`Sugary mutation` may have led to rise of humans
A genetic mutation that switched off a sugar-making enzyme in early hominids may possibly helped accelerate their evolution some three million years ago.
Washington: A genetic mutation that switched off a sugar-making enzyme in early hominids may possibly have boosted their malarial resistance and helped accelerate their
evolution some three million years ago.
According to researchers at the University of California, San Diego School of Medicine, the mutation tweaked one type of sugar molecule, Neu5Gc, in early hominids, Homo ergaster and Homo erectus, some three million years ago.
This mutation halted the production of this molecule, and the prehuman immune system began to recognise it as a threat.
As a result, the researchers said, some hominids would no longer have been able to mate and produce offspring with other populations, potentially driving early humans apart from other apes.
"Over time, this incompatibility would reduce and the eliminate individuals with Neu5Gc," study researcher Pascal Gagneux was quoted as saying by LiveScience.
Cells communicate with other cells using sugar molecules that stud the outsides of their membranes. One type of sugar molecule is sialic acid, which is found on all animal cells.
Until about three million years ago, the common ancestors of humans and other apes shared Neu5Gc, a type of sialic acid also known as N-glycolylneuraminic acid, the researchers said.
Then, a mutation stopped production of Neu5Gc in human ancestors, possibly because this mutation helped the hominids avoid strains of malaria that still infect chimpanzees today.
Instead, the ancestors with the mutation made a different version of the sialic acid, Neu5Ac, the researchers said.
Gagneux and his colleagues, who detailed their research in the Proceedings of the National Academy of Sciences, tested the idea by exposing chimpanzee sperm, with its Neu5Gc-bearing cells, to human antibodies for the molecule.
They found the antibodies killed the chimp sperm. Female mice engineered to have an immune response to Neu5Gc likewise produced fewer offspring when mated with Neu5Gc-positive males.
In other words, the researchers added, a tiny change in one little molecule could have helped drive populations to diverge from one another, as only Neu5Ac-positive ancestors
could mate with other Neu5Ac-positive ancestors, and those human ancestors without the mutation were unable to produce as many offspring.