragmente gebaseer op oorvleuelende afdelings.[xviii] DNS-streke wat honderde herhalende rye het, is om hierdie rede baie moeilik om te rekonstrueer, maar ons weet nou dat dit belangrik is vir selfunksie.


Minder as 10% van menslike DNA speel 'n funksionele rol, beweer wetenskaplikes

In die Oxford-studie is DNS 'funksioneel' as dit ons reproduktiewe fiksheid beïnvloed. Ander wetenskaplikes sê die meeste van die ander 92% is steeds op een of ander manier aktief in die liggaam. Foto: Shunyu Fan/Getty Images

In die Oxford-studie is DNS 'funksioneel' as dit ons reproduktiewe fiksheid beïnvloed. Ander wetenskaplikes sê die meeste van die ander 92% is steeds op een of ander manier aktief in die liggaam. Foto: Shunyu Fan/Getty Images

Meer as 90% van menslike DNA doen niks baie nuttig nie, en groot dele is dalk nie meer as biologiese bagasie wat oor jare se evolusie opgebou het nie, beweer Oxford-navorsers.

Die wetenskaplikes het by die figuur uitgekom nadat hulle die menslike genoom met die genetiese samestelling van ander soogdiere vergelyk het, wat wissel van honde en muise tot renosters en perde.

Die navorsers het gesoek na dele van DNS wat mense met die ander diere gedeel het, wat op verskillende punte in die geskiedenis van ons geslag geskei het. Wanneer DNS oor spesies gedeel en bewaar word, dui dit daarop dat dit iets waardevols doen.

Gerton Lunter, 'n senior wetenskaplike in die span, het gesê op grond van die vergelykings was 8,2% van menslike DNS "funksioneel", wat beteken dat dit 'n belangrike genoeg rol gespeel het om deur evolusie bewaar te word.

“Wetenskaplik gesproke het ons geen bewyse dat 92% van ons genoom hoegenaamd bydra tot ons biologie nie,” het Lunter aan die Guardian gesê.

Navorsers weet al geruime tyd dat slegs 1% van menslike DNA in gene gehou word wat gebruik word om belangrike proteïene te maak om selle – en liggame – lewendig en gesond te hou. Die jongste studie, berig in die joernaal Plos Genetics, dui daarop dat 'n verdere 7% van menslike DNS ewe noodsaaklik is, wat reguleer waar, wanneer en hoe gene uitgedruk word.

Maar as baie van ons DNS so waardeloos is, hoekom dra ons dit steeds rond? "Dit is nie waar dat die natuur spaarsamig is in terme van die behoefte aan 'n klein genoom nie. Koring het 'n baie groter genoom as ons," het Lunter gesê. "Ons is nie ontwerp nie. Ons het ontwikkel en dit is 'n morsige proses. Hierdie ander DNA is regtig net vuller. Dit is nie vullis nie. Dit kan dalk eendag nuttig wees. Maar dit is nie 'n las nie."

Van ons DNS is oorgebly van antieke virusse wat hul genetiese materiaal in ons DNS – of ons voorouers DNS – ingevoeg het en oor millennia van evolusie in stukke gemuteer is. Sommige het steeds die vermoë om in ons genome rond te spring, en by te voeg tot die vuller soos hulle dit doen, maar is so kreupel dat hulle nie kan uitbreek nie.

Alhoewel 8,2% 'n klein gedeelte van DNS lyk om funksioneel te noem, is die betekenis van die woord baie spesifiek. In die Oxford-studie is DNS “funksioneel” as dit ons reproduktiewe fiksheid beïnvloed.

Maar ander wetenskaplikes neem 'n breër siening van wat dit beteken dat DNS funksioneel is. Die meeste van die 92% wat volgens Lunter se groep nie funksioneel is nie DNS is steeds op een of ander manier in die liggaam aktief.

"Baie [DNS]-elemente wat belangrike rolle in menslike siektes speel, word nie evolusionêr bewaar nie. Sommige van hierdie het mensspesifieke funksies, sommige is betrokke by siektes wat laat aanbreek soos Alzheimer's, en ander word eenvoudig gemis deur huidige vergelykende genomika-metodes," sê Manolis Kellis, 'n berekeningsbioloog by MIT wat nie by die studie betrokke was nie. “Ons kan nie bloot die oorblywende 90% van die genoom ignoreer wat nie evolusionêr bewaar is nie.”

"Evolusie kan vir jou sê of iets belangrik is of nie belangrik nie, maar dit vertel jou nie wat daardie iets eintlik doen nie," het hy bygevoeg.


Bepaal jou gene jou hele lewe?

WANNEER jy ook al stories lees oor identiese tweelinge wat by geboorte geskei is, is hulle geneig om die sjabloon te volg wat deur die merkwaardigste van hulle almal gestel word: die "twee Jims". James Springer en James Lewis is as een maand oud geskei, deur verskillende gesinne aangeneem en op die ouderdom van 39 herenig. Toe die Universiteit van Minnesota sielkundige Thomas Bouchard hulle in 1979 ontmoet het, het hy gevind, soos 'n Washington Post-artikel dit gestel het, het albei " met 'n vrou met die naam Linda getrou en geskei en weer met 'n Betty getrou. Hulle het belangstellings in meganiese tekeninge en timmerwerk gedeel. Hulle gunsteling skoolvak was wiskunde, hul minste gunsteling, spelling. Hulle het dieselfde hoeveelheid gerook en gedrink en op dieselfde tyd van die dag hoofpyn gekry.” Die ooreenkomste was vreemd. Baie van wie hulle sou blyk te wees, blyk in hul gene geskryf te wees.

