roughex Down-regulates G2 cyclins in G1

Barbara J. Thomas, Kenton H. Zavitz, Xinzhong Dong, Mary E. Lane, Katrin Weigmann, Russell L. Finley, Roger Brent, Christian F. Lehner, S. Lawrence Zipursky

Research output: Contribution to journalArticlepeer-review

Abstract

Cell cycle arrest in G1 at the onset of patterning in the Drosophila eye is mediated by roughex. In roughex mutants, cells accumulate Cyclin A protein in early G1 and progress into g phase precociously. When Roughex is overexpressed in S/G2 cells, Cyclin A is mislocalized to the nucleus and degraded, preventing mitosis. Whereas Roughex inhibits Cyclin A accumulation, Cyclin E down-regulates Roughex protein in vivo. Roughex binds to Cyclin E and is a substrate for a Cyclin E-Cdk complex in vitro. These data argue that Roughex inhibits Cyclin A accumulation in early G1 by targeting Cyclin A for destruction. In late G1, Roughex is destabilized in a Cyclin E-dependent process, releasing Cyclin A for its role in S/G2.

Original languageEnglish (US)
Pages (from-to)1289-1298
Number of pages10
JournalGenes and Development
Volume11
Issue number10
DOIs
StatePublished - May 15 1997
Externally publishedYes

Keywords

  • Cell cycle
  • Drosophila
  • G
  • cyclin A
  • eye development
  • protein stability

ASJC Scopus subject areas

  • Genetics
  • Developmental Biology

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