GCN5: a supervisor in all-inclusive control of vertebrate cell cycle progression through transcription regulation of various cell cycle-related genes

Kikuchi, Hidehiko; Yasuda, Takami; Nakayama, Tatsuo

doi:10.1016/j.gene.2004.12.007

Cited by 69 publications

(115 citation statements)

References 30 publications

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“…Future microarray analyses and global chromatin immunoprecipitation studies should define gene expression programs regulated by Gcn5 during development. Gcn5 and p53 both affect cell survival and proliferation (Xu et al, 2000;Jin and Levine, 2001;Kikuchi et al, 2005). However, neither of these processes is affected in an obvious way in Gcn5 flox(neo)/⌬ mutants, so Gcn5 likely affects another aspect of neural tube closure.…”

Section: Discussionmentioning

confidence: 99%

“…Gcn5 Ϫ/Ϫ embryos exhibit a large increase in apoptotic cells as early as E7.5 (Xu et al, 2000), and deletion of Gcn5 in chicken cells (Kikuchi et al, 2005) or yeast (Zhang et al, 1998) leads to defective cell cycle progression. Therefore, we next determined whether neural tube closure defects in the Gcn5 flox(neo)/⌬ mutants might be due to changes in cell proliferation or survival.…”

Section: Cell Death and Cell Proliferation Are Normal In Hypomorphic mentioning

confidence: 99%

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Proper expression of the Gcn5 histone acetyltransferase is required for neural tube closure in mouse embryos

Lin

Zhang

Srajer

et al. 2008

Developmental Dynamics

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Histone acetyltransferases (HATs) are important to gene activation, altering chromatin structures to facilitate association of transcription proteins with gene promoters. The functions of individual HATs in mammalian developmental are not well defined. Our previous studies demonstrated that Gcn5, a prototypical HAT, is required for mesodermal maintenance in early embryos. Homozygous Gcn5 null embryos die soon after gastrulation, preventing determination of Gcn5 functions later during development. We report here the creation of a Gcn5 flox(neo) allele, which is only partially functional and gives rise to a hypomorphic phenotype. Mice homozygous for this allele had an increased risk of cranial neural tube closure defects (NTDs) and exencephaly. These defects were found at an even greater penetrance in

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Section: Discussionmentioning

confidence: 99%

Section: Cell Death and Cell Proliferation Are Normal In Hypomorphic mentioning

confidence: 99%

Proper expression of the Gcn5 histone acetyltransferase is required for neural tube closure in mouse embryos

Lin

Zhang

Srajer

et al. 2008

Developmental Dynamics

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show abstract

“…In this regard, AcK9, but not AcK14, was significantly reduced in response to DNA damage or Chk1 depletion. Given that GCN5 is dispensable for acetylation of H3-K14, 32,33 it appears consistent that the reduced binding of GCN5 on cyclin B1 and cdk1 promoters did not affect AcK14. In addition to our findings, pT11 was reported to accelerate demethylation on K9 by recruitment of JMJD2C, leading to increased AcK9 and subsequent transcriptional activation on androgen receptor genes.…”

Section: Transcriptional Repression and Histone Modificationsmentioning

confidence: 93%

Checkpoints meet the transcription at a novel histone milestone (H3-T11)

Shimada

Nakanishi²

2008

Cell Cycle

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“…Note that the lack of H3K9ac decrease upon KAT2A inhibition was also observed in KO experiments using chicken cells. 18 The global levels of H2B and H3 were not altered. The decrease in H2B-ub could be due to a decrease in the monoubiquitinating enzymes hRAD6 and RNF20; however, western blots using the respective antibodies indicated that their levels were not substantially changed in KAT3B-inactivated cells (Fig.…”

confidence: 94%