Ander studies by die wêreldleier Minnesota Sentrum vir Tweeling- en Gesinsnavorsing dui daarop dat baie van ons eienskappe meer as 50% oorgeërf is, insluitend gehoorsaamheid aan gesag, kwesbaarheid vir stres en risiko-soek. Navorsers het selfs voorgestel dat wanneer dit by kwessies soos godsdiens en politiek kom, ons keuses baie meer deur ons gene bepaal word as wat ons dink.

Baie vind dit ontstellend. Die idee dat onbewuste biologiese kragte ons oortuigings en optrede dryf, blyk 'n werklike bedreiging vir ons vrye wil in te hou. Ons hou daarvan om te dink dat ons keuses maak op grond van ons eie bewuste oorwegings. Maar is al daardie denkende dinge nie irrelevant as ons finale besluit reeds in ons genetiese kode geskryf is nie? En val die hele gebou van persoonlike verantwoordelikheid nie in duie as ons aanvaar dat "my gene my dit laat doen het" nie? Om hierdie bekommernisse aan te spreek, moet ons eers 'n bietjie nader kyk na wat die ervarings van identiese tweeling werklik wys.

Professor Tim Spector studeer al meer as 20 jaar 'n identiese tweeling aan King's College in Londen. Vanaf die begin van sy navorsing in die vroeë 1990's, het dit vir Spector duidelik geword dat identiese tweeling altyd meer soortgelyk was as broers of susters of nie-identiese tweelinge. Destyds het "sosiale wetenskaplikes egter die idee gehaat" dat gene 'n belangrike determinant was van wie ons is, "veral in daardie taamlik kontroversiële gebiede soos IK, persoonlikheid en oortuigings". As "een van die vele wetenskaplikes wat die gene-sentriese siening van die heelal as vanselfsprekend aanvaar het", wou Spector "hulle verkeerd bewys, en om te bewys dat daar niks is wat nie tot 'n mate geneties is nie". Vandag kyk hy hierop terug as deel van sy “oorywerige genetiese fase”.

Dit is miskien te verstane dat Spector in geenmanie vasgevang is. Die bekendstelling in 1990 van die Menslike Genoomprojek, wat daarop gemik was om die volledige volgorde van menslike DNS te karteer, het aan die begin van 'n dekade gekom wat die hoogtepunt van optimisme sou wees oor hoeveel ons gene ons kan vertel. Daniel Koshland, destyds redakteur van die gesogte tydskrif Science, het die stemming vasgevang toe hy geskryf het: “Die voordele vir die wetenskap van die genoomprojek is duidelik. Siektes soos maniese depressie, Alzheimer's, skisofrenie en hartsiektes is waarskynlik almal multigenies en selfs moeiliker om te ontrafel as sistiese fibrose. Tog is hierdie siektes die wortel van baie huidige maatskaplike probleme.” Gene sou ons help om die geheime van allerhande kwale te ontbloot, van die sielkundige tot die fisiese.

Tien jaar later was Bill Clinton en Tony Blair onder die gaste wat bymekaargekom het om “die openbaring van die eerste konsep van die menslike boek van die lewe te vier”, soos Francis Collins, die direkteur van die Human Genome Project, dit gestel het. "Ons probeer versigtig wees op dae soos hierdie," het die ABC-nuusanker gesê, "maar hierdie kaart is die begin van 'n era van ontdekking wat die lewens van elke mens sal beïnvloed, met implikasies vir wetenskap, geskiedenis, besigheid, etiek , godsdiens en natuurlik medisyne.”

Teen daardie tyd was gene nie meer bloot die sleutel om gesondheid te verstaan ​​nie: hulle het die skeletsleutel geword om byna al die raaisels van die menslike bestaan ​​te ontsluit. Vir feitlik elke aspek van die lewe - misdadigheid, getrouheid, politieke oortuiging, godsdienstige oortuiging - sou iemand beweer dat hy 'n geen daarvoor vind. Stephen Mobley het in 2005 in Hall County, Georgia, probeer om teregstelling te vermy deur te beweer dat sy moord op 'n Domino's pizza winkelbestuurder die gevolg was van 'n mutasie in die monoamienoksidase A (MAOA) geen. Die regter het die appèl van die hand gewys en gesê dat die wet nie gereed is om sulke getuienis te aanvaar nie. Die basiese idee dat die lae-MAOA-geen 'n groot bydraende oorsaak van geweld is, het egter algemeen aanvaar, en dit word nou algemeen die "vegtergeen" genoem.

