Occupancy of upstream regulatory sites in vivo coincides with major histocompatibility complex class I gene expression in mouse tissues.

Dey, Anup; Thornton, Angela M.; Lonergan, M; Weissman, Sherman M.; Chamberlain, John W.; Ozato, Keiko

doi:10.1128/mcb.12.8.3590

Cited by 77 publications

(42 citation statements)

References 81 publications

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“…5. The CRE octamer is placed in accordance with the literature (15,27,28). Immediately 5Ј to it there is striking polymorphism, although the overall level of polymorphism is much lower than for MHC II.…”

Section: Resultssupporting

confidence: 53%

Patterned variation in murine MHC promoters

Mitchison¹,

Roes²

2002

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

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To compare variation in regulatory and coding DNA, promoter sequences have been obtained from wild-derived mice and laboratory rats. The sequences are from the proximal promoter of the H2Aa, H2Ab, H2Eb, and H2K genes of 24 wild-derived inbred strains and a sample of the corresponding exon 2 sequences and of the RT1.Ba gene of six strains of laboratory rat. They reveal a high level of variation in the mouse MHC class II promoters (H2A and H2E), a low level in MHC class I (H2K), and none in the rat. The variation is pronounced in and around the cAMP response element, a major binding site for modulating promoter activity in response to external stimulation. This finding, together with the different levels of variation in MHC classes I and II, is suggestive of natural selection. However, selection operating via the MHC coding sequences must also contribute, as indicated by the minimal variation in both the MHC class II promoter and coding sequences of the rat. Furthermore CIITA (trans-activator of class II) of the mouse has been reported to have minimal variation in its promoter and none in its coding sequence. Taken together these data suggest that the regulatory and coding sequences undergo coselection. Each of the mouse class II promoters has a pattern of variation that appears to be basically dimorphic, with further variation added by recombination͞mutation. The dimorphic allelic lineages are in marginally detectable linkage disequilibrium with the exon 2 sequences, particularly in H2Aa, thus lending further support to the coevolution hypothesis.

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Section: Resultssupporting

confidence: 53%

Patterned variation in murine MHC promoters

Mitchison¹,

Roes²

2002

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

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“…[11][12][13]. Although heterodimer binding to the RARE does not require ligand in vitro, ligand is required for heterodimer occupancy of the RARE in vivo in some promoters (14,15). These and our recent observations that RA increases in vivo endonuclease sensitivity in an RA-responsive promoter (41) suggest that transcription by liganded heterodimer occurs in conjunction with an alteration of chromatin.…”

mentioning

confidence: 63%

“…We examined whether TSA affects promoter activity of the RAR␤2 gene that had been stably integrated into P19 cells (27). The RAR␤2 promoter contains a canonical RARE and is strongly activated by RA (14,25,30,31). The promoter also contains a cAMP-like responsive element and an auxiliary RARE (CRE and rare, in Fig.…”

Section: Resultsmentioning

confidence: 99%

A histone deacetylase inhibitor potentiates retinoid receptor action in embryonal carcinoma cells

Minucci

Horn

Bhattacharyya

et al. 1997

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

104

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Histone acetylation is thought to have a role in transcription. To gain insight into the role of histone acetylation in retinoid-dependent transcription, we studied the effects of trichostatin A (TSA), a specific inhibitor of histone deacetylase, on P19 embryonal carcinoma cells. We show that coaddition of TSA and retinoic acid (RA) markedly enhances neuronal differentiation in these cells, although TSA alone does not induce differentiation but causes extensive apoptosis. Consistent with the cooperative effect of TSA and RA, coaddition of the two agents synergistically enhanced transcription from stably integrated RA-responsive promoters. The transcriptional synergy by TSA and RA required the RA-responsive element and a functional retinoid X receptor (RXR)͞retinoic acid receptor (RAR) heterodimer, both obligatory for RA-dependent transcription. Furthermore, TSA led to promoter activation by an RXR-selective ligand that was otherwise inactive in transcription. In addition, TSA enhanced transcription from a minimum basal promoter, independently of the RA-responsive element. Finally, we show that TSA alone or in combination with RA increases in vivo endonuclease sensitivity within the RA-responsive promoter, suggesting that TSA treatment might alter a local chromatin environment to enhance RXR͞RAR heterodimer action. Thus, these results indicate that histone acetylation inf luences activity of the heterodimer, which is in line with the observed interaction between the RXR͞RAR heterodimer and a histone acetylase presented elsewhere.

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“…The in vivo DNA footprinting was performed by using ligationmediated PCR as described previously (Dey et al, 1992). P and TD cells were treated with 0.1% dimethyl sulfate (DMS) for 2 min.…”

Section: In Vivo Dna Footprintingmentioning

confidence: 99%

Requirement for Down-Regulation of the CCAAT-binding Activity of the NF-Y Transcription Factor during Skeletal Muscle Differentiation

Gurtner¹,

Manni²,

Fuschi

et al. 2003

MBoC

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NF-Y is composed of three subunits, NF-YA, NF-YB, and NF-YC, all required for DNA binding. All subunits are expressed in proliferating skeletal muscle cells, whereas NF-YA alone is undetectable in terminally differentiated cells in vitro. By immunohistochemistry, we show that the NF-YA protein is not expressed in the nuclei of skeletal and cardiac muscle cells in vivo. By chromatin immunoprecipitation experiments, we demonstrate herein that NF-Y does not bind to the CCAAT boxes of target promoters in differentiated muscle cells. Consistent with this, the activity of these promoters is down-regulated in differentiated muscle cells. Finally, forced expression of the NF-YA protein in cells committed to differentiate leads to an impairment in the down-regulation of cyclin A, cyclin B1, and cdk1 expression and is accompanied by a delay in myogenin expression. Thus, our results indicate that the suppression of NF-Y function is of crucial importance for the inhibition of several cell cycle genes and the induction of the early muscle-specific program in postmitotic muscle cells.

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Occupancy of upstream regulatory sites in vivo coincides with major histocompatibility complex class I gene expression in mouse tissues.

Cited by 77 publications

References 81 publications

Patterned variation in murine MHC promoters

Patterned variation in murine MHC promoters

A histone deacetylase inhibitor potentiates retinoid receptor action in embryonal carcinoma cells

Requirement for Down-Regulation of the CCAAT-binding Activity of the NF-Y Transcription Factor during Skeletal Muscle Differentiation

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