Histone acetylation reduces nucleosome core particle linking number change

Norton, Vicki G.; Imai, Brian S.; Yau, Peter M.; Bradbury, E. Morton

doi:10.1016/0092-8674(89)90920-3

Cited by 376 publications

(274 citation statements)

References 33 publications

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“…One idea is that histone acetylation serves as a molecular tag for recruiting other factors with regulatory activity (Jenuwein and Allis, 2001;Zeng and Zhou, 2002;Mujtaba et al, 2007). Histone acetylation is also thought to influence transcription through remodeling chromatin structure, increasing accessibility by relaxing DNA interactions with histone proteins (Norton et al, 1989;Grunstein, 1997). Although both mechanisms are likely to play a role, our findings indicate that HDACi administration alone has relatively little effect on hippocampal gene and synaptic protein expression.…”

Section: Discussionmentioning

confidence: 99%

Experience Modulates the Effects of Histone Deacetylase Inhibitors on Gene and Protein Expression in the Hippocampus: Impaired Plasticity in Aging

Sewal

Patzke²,

Perez

et al. 2015

J. Neurosci.

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The therapeutic potential of histone deacetylase inhibitor (HDACi) treatment has attracted considerable attention in the emerging area of cognitive neuroepigenetics. The possibility that ongoing cognitive experience importantly regulates the cell biological effects of HDACi administration, however, has not been systematically examined. In an initial experiment addressing this issue, we tested whether water maze training influences the gene expression response to acute systemic HDACi administration in the young adult rat hippocampus. Training powerfully modulated the response to HDACi treatment, increasing the total number of genes regulated to nearly 3000, including many not typically linked to neural plasticity, compared with Ͻ300 following HDACi administration alone. Although water maze training itself also regulated nearly 1800 genes, the specific mRNAs, gene networks, and biological pathways involved were largely distinct when the same experience was provided together with HDACi administration. Next, we tested whether the synaptic protein response to HDACi treatment is similarly dependent on recent cognitive experience, and whether this plasticity is altered in aged rats with memory impairment. Whereas synaptic protein labeling in the young hippocampus was selectively increased when HDACi administration was provided in conjunction with water maze training, combined treatment had no effect on synaptic proteins in the aged hippocampus. Our findings indicate that ongoing experience potently regulates the molecular consequences of HDACi treatment and that the interaction of recent cognitive experience with histone acetylation dynamics is disrupted in the aged hippocampus.

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Section: Discussionmentioning

confidence: 99%

Experience Modulates the Effects of Histone Deacetylase Inhibitors on Gene and Protein Expression in the Hippocampus: Impaired Plasticity in Aging

Sewal

Patzke²,

Perez

et al. 2015

J. Neurosci.

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“…Although histone acetyltransferases are recruited to the ligand-bound TR-RXR, it is difficult to account for the large topological change observed through acetylation alone (Norton et al 1989, Bauer et al 1994. In fact, transcription can be activated without significant topological change from a TR A promoter complexed in chromatin with unliganded TR-RXR simply by the addition of the deacetylase inhibitor TSA .…”

Section: Chromatin Remodeling For Transcriptional Activation By Trmentioning

confidence: 99%

Nuclear receptors: coactivators, corepressors and chromatin remodeling in the control of transcription