In onlangse jare het geloof in die verduidelikende krag van gene egter gekwyn. Vandag glo min wetenskaplikes dat daar 'n eenvoudige "geen" vir enigiets is. Byna alle oorgeërfde kenmerke of eienskappe is die produkte van komplekse interaksies van talle gene. Die feit dat daar nie een genetiese sneller is nie, het egter nie op sigself die bewering ondermyn dat baie van ons diepste karaktertrekke, gesindhede en selfs opinies geneties bepaal is nie. (Hierdie bekommernis word net effens getemper deur wat ons oor epigenetika leer, wat wys hoeveel oorgeërfde eienskappe net in sekere omgewings “aangeskakel” word. Die rede waarom dit nie alle vrese verwyder nie, is dat die meeste van hierdie aan- en afskakeling plaasvind baie vroeg in die lewe – hetsy in utero of in die vroeë kinderjare.)

Wat egter ons alarm kan verminder, is 'n begrip van wat genetiese studies werklik toon. Die sleutelbegrip hier is oorerflikheid. Ons word dikwels vertel dat baie eienskappe hoogs oorerflik is: geluk, byvoorbeeld, is ongeveer 50% oorerflik. Sulke syfers klink baie hoog. Maar hulle bedoel nie wat hulle blyk te beteken vir die statisties onopgeleide oog nie.

Die algemene fout wat mense maak, is om aan te neem dat as outisme byvoorbeeld 90% oorerflik is, dan het 90% van outistiese mense die toestand van hul ouers gekry. Maar oorerflikheid gaan nie oor “kans of risiko om dit oor te dra nie”, sê Spector. “Dit beteken eenvoudig hoeveel van die variasie binne 'n gegewe populasie te danke is aan gene. Dit is uiters belangrik dat dit verskil volgens die omgewing van daardie bevolking.

Spector spel uit wat dit beteken met iets soos IK, wat 'n oorerflikheid van gemiddeld 70% het. "As jy na die VSA gaan, rondom Harvard, is dit meer as 90%." Hoekom? Omdat mense wat gekies word om daarheen te gaan, geneig is om uit middelklasgesinne te kom wat hul kinders uitstekende opvoedkundige geleenthede gebied het. Omdat almal baie soortgelyke opvoeding gekry het, is byna al die oorblywende variasie te danke aan gene. As jy daarenteen na die Detroit-voorstede gaan, waar ontbering en dwelmverslawing algemeen voorkom, is die IK-oorerflikheid "naby aan 0%", omdat die omgewing so 'n sterk uitwerking het. In die algemeen glo Spector, "Enige verandering in omgewing het 'n baie groter effek op IK as gene," soos dit op byna elke menslike eienskap het. Dit is hoekom as jy wil voorspel of iemand in God glo, dit nuttiger is om te weet dat hulle in Texas woon as wat hulle gene is.

Statistiese ongeletterdheid is nie die enigste rede waarom die belangrikheid van omgewingsfaktore so dikwels verdrink nie. Ons is geneig om betower te word deur die ooreenkomste tussen identiese tweelinge en merk die verskille baie minder op. “Wanneer jy na ’n tweeling kyk,” sê Spector, “is die een ding wat altyd uitkom, die onderbewustelike tics, maniertjies, posture, die manier waarop hulle lag. Hulle sit dieselfde, kruis hul bene dieselfde, tel koppies koffie op dieselfde, al haat hulle mekaar of is hulle hul hele lewe lank geskei.” Dit is asof ons nie kan help om te dink dat sulke dinge dieper ooreenkomste weerspieël nie, al is dit eintlik die mees oppervlakkige kenmerke om te vergelyk. If you can stop yourself staring at the similarities between twins, literally and metaphorically, and listen properly to their stories, you can see how their differences are at least as telling as their similarities. Far from proving that our genes determine our lives, these stories show just the opposite.

When Ann and Judy from Powys, mid-Wales were born in the 1940s, they were the last thing their working-class family with five children needed. So, identical or not, Ann and Judy were packed off to live with different aunts. After three months, Judy returned to her biological mother, as her aunt could not manage raising another child. But for the childless 50-year-old couple who took on Ann (without ever formally adopting her), the late opportunity for parenthood was a blessing and she stayed.

Ann and Judy, who are now well into retirement, told me their story in Ann’s home in Crickhowell on the edge of the Brecon Beacons, over coffee and home-made Welsh cakes. Their experience is a valuable corrective for anyone who has been impressed by tales of how identical twins show that we are basically nothing but the products of our genes.

Although the girls grew up in the same town, they ended up living in different areas and went to different schools. The two households in which Ann and Judy grew up were very different. Judy’s father drove trains inside the steelworks, and her mother, like most women at the time, did not have a job. The family lived in a basic two-up, two-down house with a toilet at the bottom of the garden. Judy’s four older brothers were all out working by the time she was five and she was left with her older sister Yvonne.

Ann was brought up in a newly built, semi-detached house, with a toilet indoors. Her father was also a manual labourer in the steelworks, but they were relatively well off, partly because they hadn’t had children but also because they were “very careful with money”. Ann recalled that “the sugar bowl was never filled so as not to encourage people to take too much”.

