Nuclease-hypersensitive sites in chromatin of the estrogen-inducible apoVLDL II gene of chicken

Kok, Klaas; Snippe, Lenie; Ab, Geert; Gruber, M.

doi:10.1093/nar/13.14.5189

Cited by 36 publications

(30 citation statements)

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“…With regard to alterations in chromatin, a number of studies have shown estrogen-dependent changes in DNase I-hypersensitive sites (42) and dimethyl sulfate-reactive sites (67) within 300 bp upstream of the apoll transcription initiation site. These changes may result from binding of specific transcription factors, including the receptor (4,67), but may also reflect changes in nucleosomal organization on the apoll promoter.…”

Section: Discussionmentioning

confidence: 99%

“…Analysis of the mechanisms of transcriptional regulation of these genes as well as the study of mRNA turnover in avian liver cells has been hampered by the absence of a suitable homologous cell line. Studies of gene activation and estrogen-dependent alterations in chromatin structure and DNA methylation patterns have been restricted to animal studies or tissue homogenates (2,3,14,15,38,42,67,68 …”

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Reactivation of apolipoprotein II gene transcription by cycloheximide reveals two steps in the deactivation of estrogen receptor-mediated transcription.

et al. 1994

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In this report, we describe apolipoprotein II (apoll) gene expression in cell lines derived by stable expression of the chicken estrogen receptor in LMH chicken hepatoma cells. In cell lines expressing high levels of receptor (LMH/2A), apoll gene expression is increased by estrogen 300-fold compared with levels in the receptordeficient parent LMH line. LMH/2A cells show apoll mRNA induction and turnover kinetics similar to those in chicken liver. Inhibition of protein synthesis with cycloheximide (CHX) or puromycin following estrogen withdrawal superinduces apoll mRNA without affecting apoll mRNA stability. Superinduction is due to an estrogen-independent reactivation of apoll gene transcription. The apoll gene can be reactivated by CHX for up to 24 h following hormone withdrawal, suggesting that the gene is in a repressed yet transcriptionally competent state. These results reveal two distinct events necessary for termination of estrogen receptormediated transcription. The first event, removal of hormone, is sufficient to stop transcription when translation is ongoing. The second event is revealed by the CHX-induced superinduction of apoll mRNA following hormone withdrawal. This superinduction suggests that deactivation of estrogen receptor-mediated transcription requires a labile protein. Furthermore, reactivation of apoll gene expression by CHX and estrogen is additive, suggesting that estrogen is unable to overcome repression completely. Thus, a labile protein may act to repress estrogen receptor-mediated transcription of the apoll gene.In avian liver, estrogens regulate the expression of a number of egg yolk precursor proteins required for the transport of nutrients to the developing oocyte (5). Among the proteins regulated by estrogen are vitellogenin I (VTGI), VTGII, and VTGIII (63, 64), apolipoprotein B (apoB) (17) and apoll (18) of very low density lipoprotein, and riboflavin-and biotinbinding proteins (16,66). The primary action of estrogen is to increase transcription of the genes encoding these proteins via binding to the estrogen receptor. In addition to regulating transcription, estrogen also alters the cytoplasmic stability of apoll and VTGII mRNAs (30,71). Analysis of the mechanisms of transcriptional regulation of these genes as well as the study of mRNA turnover in avian liver cells has been hampered by the absence of a suitable homologous cell line. Studies of gene activation and estrogen-dependent alterations in chromatin structure and DNA methylation patterns have been restricted to animal studies or tissue homogenates (2,3,14,15,38,42,67,68

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Reactivation of apolipoprotein II gene transcription by cycloheximide reveals two steps in the deactivation of estrogen receptor-mediated transcription.

et al. 1994

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“…However, analyses of the spectrum of nuclease-hypersensitive sites in and around both the viteilogenin and apoVLDLII genes indicates that the genes are marked in the tubular gland cells of the oviduct by a subset of the sites that are present in the liver (8,20,27). The accessibility of these sites suggests that the lack of activation of the genes in the oviduct may not simply be attributable to their sequestration in heterochromatin but may also be the consequence of either the absence of tissue-specific factors that are required for expression or the presence of negative regulators that prevent activation.…”

