Dominant and Redundant Functions of TFIID Involved in the Regulation of Hepatic Genes

Tatarakis, Antonis; Margaritis, Thanasis; Martínez-Jiménez, Celia P.; Kouskouti, Antigone; Mohan, William S.; Haroniti, Anna; Kafetzopoulos, Dimitris; Tora, Làszlò; Talianidis, Iannis

doi:10.1016/j.molcel.2008.07.013

Cited by 57 publications

(91 citation statements)

References 40 publications

(56 reference statements)

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“…Likewise, liver-specific disruption of Taf10 gene in Taf10 −/− animals leads to severe growth failure during the second week after birth, more than 50% reduction in body weight at day P30, and premature death at ∼P35 (Fig. 1C) (16). Oil Red O and PAS staining in Ercc1 −/− and Taf10 −/− livers revealed a uniform accumulation of triglycerides and glycogen resulting in a "fatty liver" appearance with unusually large glycogen depots ( Fig.…”

Section: Resultsmentioning

confidence: 90%

“…To assess the contribution of NER in transcription during development, we compared the liver phenotypes of NER-deficient Ercc1 −/− animals that closely mimic a severe form of CS (11) with transcription factor II D (TFIID)-defective Taf10 −/− mice exhibiting a liver-specific defect in transcription initiation (Taf10 −/− -Alb-Cre) (16). Ercc1 −/− mice show attenuated growth, resulting in cachectic dwarfism during the second week of life and premature death before postnatal day P35 (Fig.…”

Section: Resultsmentioning

confidence: 99%

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Defective transcription initiation causes postnatal growth failure in a mouse model of nucleotide excision repair (NER) progeria

Kamileri

Karakasilioti

Sideri

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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Nucleotide excision repair (NER) defects are associated with cancer, developmental disorders and neurodegeneration. However, with the exception of cancer, the links between defects in NER and developmental abnormalities are not well understood. Here, we show that the ERCC1-XPF NER endonuclease assembles on active promoters in vivo and facilitates chromatin modifications for transcription during mammalian development. We find that Ercc1 −/− mice demonstrate striking physiological, metabolic and gene expression parallels with Taf10 −/− animals carrying a liver-specific transcription factor II D (TFIID) defect in transcription initiation. Promoter occupancy studies combined with expression profiling in the liver and in vitro differentiation cell assays reveal that ERCC1-XPF interacts with TFIID and assembles with POL II and the basal transcription machinery on promoters in vivo. Whereas ERCC1-XPF is required for the initial activation of genes associated with growth, it is dispensable for ongoing transcription. Recruitment of ERCC1-XPF on promoters is accompanied by promoter-proximal DNA demethylation and histone marks associated with active hepatic transcription. Collectively, the data unveil a role of ERCC1/XPF endonuclease in transcription initiation establishing its causal contribution to NER developmental disorders.DNA damage | genetics | metabolism

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Section: Resultsmentioning

confidence: 90%

Section: Resultsmentioning

confidence: 99%

Defective transcription initiation causes postnatal growth failure in a mouse model of nucleotide excision repair (NER) progeria

Kamileri

Karakasilioti

Sideri

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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“…It therefore seems possible that an as yet unidentified liver-specific core promoter recognition complex partially replaces canonical TFIID during or following differentiation. Although it has been suggested that fetal or postnatal induction of transcription by TFIID would be sufficient to establish a gene's expression throughout the organism's life, and that future rounds of transcription may be core promoter recognition complex independent, such a model has the clear disadvantage of excluding alterations in expression following physiological or environmental change (11). Future identification of a hepatocyte-specific complex or complexes would provide a more parsimonious mechanism of transcriptional change during liver development, regeneration, and homeostasis.…”

Section: Discussionmentioning

confidence: 99%

“…In myotubes, an alternative core component, TAF3, is retained and required for myogenic differentiation. An additional recent example of the relative dispensability of TFIID was the finding that inactivation of TAF10 has little or no affect on adult hepatic gene expression (11). Thus, the notion of switching or "remodeling" of the core promoter machinery may be more widespread than initially appreciated.…”