Where Judy told me she “was a street kid, always out”, Ann said she always had her “nose in a book because I was on my own”. And while Ann passed the 11-plus exam and got into the grammar school, Judy didn’t, and ended up at the secondary modern. Although, aged 15, Judy was offered a place at a grammar school, when she got there she found herself suddenly studying algebra and geometry in a class where everyone else had already being doing it for three years. Unsurprisingly she struggled. After four months, Judy quit and went to work in a furniture shop.

Ann, meanwhile, breezed through school, although she, too, left early because her now 66-year-old father was retiring. “I just felt that it wasn’t fair for me to stay on at school when they were on a pension,” she said. At 16, Ann began her white-collar job in the local council offices, not long after Judy had started working on the shop floor.

Although the twins’ paths had diverged up to this point, the next stage in the story is the moment where their stories converge in an uncanny way. Less than six months into her job, Ann got pregnant and quit. Two months later, Judy also got pregnant and quit the nursing course she was enrolled in. Not only that, but both fathers, soon husbands, turned out to be very violent.

However, the differences in what happened next are instructive. Ann didn’t stay married for long. “I left and went back home, and they were very supportive when they found out what was going on.” Judy, in contrast, stayed with her husband for 17 years. “I did leave him, mind, but I kept going back. I didn’t have the support. I had three children by the time I was 21.” Her mother was no help. “My mother’s attitude was, you made your bed, you lie on it,” Judy explained. Ann understands Judy’s acquiescence perfectly. “Imagine being at home, with three children, no qualifications, nothing on the horizon to see your life was going to get better, which I did have.”

The two only really started a proper sibling relationship after Ann read about the Minnesota University research in the paper and wrote to the university about her and her sister. When they were 48, they travelled together to Minnesota to meet scientists there. Now the twins are both retired. Judy says, “I think from where we started we’ve travelled the same distance.”

But there were important differences in how their lives went, and so too in the people they became. Most obviously, Ann has always had more money, but you can also see the effects of their different backgrounds on their health. “Judy’s had a hysterectomy, I haven’t,” says Ann. “Judy’s got a problem with her kidneys. I don’t. Judy’s got blood pressure, I haven’t. But she’s stronger than me.”

There are also differences in how they think and behave socially. Although their political views are very similar, Judy says, “I’m a Christian, well, probably agnostic, I think,” whereas Ann is “a confirmed atheist”. Ann also thinks she’s “much more diplomatic. Judy is just rude. That’s probably the educational background coming through. ‘Interfering’ is too strong a word, but Judy is more involved with her children and grandchildren in an advisory capacity, whereas I wouldn’t do that.” Much of this, they agree, is surely down to culture, with Ann being encouraged to adopt more genteel middle-class ways.

Ann and Judy’s story illustrates that our genes only set down what might be described as a field of possibilities. These set limits on what we are to become – so whatever our upbringings, most of us will tend towards introversion or extroversion, jollity or sobriety, facility with words or numbers. But this is far from the claim that we become is essentially written in our genes. Rather, various options are pencilled in, and our life experiences determine which get inked.

Tim Spector’s view that environment is almost always more influential than genes is clear in the case of Ann and Judy. The sisters shared the same genes but with a middle-class background Ann did better at school, earned more money and has enjoyed better health. Too much attention to genes blinds us to the obvious truth that access to financial and educational resources remains the most important determinant of how we fare in life.

Although being more middle class might improve your odds of success in life, other non-genetic factors play a huge role. Take the war babies Margaret and Eileen from Preston, Lancashire, another set of identical twins who were brought up in different families. Margaret’s adoptive parents owned their own house. Eileen’s toilet was at the bottom of the garden. And yet it was Margaret who flunked her 11-plus, simply out of nerves, while Eileen passed hers. Margaret’s adoptive mother was “hard”, and when her daughter passed her 11-plus on the second attempt she said she couldn’t go to the grammar school anyway because she had already bought the uniform for the other school. As Margaret says to Eileen now, “Your mum told you you were loved and you had to be adopted. My mum never said that. I remember waking up when I was eight years old and thinking, somebody had me and they didn’t want me. It’s horrifying, really traumatic for an eight-year-old.”

Eileen agrees that she came out better when it came to love and affection. “My mother always said Ellen [the twins’ birth mother] was very good to give me to her. She always pointed that out, and they picked me because they wanted me. I was secure despite the fact that I had to go and live in this tatty bungalow.”

Professor Tim Spector Photograph: Orion Books

Another difference in how their lives have progressed has been their choice of husbands. “You’ve been further afield than I have,” says Eileen to Margaret, turning to me and adding, “I think she’s more or less finished her bucket list. My husband won’t go. He’s not interested in travel. I’ve had to drag him out of the country.”

Identical twins show us that in the nature-versus-nurture debate, there is no winner. Both have their role to play in shaping who we are. But although we have reason to doubt that our genes determine our lives in some absolute way, this does not solve a bigger worry about whether or not we have free will.

Who we are appears to be a product of both nature and nurture, in whatever proportion they contribute, and nothing else. You are shaped by forces beyond yourself, and do not choose what you become. And so when you go on to make the choices in life that really matter, you do so on the basis of beliefs, values and dispositions that you did not choose.