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Developmental regulation of specific protein interactions with an enhancerlike binding site far upstream from the avian very-low-density apolipoprotein II gene.

et al. 1990

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Expression of the avian very-low-density apolipoprotein II (apoVLDLII) gene is completely dependent on estrogen and restricted to the liver. We have identified binding sites for nonhistone nuclear proteins located between -1.96 and -2.61 kilobases. One of these sites, located at -2.6 kilobases (designated site 1), was found to span an MspI site that becomes demethylated between days 7 and 9 of embryogenesis, the stage of development at which competence to express the apoVLDLII gene begins to be acquired. Levels of the factor(s) involved were high at day 7 of embryogenesis, decreased two-to threefold by days 9 to 11, and continued to decline more slowly until hatching. Furthermore, the mobility of the complex formed underwent a well-defined shift between days 11 to 13 of embryogenesis. Methylation interference studies showed that modification of the outer guanosines of the MspI site resulted in marked inhibition of the formation of the protein-DNA complex. Competition studies, fractionation of nuclear extracts, and tissue distribution indicated that the factor was not the avian homolog of hepatocyte nuclear factor 1, nuclear factor 1, or CCAAT/enhancer-binding protein (C/EBP). However, site 1 could compete for binding to an oligonucleotide, previously shown to be recognized by C/EBP, in a nonreciprocal fashion. These studies demonstrate that the sequence recognized by the protein includes a C/EBP consensus sequence but that elements in addition to the core enhancer motif are essential for binding.

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“…7,1987 on May 9, 2018 by guest http://mcb.asm.org/ Downloaded from trogen alters the profile of DNase I-hypersensitive sites in regions flanking both the apoVLDLII and the vitellogenin genes and also results in demethylation at a type I receptorbinding site upstream from the vitellogenin gene (2,4,17,28). In some cases, these alterations in chromatin structure persist after a primary response has ceased and can also be propagated to a limited extent after cell division in the absence of estrogen.…”

Section: Methodsmentioning

confidence: 99%

Long-term effects of estrogen on avian liver: estrogen-inducible switch in expression of nuclear, hormone-binding proteins.

Haché¹,

Tam²,

Cochrane³

et al. 1987

Mol. Cell. Biol.

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The stimulation of chicks or embryos with estrogen results in transient, hepatic expression of the vitellogenin gene, as well as long-term, propagatable alterations in the rapidity with which the gene can be reactivated. We examined the possibility that nuclear, type H estrogen-binding sites are involved in this long-term change in response characteristics. We demonstrate that the primary induction kinetics of type II sites in embryos and chicks correlated with the expression of the vitellogenin gene and that once their induction was triggered by estrogen, they accumulated, were propagated, and persisted for months after withdrawal of the hormone. We also show that their accumulation in the embryo was accompanied by prolonged expression of both the vitellogenin and very low-density apolipoprotein II genes, in the absence of elevated levels of type I receptor, and that the type II sites, like the classical receptor, appear to be preferentially associated with active or potentially active chromatin. Finally, we describe a regulatory mechanism, tested by computer modelling, that simulated the behavioral characteristics of these nuclear estrogen-binding sites and which may explain their role in mediating the long-term effects of estrogen.

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Nuclease-hypersensitive sites in chromatin of the estrogen-inducible apoVLDL II gene of chicken

Cited by 36 publications

References 41 publications

Reactivation of apolipoprotein II gene transcription by cycloheximide reveals two steps in the deactivation of estrogen receptor-mediated transcription.

Reactivation of apolipoprotein II gene transcription by cycloheximide reveals two steps in the deactivation of estrogen receptor-mediated transcription.

Developmental regulation of specific protein interactions with an enhancerlike binding site far upstream from the avian very-low-density apolipoprotein II gene.

Long-term effects of estrogen on avian liver: estrogen-inducible switch in expression of nuclear, hormone-binding proteins.

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