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confidence: 99%

Core promoter recognition complex changes accompany liver development

D’Alessio

Willenbring

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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Recent studies of several key developmental transitions have brought into question the long held view of the basal transcriptional apparatus as ubiquitous and invariant. In an effort to better understand the role of core promoter recognition and coactivator complex switching in cellular differentiation, we have examined changes in transcription factor IID (TFIID) and cofactor required for Sp1 activation/Mediator during mouse liver development. Here we show that the differentiation of fetal liver progenitors to adult hepatocytes involves a wholesale depletion of canonical cofactor required for Sp1 activation/Mediator and TFIID complexes at both the RNA and protein level, and that this alteration likely involves silencing of transcription factor promoters as well as protein degradation. It will be intriguing for future studies to determine if a novel and as yet unknown core promoter recognition complex takes the place of TFIID in adult hepatocytes and to uncover the mechanisms that down-regulate TFIID during this critical developmental transition.TATA box-binding protein-associated factor | hepatoblast | hepatogenesis T he precise and orderly differentiation of embryonic progenitors to committed adult cell types requires exquisite spatial and temporal control of gene expression. Until recently, the dynamic changes in transcriptional output that accompany developmental transitions were assumed to depend exclusively on regulatory DNA and its associated sequence-specific activators and repressors, whereas core promoter recognition, coactivator, and chromatin modifier complexes were generally taken to be ubiquitous and invariant from one cell type to the next. Indeed, these so-called core factors are highly conserved from yeast to man (1). However, recent evidence suggests that several key developmental transitions are accompanied by, and actually require, dramatic changes in components of this general machinery including transcription factor IID (TFIID) composed of the TATA box-binding protein (TBP) and its associated factors (TAFs), the cofactor required for Sp1 activation/Mediator (CRSP/Med) complex, and the Brg1/Brm-associated factor (BAF) complex (for review, see 2).The first evidence that some cell types may contain alterations of the general machinery came with the identification of germcell-specific TFIID subcomplexes in which key subunits are replaced by paralogous components. Initially oogenesis and spermatogenesis were found to require an altered TFIID in which paralogous TAF4b replaces the canonical TAF4 (3, 4). Later spermatocytes were found to also express paralogous TAF7L that may cooperate with TBP and

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“…Notably, it has been shown that individual TAFs are required for the expression of only a specific subset of genes (35)(36)(37)(38), and that the TFIID, or any of its other forms, was recruited in core promoters by a direct interaction between TAFs and their genespecific activators (39). Given that TAF4b target promoter selectivity is enhanced by activators such as c-Jun and Sp-1 (12), we propose a synergistic function of the two factors, c-Jun and TAF4b, through their interaction in which TAF4b is the coactivator of AP-1 during regulation of AP-1 target genes (Fig.…”

Section: Discussionmentioning

confidence: 99%

TAF4b and Jun/Activating Protein-1 Collaborate to Regulate the Expression of Integrin α6 and Cancer Cell Migration Properties

Kalogeropoulou

Voulgari

Kostourou

et al. 2010

Molecular Cancer Research

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The TAF4b subunit of the transcription factor IID, which has a central role in transcription by polymerase II, is involved in promoter recognition by selective recruitment of activators. The activating protein-1 (AP-1) family members participate in oncogenic transformation via gene regulation. Utilizing immunoprecipitation of endogenous protein complexes, we documented specific interactions between Jun family members and TATA box binding protein-associated factors (TAF) in colon HT29 adenocarcinoma cells. Particularly, TAF4b and c-Jun were found to colocalize and interact in the nucleus of advanced carcinoma cells and in cells with epithelial-tomesenchymal transition (EMT) characteristics. TAF4b was found to specifically regulate the AP-1 target gene involved in EMT integrin α6, thus altering related cellular properties such as migration potential. Using a chromatin immunoprecipitation approach in colon adenocarcinoma cell lines, we further identified a synergistic role for TAF4b and c-Jun and other AP-1 family members on the promoter of integrin α6, underlining the existence of a specific mechanism related to gene expression control. We show evidence for the first time of an interdependence of TAF4b and AP-1 family members in cell type-specific promoter recognition and initiation of transcription in the context of cancer progression and EMT. Mol Cancer Res; 8(4); 554-68. ©2010 AACR.

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Dominant and Redundant Functions of TFIID Involved in the Regulation of Hepatic Genes

Cited by 57 publications

References 40 publications

Defective transcription initiation causes postnatal growth failure in a mouse model of nucleotide excision repair (NER) progeria

Defective transcription initiation causes postnatal growth failure in a mouse model of nucleotide excision repair (NER) progeria

Core promoter recognition complex changes accompany liver development

TAF4b and Jun/Activating Protein-1 Collaborate to Regulate the Expression of Integrin α6 and Cancer Cell Migration Properties

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