Transcriptomics

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Comparative analysis of gene expression changes upon Cabut or dE2F1/dDP overexpression in the Drosophila wing


ABSTRACT: Investigation of whole genome gene expression level changes in dissected Drosophila wings at the wandering L3 larval stage, 24h after pupa formation and 36h after pupa formation, expressing either UAS-Cabut or UAS-dE2F1 + UAS-dDP under control of apterous-gal4 with a tubulin driven temperature-sensitive gal80 transgene, compared to the parental strain lacking UAS transgenes. A 36-chip study using total RNA recovered from four independently isolated samples of 10 dissected Drosophila wings at the indicated developmental stages expressing the indicated UAS-transgenes or the non-UAS-containing matched control strain. One sample (2D) did not pass our internal quality control and, therefore, was not included in the analysis. The dE2F1+dDP data included here is further discussed in L. Buttitta, A.J. Katzaroff, B.A. Edgar (2010). A robust cell cycle control mechanism limits E2F-induced proliferation of terminally differentiated cells in vivo. Journal of Cell Biology vol. 189, 981-96 (PMID 20548101). The Cabut data included here is further discussed in A.J. Katzaroff et al. (2011). The Krüppel-like-factor cabut has cell cycle regulatory properties similar to E2F.

ORGANISM(S): Drosophila melanogaster  

SUBMITTER: Alexia J Katzaroff   Bruce A Edgar  Laura Buttitta  Laura A Buttitta 

PROVIDER: E-GEOD-30484 | ArrayExpress | 2011-07-08

SECONDARY ACCESSION(S): GSE30484PRJNA143475

REPOSITORIES: GEO, ArrayExpress

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Publications

A robust cell cycle control mechanism limits E2F-induced proliferation of terminally differentiated cells in vivo.

Buttitta Laura A LA   Katzaroff Alexia J AJ   Edgar Bruce A BA  

The Journal of cell biology 20100601 6


Terminally differentiated cells in Drosophila melanogaster wings and eyes are largely resistant to proliferation upon deregulation of either E2F or cyclin E (CycE), but exogenous expression of both factors together can bypass cell cycle exit. In this study, we show this is the result of cooperation of cell cycle control mechanisms that limit E2F-CycE positive feedback and prevent cycling after terminal differentiation. Aberrant CycE activity after differentiation leads to the degradation of E2F  ...[more]

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