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Mitotic cells: separate but unequal

Mitotic cell divisions, long thought to produce two identical daughter cells, are not entirely equal, according to a new linkurl:study;http://www.pnas.org/cgi/doi/10.1073/pnas.0803027105 published this week in __Proceedings of the National Academy of Sciences__. Proteins destined for degradation are preferentially inherited by one cell over the other, the researchers found. "We hit on an observation that people had missed for 100 years," said linkurl:Eddy De Robertis;http://www.hhmi.ucla.edu/de

By | May 19, 2008

Mitotic cell divisions, long thought to produce two identical daughter cells, are not entirely equal, according to a new linkurl:study;http://www.pnas.org/cgi/doi/10.1073/pnas.0803027105 published this week in __Proceedings of the National Academy of Sciences__. Proteins destined for degradation are preferentially inherited by one cell over the other, the researchers found. "We hit on an observation that people had missed for 100 years," said linkurl:Eddy De Robertis;http://www.hhmi.ucla.edu/derobertis/ of the University of California, Los Angeles, who led the study. Chromosomes and the mitotic machinery are usually partitioned equally into each new daughter cell during mitosis. Researchers generally assumed this was also true of all other cellular material. But De Robertis and his colleagues now show that for spent proteins, cell division yields an uneven split -- even when dividing cells are bound for the same linkurl:cell fate.;http://www.the-scientist.com/article/display/21075/ De Robertis' team focused on a cell signaling protein called Smad1. After Smad1 is activated, it becomes primed for destruction through a series of phosphorylation events. The researchers used antibodies specific to phosphorylated Smad1 and found that 80-90% of dividing human embryonic stem cells shared the protein unequally. Smad1 proteins when not phosphorylated, however, were entirely uniform. Asymmetric mitoses were also observed in two other phosphorylated proteins primed for destruction, and in two other cell types: monkey cells __in vitro__, and __Drosophila__ embryos __in vivo__. What's more, the researchers showed that unequal distributions were maintained through three consecutive cell divisions. De Robertis hypothesizes that that when centrosomes -- a main component of the linkurl:microtubule;http://www.the-scientist.com/article/display/20525/ organizing center -- duplicate and separate to occupy opposite poles of the dividing cell, the material surrounding the centrosomes remains largely in one pole. Such imbalance may act as a cleansing mechanism to keep one daughter cell "pristine," while the other cell undergoes apoptosis, he said. linkurl:Yukiko Yamashita;http://lsi.umich.edu/facultyresearch/labs/yamashita/pi of the University of Michigan, Ann Arbor, however, was not convinced that asymmetrical mitoses are necessarily an adaptive cellular clean-up process. An alternative scenario, she told __The Scientist__, is that some centrosomes build more microtubules than others. These microtubules then attract more organelles, which results in proteasomes and their target proteins becoming unequally distributed. To test whether "bad" proteins are indeed confined into one cell to protect the other, linkurl:Yamashita;http://www.the-scientist.com/article/display/21585/ proposed disrupting the asymmetric segregation of proteins destined for degradation to see whether it leads to premature cell linkurl:aging and senescence.;http://www.the-scientist.com/article/display/23041/
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Comments

Avatar of: anonymous poster

anonymous poster

Posts: 1

May 21, 2008

Could you please update the reference to the supporting article. There is no article from Dr. Robertis listed in the PNAS journal dated 5/20/2008. \n\nThanks for an interesting post!
Avatar of: Alla Katsnelson

Alla Katsnelson

Posts: 17

May 22, 2008

Thanks for your note. As you rightly point out, the link we provided to the study is not yet active According to PNAS, the article will be published at that link at some point this week, so please check back.\n-Alla Katsnelson, news editor

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