Main Category: Stem Cell Research
Also Included In: Genetics
Article Date: 16 Sep 2013 – 1:00 PDT
Working with Dr. Zwaka and Dr. Dejosez on the study were co-authors V. L. Brandt from the Black Family Stem Cell Institute, and Hiroki Ura, PhD, from Baylor College of Medicine in Houston.
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“We could understand that p53 might foster cooperation, because loss of p53 function is a step in the development of many cancers. But finding that top1 and olfactory receptors may have the same function was a surprise,” he says. “We think these genes have the ancient function of safeguarding multicellular organisms by helping cells to coordinate their activities.”
The work was funded by the Huffington Foundation and by the National Institutes of Health (grants R01 GM077442 and P01 GM81627).
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The findings, if backed by future research, offer a new way to address disease, Dr. Zwaka says. Understanding the genetic basis of cooperative and competitive cellular behaviors could explain how cancer and immune system dysfunction develops, he says. “If a cell has lost a gene that fosters communication among cells, it may dominate other cells by ignoring signals to stop proliferating. It also makes sense that the immune system might detect and attack cells that are not cooperating. Failure to cooperate may also underlie development of birth defects.”
A network of genes with an ancient function
We often think of human cells as tiny computers that perform assigned tasks, where disease is a result of a malfunction. But in the current issue of Science, researchers at The Mount Sinai Medical Center offer a radical view of health – seeing it more as a cooperative state among cells, while they see disease as result of cells at war that fight with each other for domination.
“Cell misbehave, they are unpredictable. They do not operate like little machines,” he says. “What our study suggests is that cooperation is so central to our evolution that we have genetic mechanisms to protect us against cheating and dominating behavior.”
The scientists then tested the effects of knocking down these genes in developing mouse embryos. To their surprise, p53 and Top1 knockdown embryos developed normally – perhaps because other intact social enforcement genes took over.
They conducted a genetic screen in stem cells to look for mutants that allow cells to “misbehave – to become a little antisocial and do things they wouldn’t normally do,” Dr. Zwaka says. The screen picked up about 100 genes, which seem to cluster together into a network.
The research team, which also includes study first author Marion Dejosez, PhD, Assistant Professor at the Icahn School at Mount Sinai, took a long view toward the behavior of cells. They wondered how it was that cells, which lived on earth as single units for hundreds of millions of years, could effectively bundle themselves together to perform specific tasks. “Cells started somehow to form alliances, and to cooperate, and obviously this multicellularity had certain advantages.”
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“Both competition and cooperation drive evolution, and we are wired for cooperation all the way down to our genes,” says the study’s senior investigator, Thomas P. Zwaka, MD, PhD, Professor at the Black Family Stem Cell Institute at the Icahn School of Medicine at Mount Sinai.
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