Histone deacetylase 1 is required for cell cycle exit and differentiation in the zebrafish retina

Stadler, Jochen A.; Shkumatava, Alena; Norton, William; Rau, Marlene J.; Geisler, Robert; Fischer, Sabine; Neumann, Carl J.

doi:10.1002/dvdy.20427

Cited by 52 publications

(63 citation statements)

References 28 publications

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“…To test this possibility, we treated embryos with a histone deacetylase I inhibitor, TSA. Recent studies have demonstrated that either genetic mutations in histone deacetylase I or treatment with TSA completely inhibits retinal neurogenesis in zebrafish embryos (Stadler et al, 2005;Yamaguchi et al, 2005). We confirmed that TSA-treated embryos completely blocked expression of the neurogenic marker huc:GFP (Fig.…”

Section: Promoting Proliferative Cell Fates Does Not Bias Nuclear Migsupporting

confidence: 80%

Interkinetic Nuclear Migration and the Selection of Neurogenic Cell Divisions during Vertebrate Retinogenesis

Baye¹,

Link²

2007

J. Neurosci.

162

193

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During retinal development, neuroepithelial progenitor cells divide in either a symmetric proliferative mode, in which both daughter cells remain mitotic, or in a neurogenic mode, in which at least one daughter cell exits the cell cycle and differentiates as a neuron. Although the cellular mechanisms of neurogenesis remain unknown, heterogeneity in cell behaviors has been postulated to influence this cell fate. In this study, we analyze interkinetic nuclear migration, the apical-basal movement of nuclei in phase with the cell cycle, and the relationship of this cell behavior to neurogenesis. Using time-lapse imaging in zebrafish, we show that various parameters of interkinetic nuclear migration are significantly heterogeneous among retinal neuroepithelial cells. We provide direct evidence that neurogenic progenitors have greater basal nuclei migrations during the last cell cycle preceding a terminal mitosis. In addition, we show that atypical protein kinase C (aPKC)-mediated cell polarity is essential for the relationship between nuclear position and neurogenesis. Loss of aPKC also resulted in increased proliferative cell divisions and reduced retinal neurogenesis. Our data support a novel model for neurogenesis, in which interkinetic nuclear migration differentially positions nuclei in neuroepithelial cells and therefore influences selection of progenitors for cell cycle exit based on apical-basal polarized signals.

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Section: Promoting Proliferative Cell Fates Does Not Bias Nuclear Migsupporting

confidence: 80%

Interkinetic Nuclear Migration and the Selection of Neurogenic Cell Divisions during Vertebrate Retinogenesis

Baye¹,

Link²

2007

J. Neurosci.

162

193

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“…during differentiation to neurons specifically . A similar phenotype has been noted in a lower organism such as zebrafish where mutants for HDAC1 show a blockade of neuronal differentiation in vivo through the activation of the neurogenic repressor which in consequence leads to significant apoptosis of neural progenitor cells in hindbrain (Cunliffe et al, 2004;Stadler et al, 2005). Moreover, neuronal precursors transduced with a mutant HDAC1 devoid catalytic activity showed a 50% reduction in neuronal specification (Humphrey et al, 2008).…”

Section: The Involvement Of Hdac1 and Hdac2 In Neurogenesismentioning

confidence: 60%

Histone deacetylases 1 and 2 are required for brain development

Jaworska

Ziemka‐Nałęcz

Zalewska³

2015

Int. J. Dev. Biol.

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Epigenetic modifications of histones have been implicated in the regulation of cell specific expression of genes required for neuronal development. The best studied post-translational (epigenetic) modification of histones is the process of reversible acetylation. Two types of enzymeshistone acetyltransferases (HATs) and histone deacetylases (HDACs) establish and maintain specific patterns of histone acetylation in balance, thereby contributing to both transcriptional activation and repression of specific sets of genes. Histone deacetylases catalyze the removal of acetyl groups from selected lysine residues in the conserved tails of core histone proteins and are considered as transcriptional corepressors. A significant amount of data implicates HDACs in diverse biological processes, including tissue specific developmental program by silencing specific growth-inhibitory genes. In line with this, gene disruption studies have shown that the class I deacetylases, HDAC1 and HDAC2 play an essential role in nervous system development. In the present review, we briefly highlight current insights supporting the function of histone deacetylases in rodent brain development and discuss present knowledge referring to their role in neurogenesis, taking into consideration results obtained in culture systems and in in vivo studies.

