Transcriptional regulation of liver development

Duncan, Stephen A.

doi:10.1002/1097-0177(2000)9999:9999<::aid-dvdy1051>3.3.co;2-e

Cited by 102 publications

(86 citation statements)

References 92 publications

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“…In P15 wt livers, we also find that XPA and XPG recruit on promoters; intriguingly, disruption of Ercc1 did not affect the assembly of these NER factors on promoters (SI Appendix). In P15 wt livers, ChIP data obtained for the Hprt gene which expresses at high levels in fetal livers (19) and continues to be active postnatally (11,12) showed that all of the tested factors occupied the promoter. In P15 Ercc1 −/− livers, the Hprt mRNA levels and the occupancy of all factors tested on Hprt promoter were not significantly affected; however ChIP signals for the XPF were reduced to background levels ( Fig.…”

Section: Ercc1-xpf Is Not Required For Ongoing Hepatic Gene Transcripmentioning

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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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: Ercc1-xpf Is Not Required For Ongoing Hepatic Gene Transcripmentioning

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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“…127 Since then, several transcription factors have been identified that are essential for expression of the complete repertoire of proteins that define hepatocyte function. 73,81,128,129 These include the hepatocyte nuclear factors HNF1␣ and ␤, c/EBP␣, HNF4␣, and FoxA, which act in combination to control aspects of hepatocyte differentiation and liver function. 67,73,[130][131][132][133][134][135][136][137][138] Of these transcriptional regulators, the nuclear hormone receptor HNF4␣ appears to be particularly potent in controlling hepatocyte differentiation.…”

Section: What Governs the Establishment Of Hepatic Architecture And Mmentioning

confidence: 99%

Embryonic development of the liver†

2005

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“…Thus, emergence of new transcription factors in fully differentiated cells transcends the appearance of mere single-gene markers and is interpreted to signify large-scale reprogramming in gene expression. 1,2 Whereas in normal adult liver, the expression of hepatocyte-or BEC-associated single genes is localized to the specific cell types, cells with promiscuous expression of both hepatocytic and BEC single-gene markers are often seen in chronic liver disease. [3][4][5][6][7] The appearance of 'marker genes' from the other (hepatocyte or BEC) cell type suggests that a reprogramming in gene expression is taking place, as an adaptation to a specific pathobiologic or physiological challenge.…”

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confidence: 99%

“…18 Hepatocytic and BEC lineage is specified in part by a set of specific liver-enriched transcription factors. 1,2,19,20 Studies with knockout mice have shown that hepatocyte nuclear factor (HNF)1a and HNF4a regulate transcription of genes essential for the hepatocytic cell lineage, [21][22][23] whereas HNF1b and HNF6 are involved in development of the gallbladder and bile ducts. [24][25][26] Previous studies with rodents have shown that the earliest step in the generation of the oval cells is the appearance of hepatocyte-associated transcription factors in BEC of portal ductules and canals of Hering.…”

mentioning

confidence: 99%

Expression of specific hepatocyte and cholangiocyte transcription factors in human liver disease and embryonic development

Limaye

Alarcón

Walls

et al. 2008

Laboratory Investigation

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Transcription factors are major determinants of cell-specific gene expression in all cell types. Studies in rodent liver have shown that alterations in transcription factor expression determine lineage specification during fetal liver development and signify transdifferentiation of cells of the biliary compartment into 'oval' cells and eventually hepatocytes in adult liver. We examined the cellular localization of hepatocyte-or BEC-associated transcription factors in human fetal and adult liver and in diseases in which transdifferentiation between hepatocytes and biliary cells may play a role. In the normal adult human liver, hepatocyte nuclear factor (HNF)4a and HNF6 appeared exclusively in hepatocytes; HNF1b, HNF3a, and HNF3b were observed only in BEC. During fetal development both BEC and hepatocytes expressed HNF3a, HNF3b, and HNF6. HNF1a was expressed only in fetal hepatocytes. We further examined expression of transcription factors in massive hepatic necrosis and in specific types of chronic liver disease. Hepatocyte-associated transcription factors HNF4a and HNF6 also appeared in BEC in massive hepatic necrosis and chronic hepatitis C virus infection. Similarly, HNF3b that is expressed only in BEC in normal adult liver was also observed in hepatocytes in primary biliary cirrhosis and chronic biliary obstruction. These data mimic previous findings in rodents in which hepatocyte-associated transcription factors appear in biliary cells prior to emergence of oval cells, which function as progenitor cells for hepatocytes when the regenerative capacity of the latter is compromised.

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Transcriptional regulation of liver development

Cited by 102 publications

References 92 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

Embryonic development of the liver†

Expression of specific hepatocyte and cholangiocyte transcription factors in human liver disease and embryonic development

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