Although this may appear troubling, it is hard to see how it could be any other way. For example, say you support a more redistributive tax system, because you think that is fair. Where did that sense of fairness come from? You may well have thought it through and come to a conclusion. But what did you bring to that process? A combination of abilities and dispositions that you were born with, and information and thinking skills that you acquired. In other words, a combination of hereditary factors and environment. There is no third place for anything else to come from. You are not responsible for how you emerged from the womb, nor for the world you found yourself in. Once you became old enough and sufficiently self-aware to think for yourself, the key determinants in your personality and outlook were already set. Yes, your views might be changed later in life by powerful experiences or persuasive books. But again, you do not choose for these things to change you. The very way we speak about such experiences suggests this. “This book changed my life,” we say, not “I changed my life with this book”, acknowledging that having read it, we did not choose to be different we simply could never be the same again.

The literature on free will tends to focus on moments of choice: was I free at that point to do other than what I did? When we ask this, it often seems to us that only one option was viable. Sometimes this is because we think circumstances constrain us. But perhaps a more fundamental reason why at the moment of choice we cannot do otherwise is that we cannot be other than who we are. The nature of the chooser is the key determinant at the moment of choice: who we are comes first and what we do follows.

To be considered truly free, then, it would seem to be necessary for us to be in some sense responsible for being the people we are, and that responsibility needs to go “all the way down”: it has to be up to you and you alone what values and beliefs you hold dear and act upon. If we are not responsible for who we are, how can we be held responsible for what we do? But when we consider the dual roles of nature and nurture, the values we hold and beliefs we assert do not appear to be a matter of choice. We are formed by forces ultimately beyond our control. This thought, once made explicit, leads many to the conclusion that free will and responsibility are impossible. If you dig deep enough into what made us who we are, eventually you come across some key formative factors that we did not control. And if they are beyond our control, how can we be responsible for them?

On reflection, though, we ought to be more sanguine about not having complete control. The first step towards acceptance is to realise that it would be a very odd person whose actions did not in some sense flow from her values and beliefs. And yet the more strongly we hold these, the less we really feel free to choose other than the way we do. In 1521, the Reformation priest Martin Luther, for example, is reported to have told those who accused him of heresy at the Diet of Worms, “Here I stand. I can do no other.” This is not a denial of his freedom but an assertion of his freedom to act according to his values.

We cannot change our characters on a whim, and we would probably not want it any other way. A committed Christian does not want the freedom to wake up one day and become a Muslim. A family man does not want to find it as easy to run off with the au pair as to stick with his children and their mother. A fan of Shostakovich does not, usually at least, wish she could just decide to prefer Andrew Lloyd Webber. The critical point is that these key commitments don’t strike us primarily as choices. You don’t choose what you think is great, who you should love, or what is just. To think of these fundamental life commitments as choices is rather peculiar, perhaps a distortion created by the contemporary emphasis on choice as being at the heart of freedom.

What’s more, the idea that any kind of rational creature could choose its own basic dispositions and values is incoherent. For on what basis could such a choice be made? Without any values or dispositions, one would have no reason to prefer some over others. Imagine the anteroom in heaven, where people wait to be prepared for life on Earth. Some angel asks you, would you like to be a Republican or a Democrat? How could you answer if you did not already have some commitments and values that would tip the balance either way? It would be impossible.

Throughout human history, people have had no problem with the idea that their basic personality types were there from birth. The idea of taking after your parents is an almost universal cultural constant. Discovering just how much nature and nurture contribute to who we are is interesting, but doesn’t change the fact that traits are not chosen, and that no one ever thought they were.

Accepting this is ultimately more honest and liberating than denying it. Recognising how much our beliefs and commitments are shaped by factors beyond our control actually helps us to gain more control of them. It allows us to question our sense that something is obviously true by provoking us to ask whether it would appear so obvious if our upbringing or character had been different. It is only by recognising how much is not in our power that we can seize control of that which is. Perhaps most importantly, accepting how much belief is the product of an unchosen past should help us to be less dogmatic and more understanding of others. It doesn’t mean anything goes, of course, or that no view is right or wrong. But it does mean that no one is able to be perfectly objective, and so we should humbly accept that although objective truth is worth striving for, none of us could claim to have fully attained it.

Some may not be convinced yet that we should be so relaxed about our debt to nature and nurture. Unless we are fully responsible, it might seem unjust to blame people for their actions. If this seems persuasive, it is only because it rests on the false assumption that the only possible form of real responsibility is ultimate responsibility: that everything about who you are, what you believe and how you act is the result of your free choices alone. But our everyday notion of responsibility certainly does not and could not entail being ultimately responsible in this way. This is most evident in cases of negligence. Imagine you postpone maintaining a roof properly and it collapses during an exceptionally fierce storm, killing or injuring people below. The roof would not have collapsed if there had not been a storm, and the weather is clearly not in your control. But that does not mean you should not be held responsible for failing to maintain the building properly.

If the only real responsibility were ultimate responsibility, then there could never be any responsibility at all, because everything that happens involves factors both within and outside of our control. As the philosopher John Martin Fischer succinctly and accurately puts it, “Total control is a total fantasy – metaphysical megalomania.”

