Three million years ago , a cistron mutation change over off a sugar - making enzyme in early hominids . Our root really became unable to engender with those who still had the enzyme , possibly causing the egress of our evolutionary grandparent , Homo erectus .
All animal cells are covered in a specific case of sugar atom known as sialic acids . These speck are an essential part of every jail cell ’s interaction with other cells and the wide environment , which means they ’re often the first tip of physical contact between the cubicle and dangerous pathogen . All living apes except humanity portion out a particular type of siliac acid , called N - glycolylneuraminic dot , or Neu5Gc .
Until about three million geezerhood ago , our hominid ascendant also carried Neu5Gc , along with all the other apes . But then a factor mutation caused the enzyme creditworthy for making Neu5Gc to switch off . We do n’t know why this mutation take grasp , although one possible action is that a specially virulent tune of malaria play havoc on Neu5Gc , which imply hominid that could do without that exceptional sugar molecule would have an adaptive vantage .
To compensate for the loss of Neu5Gc , some hominids started producing more of a related siliac acid , Neu5Ac . What ’s more , they really embark on to develop a resistance in their resistant scheme to Neu5Gc . UC San Diego evolutionary biologist Pascal Gagneux explains :
“ This pass at about the same meter as former humankind were on the face of it becoming major predators in their surround . It ’s hard to be sure exactly what happened because evolution works on so many things at the same time , but the change in sialic acid meant that early mankind developed an immune response to Neu5Gc . It became viewed by their resistant systems as strange , something to be destroyed . At about the same time , they commence eating flushed meat , a major generator of Neu5Gc , which may have further cause the resistant response . ”
The tonality here is that some hominid still carried Neu5Gc while others had now develop an resistant response against this sugar molecule . Now , envisage what would happen if a male person from the first grouping hear to match with a female from the second group . The male person ’s Neu5Gc - carrying sperm would be targeted and destroy by the female person ’s Neu5Gc - insubordinate resistant system .
It would of a sudden become passing difficult for the first group to mate with the second group . And when two groups can no longer successfully procreate with each other , you have the birth of two novel distinct species . Gagneux and his fellow researchers were able to demonstrate this event by by artificial means exposing chimp sperm , which has Neu5Gc , to human antibodies . The antibodies consistently eliminated the chimp sperm before construct could ever have taken place .
Subsequent experiment with genetically altered mouse – some of whom carry Neu5GC while the rest carry Neu5Gc - repellent antibodies – suggests the fertility rate between the two groups did n’t drop immediately to zero , but rather it slow became more and more difficult for successful reproduction to pass . Gagneux explain that this slow process really crap speciation easier than a sudden drop , perhaps because it allows for the divergent populations to stabilise before being completely set apart from one another .
In any issue , this is grounds for an evolutionary cognitive operation known as speciation by contagion , in which disease can actually make one universe reproductively incompatible with another . We know from previous study that our ancestors lose Neu5Gc powerful around the same metre as when Homo erectus first come forth , lend credenza to the idea that , rather signally , infection and bread helped put us on our current evolutionary path .
ViaPNAS . icon of Homo erectus by Smithsonian National Museum of Natural History ’s Human Origins Program . graphical by UC San Diego School of Medicine .
BiologyEvolutionHuman evolutionInfectionMalariaScienceSugar
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