Physical and Functional Interactions between Drosophila Homologue of Swc6/p18Hamlet Subunit of the SWR1/SRCAP Chromatin-remodeling Complex with the DNA Repair/Transcription Factor TFIIH

Herrera-Cruz, Mariana; Cruz, Grisel; Valadéz-Graham, Viviana; Fregoso-Lomas, Mariana; Villicaña, Claudia; Vázquez, Martha; Reynaud, Enrique; Zurita, Mario

doi:10.1074/jbc.m112.383505

Cited by 10 publications

(27 citation statements)

References 55 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We have previously reported a p8 gene null allele ( p8 − ), which is semilethal, though the males are sterile [16]. Semi-lethality and sterile organisms were also observed from heteroallelic combinations between a P-element insertion allele ( p52 EP3605 ) and point mutation alleles ( p52 mrn 3 and p52 mrn 5 ) in the p52 subunit of TFIIH [15].…”

Section: Resultsmentioning

confidence: 99%

“…The Pc-GFP transgenic line (BL9593) was obtained from the Bloomington Stock Center. The p52 EP3605 , p52 mrn 5 , p52 mrn 3 and p8 − alleles were previously described [15,16]. …”

Section: Methodsmentioning

confidence: 99%

“…Total protein extracts were analysed by immunoblotting using standard procedures. Primary antibodies used were: 8WG16 (1 : 1500; Covance), H14 (1 : 1500; Covance), XPD (1 : 1500; our own preparation), XPB (1 : 2000; our own preparation), p52 (1 : 1500 [16]), p8 (1 : 1000 [16]), Cdk7 (1 : 1000, Santa Cruz Biotechnology), TBP (1 : 500; Santa Cruz Biotechnology), E7 (1 : 2000; DSHB), A12 (1 : 1500; DSHB), F2F4 (1500; DSHB), JLA20 (1 : 3000; DSHB), GFP (1 : 2500; GenScript); p18 (1 : 1000; [16]) HRP-coupled secondary antibodies (1 : 3500; Invitrogen) were used for chemioluminiscence detection with Thermo Scientific Pierce ECL. Densitometric analyses in western blots were performed using I mage J software.…”

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Analysis ofDrosophila p8andp52mutants reveals distinct roles for the maintenance of TFIIH stability and male germ cell differentiation

Cruz‐Becerra¹,

Juárez²,

Valadéz-Graham³

et al. 2016

Open Biol.

Self Cite

View full text Add to dashboard Cite

Eukaryotic gene expression is activated by factors that interact within complex machinery to initiate transcription. An important component of this machinery is the DNA repair/transcription factor TFIIH. Mutations in TFIIH result in three human syndromes: xeroderma pigmentosum, Cockayne syndrome and trichothiodystrophy. Transcription and DNA repair defects have been linked to some clinical features of these syndromes. However, how mutations in TFIIH affect specific developmental programmes, allowing organisms to develop with particular phenotypes, is not well understood. Here, we show that mutations in the p52 and p8 subunits of TFIIH have a moderate effect on the gene expression programme in the Drosophila testis, causing germ cell differentiation arrest in meiosis, but no Polycomb enrichment at the promoter of the affected differentiation genes, supporting recent data that disagree with the current Polycomb-mediated repression model for regulating gene expression in the testis. Moreover, we found that TFIIH stability is not compromised in p8 subunit-depleted testes that show transcriptional defects, highlighting the role of p8 in transcription. Therefore, this study reveals how defects in TFIIH affect a specific cell differentiation programme and contributes to understanding the specific syndrome manifestations in TFIIH-afflicted patients.

show abstract

Section: Resultsmentioning

confidence: 99%

“…The Pc-GFP transgenic line (BL9593) was obtained from the Bloomington Stock Center. The p52 EP3605 , p52 mrn 5 , p52 mrn 3 and p8 − alleles were previously described [15,16]. …”

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Analysis ofDrosophila p8andp52mutants reveals distinct roles for the maintenance of TFIIH stability and male germ cell differentiation

Cruz‐Becerra¹,

Juárez²,

Valadéz-Graham³

et al. 2016

Open Biol.