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“…It is likely the transient and incomplete nature of pharmacological inhibition allows for the survival of neuronal precursors; and the derepression of proneurogenic genes allows for the specific induction of neurogenesis, whereas the genetic loss of HDAC1 and HDAC2 is so robust, differentiation is blocked and cellular death ensues. A similar phenotype is seen in lower organisms such as zebrafish, where loss-offunction mutants for hdac1 show a blockade of neuronal differentiation in vivo through the activation of the neurogenic repressor, Hes, and show significant apoptosis in hindbrain neural progenitor cells (22)(23)(24). Additionally, neuronal precursors transduced with a mutant HDAC1 that lacks catalytic activity show a fifty percent reduction in neuronal specification (25).…”

Section: Contrasting Phenotypes Between Inhibitors and Genetic Deletionmentioning

confidence: 65%

Histone deacetylases 1 and 2 control the progression of neural precursors to neurons during brain development

Montgomery¹,

Hsieh²,

Barbosa³

et al. 2009

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

275

254

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The molecular mechanism by which neural progenitor cells commit to a specified lineage of the central nervous system remains unknown. We show that HDAC1 and HDAC2 redundantly control neuronal development and are required for neuronal specification. Mice lacking HDAC1 or HDAC2 in neuronal precursors show no overt histoarchitectural phenotypes, whereas deletion of both HDAC1 and HDAC2 in developing neurons results in severe hippocampal abnormalities, absence of cerebellar foliation, disorganization of cortical neurons, and lethality by postnatal day 7. These abnormalities in brain formation can be attributed to a failure of neuronal precursors to differentiate into mature neurons and to excessive cell death. These results reveal redundant and essential roles for HDAC1 and HDAC2 in the progression of neuronal precursors to mature neurons in vivo.cerebellum ͉ hippocampus ͉ neurogenesis ͉ neuronal precursors H istone acetyltransferases (HATs) and histone deacetylases (HDACs) provide the enzymatic basis for transcriptional activation and repression, respectively, through alterations of the chromatin landscape (1). Transcription factors recruit HDACs, either individually, or in repressive complexes to deacetylate lysine residues on histone tails, resulting in chromatin condensation and repression of gene expression (2). There are 4 classes of HDACs that coordinate proper gene regulation for numerous cellular processes: class I (HDAC1, -2, -3, and -8), class II (HDAC4, -5, -6, -7, -9, and -10), sirtuin class III, and class IV (HDAC11) (3). Although much has been learned through in vitro and inhibitor studies, little is known about the biological function of these individual enzymes in vivo (4). We have shown that the class I HDACs, HDAC1 and HDAC2, redundantly regulate cardiac growth and morphogenesis (5), however, the functions of HDAC1 and HDAC2 in other tissues remain unknown.HDAC inhibitors have shown significant potential for therapeutic use in a variety of disorders, including those of the central nervous system (CNS), such as neurodegenerative disease, motor neuron disease, and a number of other neurological disease states (6). Furthermore, it has been shown that HDAC inhibitors induce differentiation of both embryonic and adult cortical neuronal progenitor cells to neurons specifically (7-9). The wide expression pattern of a number of HDACs in the developing brain suggests specific roles for individual HDACs in neuronal development (10), however, the broad inhibition of classical HDAC inhibitors has precluded the analysis of individual HDACs pharmacologically. Additionally, the early lethality associated with global deletion of class I HDACs in knockout mice has compounded the difficulties in analyzing the functions of these enzymes during specific stages of neurogenesis in vivo (5, 11).To further investigate the specific roles of HDAC1 and HDAC2 in neuronal development, we generated conditional deletions of HDAC1 and HDAC2 in the central nervous system. Here, we show both HDAC1 and HDAC2 are required for multip...

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Histone deacetylase 1 is required for cell cycle exit and differentiation in the zebrafish retina

Cited by 52 publications

References 28 publications

Interkinetic Nuclear Migration and the Selection of Neurogenic Cell Divisions during Vertebrate Retinogenesis

Interkinetic Nuclear Migration and the Selection of Neurogenic Cell Divisions during Vertebrate Retinogenesis

Histone deacetylases 1 and 2 are required for brain development

Histone deacetylases 1 and 2 control the progression of neural precursors to neurons during brain development

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