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Are genetic determinants of asymmetric stem cell division active in hematopoietic stem cells?

Abstract

Stem cells have acquired a golden glow in the past few years as they represent possible tools for reversing the damage wreak on organs. These cells are found not only in major regenerative tissues, such as the epithelia, blood and testes, but also in ‘static tissues’, such as the nervous system and liver, where they play a central role in tissue growth and maintenance. The mechanism by which stem cells maintain populations of highly differentiated, short-lived cells seems to involve a critical balance between alternate fates: daughter cells either maintain stem cell identity or initiate differentiation. Recent studies in lower organisms have unveiled the regulatory mechanisms of asymmetric stem cell divisions. In these models, the surrounding environment likely provides key instructive signals for the cells to choose one fate over another. Our understanding now extends to the intrinsic mechanisms of cell polarity that influence asymmetrical stem cell divisions. This article focuses on the genetic determinants of asymmetric stem cell divisions in lower organisms as a model for studying the process of self-renewal of mammalian hematopoietic stem cells.

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Acknowledgements

We wish to acknowledge all members of our laboratory for insightful discussion and for their constant support. We also thank Dr Ihor R Lemischka and Jason A Hackney for the access to the updated version of the StemCell Database. This work was funded by a research grant from the National Cancer Institute of Canada (#013241). AF is a recipient of a FRSQ studentship; JL is a recipient of a post-doctoral fellowship from the Human Frontiers in Science Program (HFSP) and GS is a scholar of the Leukemia and Lymphoma Society of America.

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Correspondence to Guy Sauvageau.

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StemCell Database: stemcell.princeton.edu/search_page.html

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Faubert, A., Lessard, J. & Sauvageau, G. Are genetic determinants of asymmetric stem cell division active in hematopoietic stem cells?. Oncogene 23, 7247–7255 (2004). https://doi.org/10.1038/sj.onc.1207944

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