Many arguments that purport to debunk free will are powerful only if you buy into the premise that real responsibility is ultimate responsibility. Almost all those who deny free will define responsibility as though it must be total and absolute, or it is nothing at all. The Dutch neuroscientist Dick Swaab, who calls free will “an illusion”, does so by endorsing the definition of free will by Joseph L Price (a scientist, not a philosopher) as “the ability to choose to act or refrain from action without extrinsic or intrinsic constraints”. No wonder he is forced to conclude that, “Our current knowledge of neurobiology makes it clear that there is no such thing as absolute freedom.” Similarly, he claims that the existence of unconscious decision-making in the brain leaves “no room for a purely conscious, free will”. That’s true. The only question is why one would believe such absolute or pure freedom is possible or necessary.

The answer would appear to be to justify eternal damnation. As Augustine put it in the fourth century, “The very fact that anyone who uses free will to sin is divinely punished shows that free will was given to enable human beings to live rightly, for such punishment would be unjust if free will had been given both for living rightly and for sinning.” If the buck doesn’t stop with us, then it can only stop with the one who created us, making God ultimately responsible for our wickedness. Hence, as Erasmus put it, free will is theologically necessary “to allow the ungodly, who have deliberately fallen short of the grace of God, to be deservedly condemned to clear God of the false accusation of cruelty and injustice to free us from despair, protect us from complacency, and spur us on to moral endeavour.”

The ultimate punishment requires an ultimate responsibility which cannot exist. That is why we should not be worried to discover that factors outside our control, such as our genetic makeup, are critical to making us the people we have become. The only forms of freedom and responsibility that are both possible and worth having are those that are partial, not absolute. There is nothing science tells us that rules out this kind of free will. We know people are responsive to reasons. We know we have varying capacities of self-control which can be strengthened or weakened. We know there is a difference between doing something under coercion or because you decide yourself you want to. Real free will, not a philosopher’s fantasy, requires no more than these kinds of abilities to direct our own actions. It does not require the impossible feat of having written our own genetic code before we were even born.

If we become accustomed to thinking of freedom as completely unfettered, anything more limited will at first sight look like an emaciated form of liberty. You might even dismiss it as mere wiggle room: the ability to make limited choices within a framework of great restraint. But that would be a mistake. Unfettered freedom is not only an illusion it makes no sense. It would not be desirable even if we could have it. Quite simply, the commonplace idea of free will we must ditch was always wrong. Good riddance to it.


Science Says Dogs And Humans Have More In Common Than Treats And Play

Have you ever looked at your dog and thought, “Wow, sometimes I feel like we have so much in common”? Well, you will be happy to know that there is some truth in that statement. It turns out that 25% of the DNA sequence in the dog genome is an exact match for the human DNA sequence.

Wait a minute. Does that mean humans are a quarter dog? Or dogs are a quarter human? As much as I wish that was true, unfortunately, it doesn’t quite work like that.

To understand how humans and dogs can share the same DNA, we first need to have a quick biology lesson. Whether you’re a dog or a human, every living thing is made up of the same DNA-base, or building blocks, of A’s, T’s, G’s, and C’s.

The crazy thing about these building blocks is that there are a TON of them. Humans have a total of 3.3 billion and dogs have a total of 2.8 billion – a little less, but still a lot.

The number of building blocks isn’t the only difference between humans and dogs. We actually differ in the number of chromosomes we have as well, humans have 23 and dogs have 39. What’s interesting though, is that these differences in the number of building blocks and chromosomes aren’t that important when it comes to differentiating between humans and dogs.

What makes each person, or species, unique is the order in which these building blocks are assembled. Where you may have an A in spot 15, 1500, and 15,000, your dog may have a T or a G. Not surprisingly, these differences in building block assembly are greater between species, such as the case with humans and dogs, than within a species.

Now that our biology lesson is over, you may be asking yourself “If our number of chromosomes, building blocks, and the way they’re assembled are different, how can we possibly share any DNA with a dog?”

The answer to that is simple. Since humans and dogs have so many similar body parts that carry out the same biological functions, we see a lot of overlap in how the DNA for those parts are put together. This is why we have an exact match for 25% of dog and human DNA. It’s also why dogs are used in so many health studies we have similar parts that are prone to the same illnesses, such as cancer or heart disease.

While there is a quarter of our design that is exactly like a dog’s, it’s the small differences in the remaining 75% that result in two very different species. The other 75% of our genes are a mixture of totally unique human DNA and other DNA that is somewhat similar to a dog’s.

All in all, while humans and dogs do share 25% of their DNA, the remaining 75% is what really counts. But hey, if it makes you happy you can still consider yourself 25% dog!


How Much Neanderthal DNA do Humans Have?

We all have a little Neanderthal in us. The amount varies a bit, from less than a percent to likely over 2 percent, depending on our heritage. East Asians seem to have the most Neanderthal DNA in their genomes, followed by those of European ancestry. Africans, long thought to have no Neanderthal DNA, were recently found to have genes from the hominins comprising around 0.3 percent of their genome.

That genetic material is the result of interbreeding between our two groups at some point in the past. There were multiple trysts between human- and Neanderthal-kind, and the offspring of those unions would go on to cement the Neanderthal legacy in our genomes.

