October 9 - 12, 2012
Building 10 & Natcher Conference Center
- General Schedule of Events
- Opening Plenary Session
- Concurrent Symposia Sessions
- Poster Sessions
- National Graduate Student Research Conference
- FARE Award Ceremony
- Special Exhibits on Resources for Intramural Research
- TSA Research Festival Exhibit Show
- Clinical Center Tours
- Research Festival Committees
- Past Research Festivals
Centriole disengagement in the absence of microtubules
| Thursday, November 07, 2013 — Poster Session II | |||
|---|---|---|---|
12:00 p.m. – 2:00 p.m. |
FAES Academic Center (Upper-Level Terrace) |
NCI |
CHEMCELL-24 |
Authors
- A.K. Shukla
- J. Loncarek
Abstract
Cells control centrosome number by controlling centriole duplication. Centrioles duplicate by forming new centriole (procentriole) in close association (engagement) with pre-existing mother centriole, an association which persists until the end of the cell cycle. Premature disengagement between two centrioles creates permissive conditions for erroneous centriole reduplication within the same cell cycle. Supernumerary centrosomes are a hallmark of most tumors, however, how centrioles disengage and reduplicate is still not clear at molecular level. In this study, we are testing whether centriole disengagement requires functional microtubule (MT) network. In order to test the requirement of MTs for centriole disengagement during mitosis, we disrupted MTs during various stages using inhibitor of MT polymerization (nocodazole), and assessed centriole disengagement status by live and fixed cell microscopy. In addition, we compared the process of centriole disengagement during prolonged interphase in the cells with or without interphase MTs. For that purpose, we generated mammalian cell lines where rapid centriole disengagement during S or G2 phase arrest can be induced upon Plk1-RFP expression by doxycycline. Our results demonstrate that centrioles can efficiently disengage without functional microtubule network during mitosis as well as interphase.
