Intermediate filament protein synthesis in preimplantation murine embryos

Oshima, Robert G.; Howe, W E; Klier, F. George; Adamson, Eileen D.; Shevinsky, L H

doi:10.1016/0012-1606(83)90294-4

Cited by 184 publications

(71 citation statements)

References 25 publications

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“…The mouse endoA gene is a useful model for studies on developmental regulation [1,2], and particularly the features of chromatin structure that differ in active and inactive genes [3].…”

Section: Introductionmentioning

confidence: 99%

Activation of the mouse cytokeratin A (endo A) gene in teratocarcinoma F9 cells by the histone deacetylase inhibitor Trichostatin A

Miyashita¹,

Yamamoto²,

Nishimune³

et al. 1994

FEBS Letters

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Absa'aet Treatment of cultured ceils with sodium butyrate, that is the histone deacetylase inhibitor, induces the historic hyperacetylation and the expressions of various mammalian genes without affecting the level of protein synthesis. However, butyrate is a non-specific inhibitor of deacetylase because of its effects on various other enzymes and nuclear proteins other than histones. On the other hand, Trichostatin A (TSA) was recently found to be a potent and specific inhibitor of histone deacetylase. We examined the effect of TSA on the expression of mouse cytokeratin A (endoA). TSA increased endoA expression in F9 ceils, and was efffective at a much lower concentration than sodium butyrate. We also examined the changes of chromatin structure induced by the two drugs by a DNase 1-hypersensitivity assay. Both drugs induced the formation of a DNase 1-hypersensitive site (DH site) in only the promoter region. The precise mechanism(s) by which the two drugs increase endoA gene expression is unknown, but these results suggest that endoA expression is induced by inhibition of histone deacetylase and that the effect is at the transcriptional level.

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“…The mouse endoA gene is a useful model for studies on developmental regulation [1,2], and particularly the features of chromatin structure that differ in active and inactive genes [3].…”

Section: Introductionmentioning

confidence: 99%

Activation of the mouse cytokeratin A (endo A) gene in teratocarcinoma F9 cells by the histone deacetylase inhibitor Trichostatin A

Miyashita¹,

Yamamoto²,

Nishimune³

et al. 1994

FEBS Letters

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“…Keratin 8 (mK8) and its partner keratin 18 (mK18) are the first IF proteins to be expressed during mouse embryogenesis (Jackson et al 1980;Kemler et al 1981;Oshima et al 1983). They are expressed in several extraembryonic tissues, including the trophectoderm, the endoderm, the visceral yolk sac, and the placenta.…”

mentioning

confidence: 99%

Mid-gestational lethality in mice lacking keratin 8.

Baribault¹,

Price²,

Miyai³

et al. 1993

Genes & Development

243

174

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Keratin 8 (mK8) and its partner keratin 18 (mK18) are the first intermediate filament proteins expressed during mouse embryogenesis. They are found in most extraembryonic and embryonic simple epithelia, including trophectoderm, visceral yolk sac, gastrointestinal tract, lungs, mammary glands, and uterus. We report that a targeted null mutation in the inK8 gene causes mid-gestational lethality. Mutant embryos are growth retarded and suffer from internal bleeding, with an abnormal accumulation of erythrocytes in fetal livers. The mK8-phenotype has 94% penetrance, with a few mice surviving into adulthood. We suggest that mK8/mK18 filaments are important for the integrity of the fetal liver, like specialized human epidermal keratins for the integrity of the epidermis. This phenotype in mice differs from the reported function of simple epithelium keratins in Xenopus at the gastrulation stage. In mice, mK8 fulfills a vital function at 12 days postcoitum.

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“…The mouse homolog of the K18 protein (Endo B or mK18) copolymerizes with the complementary and coexpressed type II murine keratin 8 (mK8 or Endo A) (6,10,22,23) to form the first intermediate filaments expressed during mouse development (14,26). In murine embryonal carcinoma cells, expression of mouse and human K18 genes appears to be limited, at least in part, by low levels of AP1 transcription factor activity.…”

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confidence: 99%

cis regulation of the keratin 18 gene in transgenic mice.

Neznanov¹,

Oshima²

1993

Mol. Cell. Biol.

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The gene coding for human keratin 18 (K18), a type I intermediate filament protein found in a variety of simple epithelia, is regulated correctly in transgenic mice but is promiscuously expressed after direct transfection into cell culture lines. We have begun an investigation of the mechanisms responsible for the correct regulation of K18 with a comparison of the chromatin state of K18 in permissive and nonpermissive transgenic mouse tissues to identify seven expression-specific, DNase-hypersensitive sites that correlate with known or potential regulatory regions of the gene. Four of these sites are associated with the proximal promoter region and the first intron that has been implicated previously in the transcriptional control of K18. Two hypersensitive sites are associated with a conserved Alu repetitive sequence located immediately upstream of the proximal promoter elements. Transcription of this Alu element in a direction opposite that of K18 was correlated with K18 expression in transgenic tissues. The final hypersensitive site was mapped to exon 6. The potential importance of this region for the expression of K18 was supported by the results of transient expression of the gene and various deleted constructions. In addition, exon 6 and the intron 1 regulatory region were distinguished from the remainder of K18 by differential DNA methylation in expressing and nonexpressing tissues. The CpG-rich proximal promoter and first exon regions remain unmethylated in both permissive and nonpermissive tissues. These results suggest that DNA methylation is not the primary mechanism of control of the gene. An Alu RNA polymerase III transcription unit and exon 6 are implicated in regulation of K18.

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Intermediate filament protein synthesis in preimplantation murine embryos

Cited by 184 publications

References 25 publications

Activation of the mouse cytokeratin A (endo A) gene in teratocarcinoma F9 cells by the histone deacetylase inhibitor Trichostatin A

Activation of the mouse cytokeratin A (endo A) gene in teratocarcinoma F9 cells by the histone deacetylase inhibitor Trichostatin A

Mid-gestational lethality in mice lacking keratin 8.

cis regulation of the keratin 18 gene in transgenic mice.

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