Neanderthal genes are thought to be linked to a number of different traits in humans. They might help protect us from some pathogens, for example, but also make us more susceptible to heart disease. Neanderthal DNA probably also plays a role in hair color, our sense of smell and even our sleeping habits, to some extent.

This story is part of an ongoing series covering readers’ biggest questions about human origins. Read more:


How much DNA do humans have? - Biology

Genes. They are a piece of the complicated puzzle that separate man from animal and from one another. Made up of the DNA that is inherited from one’s parents, our genes are roadmaps and instruction manuals. They tell our cellular machinery which functional molecules to make, impacting the ingredients that make up the processes of life. Eye color, height, vision, and intellect can all be influenced by our genes.

In April 2003, the complete human genome was published by the International Human Genome Sequencing Consortium. It marked a pivotal moment in our ability to understanding the inner workings of the human organism. As Francis Collins, Director of the National Human Genome Research Center, explains: “It’s a history book – a narrative of the journey of our species through time. It’s a shop manual, with an incredibly detailed blueprint for building every human cell. And it’s a transformative textbook of medicine, with insights that will give health care providers immense new powers to treat, prevent and cure disease.” He was right.

Before we started sequencing the human genome, scientists believed that the species Homo Sapien had between 50,000 and 140,000 genes. They had drastically overestimated. Human beings have roughly 20,500 genes, all coiled up in DNA, housed in each and every one of the trillions of cells that make you who you are. That’s 20,500 places where the machinery of human life can be altered. Many of these alterations would make life impossible.

Life didn’t begin with this many genes, and our gene count varies significantly from other organisms. According to the theory of common descent, all life on earth originated from a common ancestor that lived around 3.9 billion years ago. In that time, incremental mutations in DNA have resulted in everything from wispy ocean plants through complex animal organisms like human beings.

This common history ensures that earthly DNA shares some similarities, but 3.9 billion years is also an incredibly long time. The planet’s biodiversity includes creatures that are single-celled and multicelled, propelled by legs, wings or fins, equipped with enhanced smell, hearing or even echolocation. The makeup of our DNA and the genes it comprises is equally diverse.

Scientist believe that sponges were the first animal to branch off from the tree of life, though Comb Jellies were considered for a short time. The farther back an organism breaks away from the tree, the less similar their DNA. The sponge genome contains 18,000 genes, many of which are similar to people. In fact, humans and sponges share around 70 percent of their DNA.

Since all organisms on earth share a common ancestor, the connection and commonality goes back further than the sponge. You may have heard that people share over half their genes with bananas, and this true. We all recognize, however, that people are a far cry from bananas. Half of thousands and thousands is still a large number, especially when you take into account that genes determine our form and functions as organisms. There is still plenty of room for the changes that make us so very different from plant-relatives, just as only a difference of 30 percent is enough to distinguish us from our sponge-brethren.

When comparing homo sapiens to more similar creatures, the gene-specific differences between us shrink considerably. We share about 99 percent of our DNA with chimpanzees. Though this still leaves a large number of genes that separate us, it is small enough to think about how those genes might influence our behaviors. Deciphering which genes are responsible for which attributes is a monumental task and, though we are far from solving this mystery, scientists are beginning to ask the questions.

Another factor of gene diversity is the sheer number of genes each organism has.

Though it surprises most people, human beings are not the most genetically complex animal. We may have 20,500 genes, but a teeny, tiny crustacean known as the water flea Daphnia holds the record at 31,000 genes. More than a third of this creature’s genes are unique, unknown to science until the Daphnia’s genome was sequenced in 2011

Why does such a tiny, seemingly simple creature need so many genes? Size can be deceiving, and the Daphnia is far from simple. Its aquatic environment is much more variable than ours, and it needs to adapt quickly if it wants to survive. This hypothesis fits in neatly with our data, as most of its unique genes are indeed slated to shift with environmental factors.

As project leader John Colbourne explains, “since the majority of duplicated and unknown genes are sensitive to environmental conditions, their accumulation in the genome could account for Daphnia‘s flexible responses to environmental change.”

Underlying the mystery of Daphnia is epigenetics, which is the study of “changes in organisms caused by modification of gene expression rather than alteration of the genetic code itself.” Just because an organism has a particular gene, doesn’t mean it is being used. In order for genes to have an impact on an organism, they need to be read by the cell’s machinery. Any number of environmental factors can impact whether a gene is loosely waiting to be read, or coiled tightly up. At the end of the day, it isn’t only genes that matter. Epigenetics accounts for many of the differences between people. Genetically, every person in the world is 99.9 percent the same. Though some of the differences that make us unique from one another are genetics, many are epigenetic.

The exciting thing about this discovery is that they way our genes impact who we are and who we become is a fluid process – it is not set in stone. What you do can impact which genes are activated and which become, or remain, dormant. This is why identical twins, who share DNA, become more and more distinct over time. Experience matters. It really is a combination of nurture and nature, even when it comes to your genes.

Erin Wildermuth is a science writer based in Miami. She is passionate about using technology to improve human health.


