Washington, Aug 25 : A mother and a daughter can be similar yet so different. Northwestern University researchers now know the reason why, at least in yeast cells.
A new mechanism had been found to be responsible for cell fate determination - how one cell, the daughter, becomes dramatically different from the mother, in spite of sharing the same genetic material.
When a yeast cell divides it produces a mother cell and a smaller, different daughter cell. The latter is the one that actually performs the final act of separation. And the daughter takes longer than the mother to begin the next cycle of division, since it needs time to grow up.
The key to the researchers' discovery of how this differentiation works is the gene regulator Ace2, a protein that directly turns genes on. The researchers found the protein gets trapped in the nucleus of the daughter cell, turning on genes that make daughter different from mother.
Researchers also found that the differentiation of the mother and daughter cell - this trapping of the regulator in the daughter nucleus - occurs while the two are still connected.
Many of the fundamental mechanisms for cell division in yeast are also very similar in mammals; many of the proteins involved in human disease are related to proteins involved in yeast cell division.
The new knowledge about cell fate determination could lead to a better understanding of healthy human cells, what goes awry in cancer cells and how stem cells and germ cells work.
"Cancer may reflect a partial and aberrant loss of differentiated character, in which cells that were formerly specified to perform a specific task 'forget' that, and become more like the rapidly dividing stem cells from which they came," said Eric L. Weiss, assistant professor at the Northwestern's Weinberg College of Arts and Sciences. He led the research team.
The co-authors are Emily Mazanka, Brian J. Yeh and Patrick Charoenpong from Northwestern; and Jes Alexander, Drew M. Lowery and Michael Yaffee from the Massachusetts Institute of Technology.
--- IANS
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