Format

Send to

Choose Destination
See comment in PubMed Commons below
Curr Biol. 1997 Jul 1;7(7):488-99.

S-phase function of Drosophila cyclin A and its downregulation in G1 phase.

Author information

1
Department of Genetics, University of Cologne, Weyertal 121, 50931, Cologne, Germany.

Abstract

BACKGROUND:

Cyclin E is the normal inducer of S phase in G1 cells of Drosophila embryos. Stable G1 quiescence requires the downregulation both of cyclin E and of other factors that can bypass the normal regulation of cell cycle progression.

RESULTS:

High-level expression of cyclin A triggered the G1/S transition in wild-type embryos and in mutant embryos lacking cyclin E. Three types of control downregulated this activity of cyclin A. First, cyclin destruction limited the accumulation of cyclin A protein in G1. Second, inhibitory phosphorylation of cdc2, the kinase partner of cyclin A, reduced the S-phase promoting activity of cyclin A in G1. Third, rux, a protein with unknown biochemical function, limited cyclin A function in G1. Overexpression of rux blocked S phase induction by coexpressed cyclin A and promoted the degradation of cyclin A. Rux also prevented a stable cyclin A mutant from inducing S phase, indicating that inhibition does not require cyclin destruction, and drove the nuclear localization of cyclin A.

CONCLUSIONS:

Cyclin A can drive the G1/S transition, but this function is suppressed by three types of control: cyclin A destruction, inhibitory phosphorylation of cdc2, and inhibition by rux. The partly redundant contributions of these three inhibitory mechanisms safeguard the stability of G1 quiescence until the induction of cyclin E. The action of rux during G1 resembles the action of inhibitors of mitotic kinases present during G1 in yeast, although no obvious sequence similarity exists.

PMID:
9210381
PMCID:
PMC2754254
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Support Center