Home List of Titles Asymmetric proteasome segregation as a mechanism for unequal partitioning of the transcription factor T-bet during T Lymphocyte division
Please use this identifier to cite or link to this item: http://hdl.handle.net/1959.3/190930
- Asymmetric proteasome segregation as a mechanism for unequal partitioning of the transcription factor T-bet during T Lymphocyte division
- Chang, John T.; Ciocca, Maria L.; Kinjyo, Ichiko; Palanivel, Vikram R.; McClurkin, Courtney E.; DeJong, Caitlin S.; Mooney, Erin C.; Kim, Jiyeon S.; Steinel, Natalie C.; Oliaro, Jane; Yin, Catherine C.; Florea, Bogdan I.; Overkleeft, Herman S.; Berg, Leslie J.; Russell, Sarah M.; Koretzky, Gary A.; Jordan, Martha S.; Reiner, Steven L.
- 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.
- Publication type
- Journal article
- Research centre
- Swinburne University of Technology. Faculty of Engineering and Industrial Sciences. Centre for Micro-Photonics
- Immunity, Vol. 34, no. 4 (Apr 2011), pp. 492-504
- Publication year
- FOR Code(s)
- 1107 Immunology
- Asymmetric partitioning; Cell division; Polarization; Segregation; T cells; T Lymphocytes
- Cell Press
- Publisher URL
- Copyright © 2011.
- Peer reviewed