October 9 - 12, 2012
Building 10 & Natcher Conference Center
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- Opening Plenary Session
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- National Graduate Student Research Conference
- FARE Award Ceremony
- Special Exhibits on Resources for Intramural Research
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- Past Research Festivals
RNAi knockdown of RAD51 in mouse testicular cells reveals its role in meiotic homologous recombination in mammals
| Friday, November 08, 2013 — Poster Session III | |||
|---|---|---|---|
10:00 a.m. – 12:00 p.m. |
FAES Academic Center (Upper-Level Terrace) |
NIDDK |
GEN-5 |
Authors
- J. Dai
- R.D. Camerini-Otero
Abstract
During meiosis, homologous recombination (HR) enables populations to adapt during evolution by producing new combinations of DNA sequences, and also ensures the stability of the karyotype of the organism by controlling the accurate segregation of homologous chromosome pairs. In most eukaryotes, recombinases RAD51 and DMC1 play an essential role in the repair of double strand breaks during meiotic HR. In mammals, DMC1 knockout results in an arrest of meiosis at early prophase I stage, without completion of HR. However, the function of RAD51 during meiotic HR in mammals remains unclear, due to the embryonic lethality of the RAD51 knockout mouse. Here we present our functional studies of RAD51 during mouse spermatogenesis using siRNA to knockdown RAD51 both in vivo by injecting siRNAs into mouse seminiferous tubules and in an in vitro spermatogenesis system with cultured spermatocytes. Our results reveals that RAD51 is indispensable for mouse meiotic HR, and that the knockdown of RAD51 leads to the quick death of spermatocytes from early prophase I stage through a P53 dependent apoptotic pathway. The system we have developed provides an experimental setup for the study of a number of meiotic proteins.
