Translational regulation is a crucial aspect of gene expression during oogenesis and early embryogenesis in all animals, and is also important in somatic tissues. A strategy has been developed for examining the components of this regulatory pathway using the Power of Drosophila molecular genetics. 1. The role of cytoplasmic polyadenylation in translation regulation in Drosophila will be investigated. The translational activation of bicoid mRNA during early embryogenesis is correlated with an increase in its poly (A) tail length. To study whether polyadenylation is required for translation, the rescuing ability will be determined of various bicoid transcripts injected into embryos derived from females homozygous for a null bicoid mutation. mRNA sequences that control translational activation will also be investigated using both injection of synthetic transcripts and production of transgenic files. 2. Mutations in the cortex gene behave as recessive, maternal-effect mutations. Embryos derived from females homozygous for a cortex mutations arrest early in development. Although these embryos contain normal amounts of properly spliced and localized bicoid mRNA, this mRNA is not translated. In addition, the polyadenylation of bicoid mRNA that normally accompanies early development does not occur. These results implicate the cortex gene in polyadenylation and translational activation of bicoid mRNA. Therefore, the phenotype of cortex mutants will be investigated (the time and characteristics of embryonic arrest), and the cortex gene will be cloned and sequenced to clarify its role in early development. 3. Other collections of maternal-effect mutations will be analyzed to identify additional genes that participate in maternal mRNA activation, using the same strategy that showed a role for cortex in bicoid translational control. The phenotype, nature of the gene product, and expression pattern will be determined of mutations that exhibits defects in translational activation, and their functional interactions with and genetic relationship to the cortex gene will be studied.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Research Project (R01)
Project #
3R01GM051584-04S1
Application #
2834534
Study Section
Molecular Biology Study Section (MBY)
Project Start
1994-08-01
Project End
1999-01-31
Budget Start
1997-08-01
Budget End
1999-01-31
Support Year
4
Fiscal Year
1998
Total Cost
Indirect Cost
Name
State University New York Stony Brook
Department
Pharmacology
Type
Schools of Medicine
DUNS #
804878247
City
Stony Brook
State
NY
Country
United States
Zip Code
11794