Apoptosis Is Induced in BHK Cells by the tsBN462/13 Mutation in the CCG1/TAFII250 Subunit of the TFIID Basal Transcription Factor

Sekiguchi, Toshio; Nakashima, Torahiko; Hayashida, Toshiro; Kuraoka, Akio; Hashimoto, Shuichi; Tsuchida, Nobuo; Shibata, Yosaburo; Hunter, Tony; Nishimoto, Tetsuya

doi:10.1006/excr.1995.1183

Cited by 35 publications

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“…We then examined if transfected cells had FITC-staining nuclei using ā uorescence microscope. Since exponentially growing cultures of tsBN462 cells ceased to replicate DNA after incubation for 15 h at 39.58C (Sekiguchi et al, 1995), few tsBN462 cells incorporated BUdR after 20 h at 39.58C. In contrast, a signi®cant number of cells transfected with the cyclin D1 expression vector underwent DNA replication at 39.58C as detected by BUdR incorporation, consistent with the increase in S phase population observed by FACScan analysis ( Figure 1a).…”

Section: Resultssupporting

confidence: 80%

“…A temperature dependent decrease of luciferase activity was still observed with the D-184 (Sekiguchi et al, 1995) and the pCDEB vector (hygromycin resistance) or the pCDEB vector only. Hygromycin resistant colonies were isolated at 33.58C and were analysed for their growth at 38.58C by FACScan analysis.…”

Section: Resultsmentioning

confidence: 96%

“…We coexpressed E1b19kK, because we previously observed that E1b19K e ectively protected cells from undergoing apoptosis at the restrictive temperature (Sekiguchi et al, 1995). Clones 1 and 2 expressing both E7 and E1b19K were able to proliferate and form colonies at 38.58C, whereas control clones 3 and 4 containing pCDEB vector alone did not.…”

Section: Resultsmentioning

confidence: 99%

“…CCG1/TAF II 250 is a key component of the TFIID complex, which is required for RNA polymerase II dependent transcription (Hisatake et al, 1993;Ruppert et al, 1993); CCG1/TAF II 250 has both protein kinase and acetyltransferase activities (Dikstein et al, 1996;Mizzen et al, 1996). At the restrictive temperature of 39.58C, tsBN462 cells arrest in G1 (Sekiguchi et al, 1987) and subsequently undergo apoptosis (Sekiguchi et al, 1995). Previously, we showed that D-type cyclin expression is decreased and p21 and p27 expression is increased in tsBN462 cells at 39.58C (Sekiguchi et al, 1996).…”

Section: Introductionmentioning

confidence: 96%

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Overexpression of D-type cyclins, E2F-1, SV40 large T antigen and HPV16 E7 rescue cell cycle arrest of tsBN462 cells caused by the CCG1/TAFII250 mutation

Sekiguchi

Nishimoto

Hunter³

1999

Oncogene

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Japan tsBN462 cells, which have a point mutation in CCG1/ TAF II 250, a component of TFIID complex, arrest in G1 at the nonpermissive temperature of 39.58C. Overexpression of D-type cyclins rescued the cell cycle arrest of tsBN462 cells, suggesting that the cell cycle arrest was through Rb. Consistent with this, overexpression of E2F-1, whose function is repressed by the hypophosphorylated form of Rb, also rescued the cell cycle arrest. Moreover, expression of the viral oncoproteins SV40 large T antigen and HPV16 E7, which both bind Rb and inactivate its function, rescued the cell cycle arrest, whereas HPV16 E6 did not. Mutation of the Rb-binding motif in E7 abrogated its ability to rescue the cell cycle arrest. Expression of exogenous cyclin D1, SV40 large T antigen or CCG1/TAF II 250 increased cyclin A expression at 39.58C. Coexpression of HPV16 E7 and adenovirus E1b19K, which blocks apoptosis, rescued the proliferation of tsBN462 cells at 38.58C. To investigate the mechanism underlying the lack of cyclin D1 expression, deletion analysis of cyclin D1 promoter was performed. The 0.15 kbp cyclin D1 core promoter region, which lacks any transcription factor binding motifs, still exhibited a temperature-sensitive phenotype in tsBN462 cells suggesting that CCG1/TAF II 250 is critical for the function of the cyclin D1 core promoter.

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Section: Resultssupporting

confidence: 80%

Section: Resultsmentioning

confidence: 96%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 96%

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Overexpression of D-type cyclins, E2F-1, SV40 large T antigen and HPV16 E7 rescue cell cycle arrest of tsBN462 cells caused by the CCG1/TAFII250 mutation

Sekiguchi

Nishimoto

Hunter³

1999

Oncogene

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“…Presumably this cell cycle block is the consequence of TAF II 250-mediated alterations in gene expression of certain cell cycle control genes (Wang and Tjian, 1994). Thus TAF II 250 is important not only for the regulation of transcription but also the cell cycle and possibly apoptosis (Sekiguchi et al, 1995). Recently, we have shown that Rb can bind directly to TAF II 250 both in vitro and in vivo (Shao et al, 1995) and that stimulation of Sp1-mediated transcription by Rb is conferred through a TAF II 250-dependent pathway.…”

Section: Introductionmentioning

confidence: 98%

Rb interacts with TAFII250/TFIID through multiple domains

Shao

Siegert

Ruppert³

et al. 1997

Oncogene

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The retinoblastoma tumor suppressor gene product (Rb) binds directly to the largest TFIID subunit, TATAbinding protein associated factor TAF II 250, ®rst identi®ed as the cell cycle regulatory protein CCG1. Here we map the domains in Rb and TAF II 250 important for their interaction in vitro and in vivo. Both the amino terminus and the large pocket of Rb are able to associate independently with TAF II 250. The binding domain(s) within the large pocket are distinct from the viral oncoprotein and E2F binding region since certain pocket mutations, which abolish E1A binding, do not abolish TAF II 250 binding. Consistent with the large pocket of Rb binding to TAF II 250, the large pocket domains of both p107 and p130 are able to bind to TAF II 250 in vivo. We also demonstrate that at least two regions of TAF II 250 are able to bind to the large pocket of Rb independently whereas the amino terminus of Rb binds to a distinct domain in TAF II 250. We further demonstrate that Rb can bind to TFIID in vitro, presumably in part through an interaction with TAF II 250. Our results suggest a complex interaction between Rb and TAF II 250 and imply that TAF II 250, TFIID, and potentially other basal transcription factors are targets for regulation by Rb and Rb-related proteins.

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Programmed Cell Death and Apoptosis in Fungi

Ramsdale

2006

Fungal Genomics

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Apoptosis Is Induced in BHK Cells by the tsBN462/13 Mutation in the CCG1/TAFII250 Subunit of the TFIID Basal Transcription Factor

Cited by 35 publications

References 0 publications

Overexpression of D-type cyclins, E2F-1, SV40 large T antigen and HPV16 E7 rescue cell cycle arrest of tsBN462 cells caused by the CCG1/TAFII250 mutation

Overexpression of D-type cyclins, E2F-1, SV40 large T antigen and HPV16 E7 rescue cell cycle arrest of tsBN462 cells caused by the CCG1/TAFII250 mutation

Rb interacts with TAFII250/TFIID through multiple domains

Programmed Cell Death and Apoptosis in Fungi

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