The research which I propose here will address the general question of how the cell cycle can be regulated by developmental signals, with the specific goal of investigating the pathway(s) that enable the delay of meiotic division in Drosophila males until all spermatid differentiation genes are transcribed. Initial work in several labs has implicated Twine, the male meiosis-specific Cdc25, as an important player in the G2/M transition. The onset of meiotic division is known to require Twine activity; in addition, the translation of twine depends on wild-type function of several genes, including three encoding testis-specific TBP-associated factors (TAFs, can, mia, and sa), and an RNA-binding protein (Boule). The work proposed here will address the connection between the transcription factors, Boule, and twine translation. First, I will identify the mechanism by which Boule protein accumulation is controlled, since it is known to be absent in sa and mia mutants. Second, I will characterize the shortstop mutant and investigate the molecular mode of action of its wild-type product.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
1F32GM071260-01A1
Application #
6887018
Study Section
Special Emphasis Panel (ZRG1-F05 (20))
Program Officer
Portnoy, Matthew
Project Start
2005-09-15
Project End
2007-09-14
Budget Start
2005-09-15
Budget End
2006-09-16
Support Year
1
Fiscal Year
2005
Total Cost
$43,976
Indirect Cost
Name
Stanford University
Department
Anatomy/Cell Biology
Type
Schools of Medicine
DUNS #
009214214
City
Stanford
State
CA
Country
United States
Zip Code
94305