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A more recent version of this article appeared on September 1, 2002
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Submitted on February 14, 2002
Revised on May 14, 2002
Accepted on June 14, 2002
1 Department of Genetics and Molecular Physiology, Institute of Biotechnology, Universidad Nacional Autónoma de México, Apdo Postal 510-3, Cuernavaca, Morelos 62250 México
* Corresponding author. E-mail address: marioz{at}ibt.unam.mx.
Mutations in XPB and XPD TFIIH helicases have been related with three hereditary human disorders: Xeroderma pigmentosum, Cockayne syndrome and trichothiodystrophy. The dual role of TFIIH in DNA repair and transcription makes difficult to discern which of the mutant TFIIH phenotypes are due to defects in any of these different processes. We used haywire (hay), the Drosophila XPB homologue, to dissect this problem. Our results show that when hay dosage is affected, the fly shows defects in structures that require high levels of transcription. We found a genetic interaction between hay and cdk7 and we propose that some of these phenotypes are due to transcriptional deficiencies. We also found more apoptotic cells in imaginal discs and in the central nervous system of hay mutant flies than in wild type flies. Because this abnormal level of apoptosis was not detected in cdk7 flies, this phenotype could be related to defects in DNA repair. In addition the apoptosis induced by p53 Drosophila homologue (Dmp53) is suppressed in heterozygous hay flies.
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