ArticleMolecular and cellular biology2006
Specific role of the SR protein splicing factor B52 in cell cycle control in Drosophila.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Hereditary retinoblastoma iPSC model reveals aberrant spliceosome function driving bone malignancies.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- An alternatively spliced form affecting the Marked Box domain of Drosophila E2F1 is required for proper cell cycle regulation.PLoS genetics · 2018Article
- A new function of the splicing factor SRSF2 in the control of E2F1-mediated cell cycle progression in neuroendocrine lung tumors.Cell cycle (Georgetown, Tex.) · 2013Article
- Endoreplication: polyploidy with purpose.Genes & development · 2009Review
- Article
- Specific combinations of SR proteins associate with single pre-messenger RNAs in vivo and contribute different functions.The Journal of cell biology · 2009Article
- Intrinsic negative cell cycle regulation provided by PIP box- and Cul4Cdt2-mediated destruction of E2f1 during S phase.Developmental cell · 2008Article
- Suppressors of the cdc-25.1(gf)-associated intestinal hyperplasia reveal important maternal roles for prp-8 and a subset of splicing factors in C. elegans.RNA (New York, N.Y.) · 2008Article
- dE2F2-independent rescue of proliferation in cells lacking an activator dE2F1.Molecular and cellular biology · 2007Article
- Identification of RNA binding sequences of Drosophila SR protein DX16.Molecular and cellular biochemistry · 2007Article
- The SR family proteins B52 and dASF/SF2 modulate development of the Drosophila visual system by regulating specific RNA targets.Molecular and cellular biology · 2007Article
- Eye development under the control of SRp55/B52-mediated alternative splicing of eyeless.PloS one · 2007Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
E2F and retinoblastoma tumor suppressor protein pRB are important regulators of cell proliferation; however, the regulation of these proteins in vivo is not well understood. In Drosophila there are two E2F genes, an activator, de2f1, and a repressor, de2f2. The loss of de2f1 gives rise to the G(1)/S block accompanied by the repression of E2F-dependent transcription. These defects can be suppressed by mutation of de2f2. In this work, we show that the de2f1 mutant phenotype is rescued by the loss of the pre-mRNA splicing factor SR protein B52. Mutations in B52 restore S phase in clones of de2f1 mutant cells and phenocopy the loss of the de2f2 function. B52 acts upstream of de2f2 and plays a specific role in regulation of de2f2 pre-mRNA splicing. In B52-deficient cells, the level of dE2F2 protein is severely reduced and the expression of dE2F2-dependent genes is deregulated. Reexpression of the intronless copy of dE2F2 in B52-deficient cells restores the dE2F2-mediated repression. These results uncover a previously unrecognized role of the splicing factor in maintaining the G(1)/S block in vivo by specific regulation of the dE2F2 repressor function.
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