A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Reference Report

Reference
Citation Mitchell, N.C., Johanson, T.M., Cranna, N.J., Er, A.L., Richardson, H.E., Hannan, R.D., Quinn, L.M. (2010). Hfp inhibits Drosophila myc transcription and cell growth in a TFIIH/Hay-dependent manner.  Development 137(17): 2875--2884. (Export to RIS)
FlyBase ID FBrf0211524
Publication Type Research paper
PubMed ID 20667914
PubMed Abstract An unresolved question regarding the RNA-recognition motif (RRM) protein Half pint (Hfp) has been whether its tumour suppressor behaviour occurs by a transcriptional mechanism or via effects on splicing. The data presented here demonstrate that Hfp achieves cell cycle inhibition via an essential role in the repression of Drosophila myc (dmyc) transcription. We demonstrate that regulation of dmyc requires interaction between the transcriptional repressor Hfp and the DNA helicase subunit of TFIIH, Haywire (Hay). In vivo studies show that Hfp binds to the dmyc promoter and that repression of dmyc transcription requires Hfp. In addition, loss of Hfp results in enhanced cell growth, which depends on the presence of dMyc. This is consistent with Hfp being essential for inhibition of dmyc transcription and cell growth. Further support for Hfp controlling dmyc transcriptionally comes from the demonstration that Hfp physically and genetically interacts with the XPB helicase component of the TFIIH transcription factor complex, Hay, which is required for normal levels of dmyc expression, cell growth and cell cycle progression. Together, these data demonstrate that Hfp is crucial for repression of dmyc, suggesting that a transcriptional, rather than splicing, mechanism underlies the regulation of dMyc and the tumour suppressor behaviour of Hfp.
DOI 10.1242/dev.049585
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Language of Publication English
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Publication Type Journal
Abbreviation Development
Title Development
Publication Year 1987-
ISBN/ISSN 0950-1991
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