New York, Jan 9 (IANS) For those who are curious about how life began on Earth, all it took was one random mutation more than 600 million years ago to start multicellular life on our planet, new research suggests.
With that random act, a new protein function was born that helped our single-celled ancestor transition into an organised multicellular organism.
Proteins are the workhorses of our cells, performing a wide variety of tasks such as metabolism.
Our work suggests that new protein functions can evolve with a very small number of mutations. In this case, only one was required, said biochemist Ken Prehoda from University of Oregon.
This mutation is one small change that dramatically altered the protein's function, allowing it to perform a completely different task.
You could say that animals really like these proteins because there are now over 70 of them inside of us, Prehoda added.
For the research, Prehoda's team looked at choanoflagellates which are a group of free-living, single-celled organisms considered to be the closest living relative of animals.
These sponge-like, seawater-dwelling organisms have a short, outward-facing squiggly tail called a flagellum that allows them to move and gather food.
Prehoda and colleagues then used ancestral protein reconstruction, a technique devised by co-author Joseph W Thornton, a biologist now at University of Chicago.
The team identified a mutation that was important for opening the door to organised multicellular animals that eventually no longer needed their tails.
They also found that the choanoflagellate flagellum is critical for organising its multi-cellular colony, suggesting that this may have also been the case as our single-celled ancestor transitioned to a multi-cellular lifestyle.
The protein domain that resulted from this mutation is found today in all animal genomes and their close unicellular relatives but absent in other life forms.
The research helps to address several important questions that scientists have had about evolution.
It also has implications for studying diseases such as cancer in which damaged cells no longer cooperate with other cells in our bodies and revert back to a unicellular state where each is on its own, the authors noted in a paper appeared in the journal eLife.
