Awardee OrganizationUNIVERSITY OF CALIFORNIA, SAN FRANCISCO
Description
Abstract Text
The precise patterns of embryonic cell division contribute to normal
morphogenesis and reflect tight control of cell proliferation in
metazoans. Identification of the mechanisms of this control should
illuminate aspects of embryonic patterning and of diseases resulting from
defects in the control of cell proliferation. Cell cycle regulators and
the developmental programs that influence their activity are widely
conserved. However, development does not simply impose controls on a
standard cell cycle. It changes the very nature of the cycle, deleting and
adding steps by changing the levels of fundamental cell cycle components.
Drosophila provides a powerful model system for analyses of these
developmental controls: in addition to genetic, molecular and
developmental tools, many characterized cell cycle regulators are
available in this organism. Cycles 1-7 forgo all familiar controls. Only
exit from mitosis seems regulated, perhaps by cytoskeletal influences on
cyclin B degradation. The importance of cyclin degradation will be tested
by introduction of non-destructible mutants of cyclin, and cyclin
stability will be examined in mutants defective in arrest at the first
mitosis. During cycles 1-16, progress to S phase is limited only by a
requirement to pass through mitosis. The DNA is thought to gain the
license to replicate once each time it passes through mitosis. We will
test the roles of candidate licensing factor genes cloned by homology to
yeast replication genes. Progress to mitosis is usually blocked if DNA
synthesis is arrested. This S phase checkpoint control involves inhibitory
phosphorylation of Cdc2, and becomes operative only at cycle 14 when this
inhibitory phosphorylation first occurs. We will examine regulation of a
recently cloned kinase that is apparently responsible for this inhibitory
phosphorylation. Rapid cell cycling inhibits transcription in early
embryos, and cycle lengthening appears to be a key regulator of
transcription. We will test whether the mitotic Cdc2 kinase directly
inhibits transcription by phosphorylating RNA polymerase, and whether
passage of a replication fork interferes with ongoing transcription. In
cycle 14, another feature of cell cycle control becomes evident: the
orientation of cell division planes is regulated. We will identify genes
responsible for re-orienting division planes in stereotyped patterns.
No Sub Projects information available for 5R01GM037193-12
Publications
Publications are associated with projects, but cannot be identified with any particular year of the project or fiscal year of funding. This is due to the continuous and cumulative nature of knowledge generation across the life of a project and the sometimes long and variable publishing timeline. Similarly, for multi-component projects, publications are associated with the parent core project and not with individual sub-projects.
No Publications available for 5R01GM037193-12
Patents
No Patents information available for 5R01GM037193-12
Outcomes
The Project Outcomes shown here are displayed verbatim as submitted by the Principal Investigator (PI) for this award. Any opinions, findings, and conclusions or recommendations expressed are those of the PI and do not necessarily reflect the views of the National Institutes of Health. NIH has not endorsed the content below.
No Outcomes available for 5R01GM037193-12
Clinical Studies
No Clinical Studies information available for 5R01GM037193-12
News and More
Related News Releases
No news release information available for 5R01GM037193-12
History
No Historical information available for 5R01GM037193-12
Similar Projects
No Similar Projects information available for 5R01GM037193-12