Collingwood¹,

Fd²,

Ap³

1999

Journal of Molecular Endocrinology

294

172

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A contemporary view of hormone action at the transcriptional level requires knowledge of the transcription factors including the hormone receptor that may bind to promoters or enhancers, together with the chromosomal context within which these regulatory proteins function. Nuclear receptors provide the best examples of transcriptional control through the targeted recruitment of large protein complexes that modify chromosomal components and reversibly stabilize or destabilize chromatin. Ligand-dependent recruitment of transcriptional coactivators destabilizes chromatin by mechanisms including histone acetylation and contacts with the basal transcriptional machinery. In contrast, the recruitment of corepressors in the absence of ligand or in the presence of hormone antagonists serves to stabilize chromatin by the targeting of histone deacetylases. Both activation and repression require the action of other chromatin remodeling engines of the switch 2/sucrose nonfermentable 2 (SWI2/SNF2) class. Here we summarize this information and integrate hormone action into a chromatin context. Journal of Molecular Endocrinology (1999) 23, 255-275 INTRODUCTIONThe nuclear hormone receptors provide transcription research with a clear example of how the reversible modification of chromatin structure can contribute to the control of gene expression. Remarkable progress in the definition of intermediary protein complexes that activate or repress transcription has allowed common themes in transcriptional control by a wide variety of receptors to emerge. The roles of these coactivators and corepressors in mediating the activities of nuclear receptors within chromatin is a key element of contemporary molecular endocrinology. The beststudied receptors in this regard are those for the glucocorticoid and thyroid hormones.The glucocorticoid receptor recognizes response elements within nucleosomes as a first step towards a finely orchestrated rearrangement of histone-DNA contacts concomitant with the assembly of a functional transcription complex. The determinants of chromatin remodeling and the molecular machines that carry it out are now understood in considerable detail. Likewise, the thyroid hormone receptor recognizes nucleosomal DNA and utilizes chromatin to regulate transcription. However, in this case the receptor exerts a dual function. In the absence of ligand, the thyroid hormone receptor recruits a corepressor complex that stabilizes chromatin structure. Upon addition of hormone the receptor releases this repressive complex, and recruits coactivators that destabilize chromatin and promote transcription.This review illustrates the role of chromatin, coactivators and corepressors in gene control as orchestrated by the glucocorticoid and thyroid hormone receptors. COACTIVATORS AND COREPRESSORS CoactivatorsThe interplay of distinct nuclear receptor responsive transcription pathways has been recognized for 255

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“…Histones are subject to a variety of posttranslational modifications, of which the best studied is acetylation (for review, see Turner, 2005). Histone acetylation alters chromatin structure (Norton et al, 1989) and increases accessibility for transcriptional regulatory proteins (Vettese-Dadey et al, 1996). The steady-state levels of histone acetylation are the product of proteins with histone acetyltransferase (HAT) activity that add acetyl groups to histones and proteins with histone deacetylase (HDAC) activity that remove acetyl groups.…”

Section: Introductionmentioning

confidence: 99%

Histone Deacetylase Inhibitors Enhance Memory and Synaptic Plasticity via CREB: CBP-Dependent Transcriptional Activation

Vecsey¹,

Hawk²,

Lattal³

et al. 2007

Journal of Neuroscience

757

761

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Histone deacetylase (HDAC) inhibitors increase histone acetylation and enhance both memory and synaptic plasticity. The current model for the action of HDAC inhibitors assumes that they alter gene expression globally and thus affect memory processes in a nonspecific manner. Here, we show that the enhancement of hippocampus-dependent memory and hippocampal synaptic plasticity by HDAC inhibitors is mediated by the transcription factor cAMP response element-binding protein (CREB) and the recruitment of the transcriptional coactivator and histone acetyltransferase CREB-binding protein (CBP) via the CREB-binding domain of CBP. Furthermore, we show that the HDAC inhibitor trichostatin A does not globally alter gene expression but instead increases the expression of specific genes during memory consolidation. Our results suggest that HDAC inhibitors enhance memory processes by the activation of key genes regulated by the CREB:CBP transcriptional complex.

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Histone acetylation reduces nucleosome core particle linking number change

Cited by 376 publications

References 33 publications

Experience Modulates the Effects of Histone Deacetylase Inhibitors on Gene and Protein Expression in the Hippocampus: Impaired Plasticity in Aging

Experience Modulates the Effects of Histone Deacetylase Inhibitors on Gene and Protein Expression in the Hippocampus: Impaired Plasticity in Aging

Nuclear receptors: coactivators, corepressors and chromatin remodeling in the control of transcription

Histone Deacetylase Inhibitors Enhance Memory and Synaptic Plasticity via CREB: CBP-Dependent Transcriptional Activation

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