Self Cite

View full text Add to dashboard Cite

show abstract

“…In this context, it has been shown that Dmp52, the Drosophila homolog of the p52 subunit of TFIIH, interacts with Dmp18, the homolog of Swc6/p18, a subunit of the SWR1/SRCAP complex responsible for H2AZ exchange in fungi and vertebrates (84). TFIIH might also disturb histone posttranslational modifications (PTMs) that normally occur on activated promoters (85).…”

Section: Nucleotide Excision Repairmentioning

confidence: 99%

Nucleotide Excision Repair and Transcriptional Regulation: TFIIH and Beyond

Compe

Egly

2016

Annu. Rev. Biochem.

139

122

View full text Add to dashboard Cite

Transcription factor IIH (TFIIH) is a multiprotein complex involved in both transcription and DNA repair, revealing a striking functional link between these two processes. Some of its subunits also belong to complexes involved in other cellular processes, such as chromosome segregation and cell cycle regulation, emphasizing the multitasking capabilities of this factor. This review aims to depict the structure of TFIIH and to dissect the roles of its subunits in different cellular mechanisms. Our understanding of the biochemistry of TFIIH has greatly benefited from studies focused on diseases related to TFIIH mutations. We address the etiology of these disorders and underline the fact that TFIIH can be considered a promising target for therapeutic strategies.

show abstract

“…Lysates were clarified to 13,000 rpm at 4˚C. CoIPs were performed as indicated in Herrera-Cruz et al (Herrera-Cruz et al, 2012) Antibodies Antibodies used were Dp53: D-200 and H3 (both antibodies recognize the two Dp53 isoforms), p62 Q-19, p89 S-19 and Cdk7 ds-17 (Santa Cruz); Dp53-H3 and Anti-BrdU G3G4 (Hybridoma Bank). Dmp52 antibody was raised using a carboxy-terminal peptide (-CDVKRYWKKYSKSGV-) by New England Peptides.…”

Section: Pulldown Assaymentioning

confidence: 99%

The genetic depletion or the triptolide inhibition of TFIIH in p53 deficient cells induce a JNK-dependent cell death in Drosophila

Villicaña¹,

Cruz²,

Zurita³

2013

Journal of Cell Science

Self Cite

View full text Add to dashboard Cite

SummaryTranscription factor IIH (TFIIH) participates in transcription, nucleotide excision repair and the control of the cell cycle. In the present study, we demonstrate that the Dmp52 subunit of TFIIH in Drosophila physically interacts with the fly p53 homologue, Dp53. The depletion of Dmp52 in the wing disc generates chromosome fragility, increases apoptosis and produces wings with a reduced number of cells; cellular proliferation, however, is not affected. Interestingly, instead of suppressing the apoptotic phenotype, the depletion of Dp53 in Dmp52-depleted wing disc cells increases apoptosis and the number of cells that suffer from chromosome fragility. The apoptosis induced by the depletion of Dmp52 alone is partially dependent on the JNK pathway. In contrast, the enhanced apoptosis caused by the simultaneous depletion of Dp53 and Dmp52 is absolutely JNK-dependent. In this study, we also show that the anti-proliferative drug triptolide, which inhibits the ATPase activity of the XPB subunit of TFIIH, phenocopies the JNK-dependent massive apoptotic phenotype of Dp53-depleted wing disc cells; this observation suggests that the mechanism by which triptolide induces apoptosis in p53-deficient cancer cells involves the activation of the JNK death pathway.

show abstract

Physical and Functional Interactions between Drosophila Homologue of Swc6/p18Hamlet Subunit of the SWR1/SRCAP Chromatin-remodeling Complex with the DNA Repair/Transcription Factor TFIIH

Cited by 10 publications

References 55 publications

Analysis ofDrosophila p8andp52mutants reveals distinct roles for the maintenance of TFIIH stability and male germ cell differentiation

Analysis ofDrosophila p8andp52mutants reveals distinct roles for the maintenance of TFIIH stability and male germ cell differentiation

Nucleotide Excision Repair and Transcriptional Regulation: TFIIH and Beyond

The genetic depletion or the triptolide inhibition of TFIIH in p53 deficient cells induce a JNK-dependent cell death in Drosophila

Contact Info

Product

Resources

About