Repression of dMyc expression by Wingless promotes Rbf-induced G 1 arrest in the presumptive Drosophila wing margin

Molly Duman-Scheel, Laura A. Johnston, Wei Du

Research output: Contribution to journalArticle

55 Scopus citations

Abstract

Little is known about how patterns of cell proliferation and arrest are generated during development, a time when tight regulation of the cell cycle is necessary. In this study, the mechanism by which the developmental signaling molecule Wingless (Wg) generates G1 arrest in the presumptive Drosophila wing margin is examined in detail. Wg signaling promotes activity of the Drosophila retinoblastoma family (Rbf) protein, which is required for G 1 arrest in the presumptive wing margin. Wg promotes Rbf function by repressing expression of the G1-S regulator Drosophila myc(dmyc). Ectopic expression of dMyc induces expression of Cyclin E, Cyclin D, and Cdk4, which can inhibit Rbf and promote G1-S progression. Thus, G 1 arrest in the presumptive wing margin depends on the presence of Rbf, which is maintained by the ability of Wg signaling to repress dmyc expression in these cells. In addition to advancing the understanding of how patterned cell-cycle arrest is generated by the Wg signaling molecule during development, this study indicates that components of the Rbf/E2f pathway are targets of dMyc in Drosophila. Although Rbf/E2f pathway components mediate the ability of dMyc to promote G1 progression, dMyc appears to regulate growth independently of the RSF/E2f pathway.

Original languageEnglish (US)
Pages (from-to)3857-3862
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume101
Issue number11
DOIs
StatePublished - Mar 16 2004
Externally publishedYes

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