The Human Genome Is Full of Viruses

V iruses are amazing molecular machines that are much tinier than even the smallest cells. We often think of viruses like the flu, chickenpox, or herpes as “external” invaders, but viruses are more inherently associated with human life than we often realize. Even after recovering from an infection there will always be a piece of that virus encoded within your DNA (depending on the type of virus). Approximately 8% of the human genome is made up of endogenous retroviruses (ERVs), which are viral gene sequences that have become a permanent part of the human lineage after they infected our ancient ancestors. And these endogenous retroviruses don’t just sit silently in the genome — their expression has been implicated in diseases like autoimmune disorders and breast cancer.

But endogenous retroviruses don’t only harm our health they can also be extremely useful for human survival. For example, they play a very important role as an interface between a pregnant mother and her fetus by regulating placental development and function. It has been suggested that viruses are not only necessary for the existence of placental mammals, but also for the existence of life in general. Professor Luis P. Villarreal, the Founding Director of the Center for Virus Research at UC Irvine, says it like this: “So powerful and ancient are viruses, that I would summarize their role in life as ‘Ex Virus Omnia’ (from virus everything).”

Viruses are powerful, ancient, and vital to our existence, but they are extremely simple constructions. They tend to be nothing more than a few pieces: a protein capsid, which is a simplistic and protective shell a protein called a polymerase, which carries out most of the functions related to replicating the viral genome and a sequence of nucleotides — either RNA or DNA — that encode for the previously mentioned viral proteins. The image below shows one of the ways that these viral components can be assembled into a unified whole. Unlike a human genome, a viral genome can be thought of as a self-contained model of the entire viral form. Within its RNA or DNA, a virus contains all the instructions necessary to create an entirely new body for itself and to replicate those same instructions. The simplicity and self-contained nature of viruses makes them phenomenal tools for biological engineering and medicine.

Viruses are so simple that they don’t always need their own body to survive they have circadian rhythms like all living things. We experience these rhythms through cycles of sleep and wakefulness, whereas viral rhythms occur as periods of dormancy between rounds of infection. Viruses don’t technically have a body during their dormant phase — they are nothing more than a string of letters in the book of the genome. But, as soon as something disturbs their sleep (like a mutation or a new virus invading the host) viruses can awaken and rebuild their physical bodies from a purely genetic form. When the wrong (or right, depending on your perspective) protein manages to leak out of a dormant viral gene, it is like the virus is suddenly awake again. A new physical body means that it has all the tools necessary to replicate.

Even beyond these rhythmic cycles, certain kinds of viruses don’t need a physical form at all. These disembodied viruses are called transposable elements, or transposons. True viruses have a body made from proteins, but transposons are mobile genetic elements — sequences of DNA that physically move in and out of genomes. For this reason, they are often referred to as “jumping genes.” Transposons do very much the same thing as true viruses, i.e. they copy and paste themselves throughout genomes. They are so similar to true viruses that some endogenous retroviruses (ERVs) are themselves transposons. As stated above,

8% of the human genome is made up of ERVs, but nearly 50% of the human genome is made of transposons! Humans are basically just big piles of viral-like sequences.

Transposons have a disturbing capacity to disrupt important genes by inserting themselves into the DNA sequences. It’s like if a series of words in a book could physically move around from page to page — these words would have a high likelihood of jumping into the middle of a sentence, thereby making it nonsensical. Amazingly, transposons preferentially insert themselves into important and functional genes — as if those jumping words wanted to disrupt the most interesting parts of the book rather than the index or bibliography. This is a powerful evolutionary strategy, since transposons are much more likely to get “read” by a cell if they jump into the middle of an important (and therefore, active) gene.

Transposons can very easily mess up important genes that we need to survive, so it has been theorized that epigenetic mechanisms evolved to stop transposons from moving around the genome. Furthermore, since transposons can rapidly alter DNA sequences, they are thought to play a major role in the processes of evolution and speciation (how a species evolves into a new form). In plants, transposons become highly active in response to stressful conditions, and this could act as a rapid source of short-term mutation when the environment starts pressuring you to survive or die. In addition, an animal’s genome changes when they are domesticated (like going from a wolf to a dog, or from an aurochs to a cow), and a majority of these changes occur in transposon sequences. No one is really sure why or how this happens, but it is clear that viruses play a very important role in rapid genetic change.

A biological virus (whether it is a true virus, an endogenous retrovirus, or a transposon) can literally lay dormant in a word document as a string of As, Ts, Cs, and Gs. In other words, viruses can exist independently of genetics, solely in the symbolic dimension of evolution. A virus is nothing more than an idea until it finds a host within which it can replicate itself. Despite their ephemerality, viral sequences are clearly important for our lives as humans. After all, they compose nearly half of our genome and seem to play an important role in our long-term evolution.

In many ways, viruses are eerily reminiscent of the idea of ancient spells, which sit quietly as words in a book until someone utters the mystical syllables and unleashes the magic contained within. Perhaps due to the mysticism of this concept, many scientists and philosophers have a hard time accepting viruses as living things. But, whether or not you classify viruses as living entities, they certainly show us that the line between living things and pure information is a lot fuzzier than we often think…

Copyright © 2019 by Ben L. Callif. Used by permission of S. Woodhouse Books, an imprint of Everything Goes Media. All rights reserved.

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