Journal
IMMUNITY
Volume 34, Issue 4, Pages 492-504Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2011.03.017
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Categories
Funding
- NIH [AI042370, AI076458, AI061699, DK080949, AGA-FDHN, T32HD007516, AI37584, AI46564, CA093615, GM053256, AR052802]
- Abramson Family
- NHMRC
- Peter MacCallum Cancer Centre
- HFSP
- ARC
- UCSD Digestive Diseases Research Development Center [DK80506]
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Polarized segregation of proteins in T cells is thought to play a role in diverse cellular functions including signal transduction, migration, and directed secretion of cytokines. Persistence of this polarization can result in asymmetric segregation of fate-determining proteins during cell division, which may enable a T cell to generate diverse progeny. Here, we provide evidence that a lineage-determining transcription factor, T-bet, underwent asymmetric organization in activated T cells preparing to divide and that it was unequally partitioned into the two daughter cells. This unequal acquisition of T-bet appeared to result from its asymmetric destruction during mitosis by virtue of concomitant asymmetric segregation of the proteasome. These results suggest a mechanism by which a cell may unequally localize cellular activities during division, thereby imparting disparity in the abundance of cell fate regulators in the daughter cells.
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