Chromatin remodeling complexes: ATP-dependent machines in action

Johnson, Cotteka N; Adkins, Nicholas L.; Georgel, Philippe

doi:10.1139/o05-115

Cited by 69 publications

(51 citation statements)

References 126 publications

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“…In addition, NDR is a Brg1-enriched region. Brg1 has been shown to affect nucleosomes, phasing in the region surrounding TSS in vivo and alters the structure and/or position of nucleosome of target promoters (26,72). In this study, however, IUGR did not affect the position of nucleosomes on the GR promoters in male hippocampus.…”

Section: Discussioncontrasting

confidence: 70%

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IUGR increases chromatin-remodeling factor Brg1 expression and binding to GR exon 1.7 promoter in newborn male rat hippocampus

McKnight

Maniar

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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Ke X, McKnight RA, Maniar LE, Sun Y, Callaway CW, Majnik A, Lane RH, Cohen SS. IUGR increases chromatin-remodeling factor Brg1 expression and binding to GR exon 1.7 promoter in newborn male rat hippocampus. Am J Physiol Regul Integr Comp Physiol 309: R119 -R127, 2015. First published May 13, 2015 doi:10.1152/ajpregu.00495.2014.-Intrauterine growth restriction (IUGR) increases the risk for neurodevelopment delay and neuroendocrine reprogramming in both humans and rats. Neuroendocrine reprogramming involves the glucocorticoid receptor (GR) gene that is epigenetically regulated in the hippocampus. Using a wellcharacterized rodent model, we have previously shown that IUGR increases GR exon 1.7 mRNA variant and total GR expressions in male rat pup hippocampus. Epigenetic regulation of GR transcription may involve chromatin remodeling of the GR gene. A key chromatin remodeler is Brahma-related gene-1(Brg1), a member of the ATPdependent SWItch/Sucrose NonFermentable (SWI/SNF) chromatin remodeling complex. Brg1 regulates gene expression by affecting nucleosome repositioning and recruiting transcriptional components to target promoters. We hypothesized that IUGR would increase hippocampal Brg1 expression and binding to GR exon 1.7 promoter, as well as alter nucleosome positioning over GR promoters in newborn male pups. Further, we hypothesized that IUGR would lead to accumulation of specificity protein 1 (Sp1) and RNA pol II at GR exon 1.7 promoter. Indeed, we found that IUGR increased Brg1 expression and binding to GR exon 1.7 promoter. We also found that increased Brg1 binding to GR exon 1.7 promoter was associated with accumulation of Sp1 and RNA pol II carboxy terminal domain pSer-5 (a marker of active transcription). Furthermore, the transcription start site of GR exon 1.7 was located within a nucleosome-depleted region. We speculate that changes in hippocampal Brg1 expression mediate GR expression and subsequently trigger neuroendocrine reprogramming in male IUGR rats.intrauterine growth restriction; Brahma-related gene 1; glucocorticoid receptor; hippocampus UTEROPLACENTAL INSUFFICIENCY (UPI) leads to intrauterine growth restriction (IUGR) and complicates up to 4 -6% of all pregnancies in developed countries (13). IUGR predisposes affected newborns toward poor neurological outcomes and impaired neuroendocrine programming (18,20,46,67,71). Neuroendocrine programming of the hypothalamo-pituitary axis (HPA) axis is regulated, in part, by the hippocampus (24,40). Multiple studies suggest that IUGR-induced neuroendocrine reprogramming involves altered glucocorticoid receptor (GR) expression in the hippocampus and dysregulation of HPA axis reactivity (24,34,42,43,74,75,80

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Section: Discussioncontrasting

confidence: 70%

“…Brg1 regulates gene transcription epigenetically by affecting the chromatin structure of target promoters (26,72). In addition, Brg1 interacts with GR for GR-regulated transactivation on target genes (5).…”

Section: Discussionmentioning

confidence: 99%

IUGR increases chromatin-remodeling factor Brg1 expression and binding to GR exon 1.7 promoter in newborn male rat hippocampus

McKnight

Maniar

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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“…ATP-dependent chromatin-remodeling complexes use energy derived from the hydrolysis of ATP to break histone-DNA contacts and reposition nucleosomes in a noncovalent manner (13). Generally, ATP-dependent chromatin remodelers are grouped into five major families, i.e., SWI/SNF, ISWI, Mi-2/NuRD, INO80, and SWR1, each being derived from the SNF2 helicase superfamily, which has a common structural core consisting of two RecA helicase-like domains that bind and hydrolyze ATP (1,(14)(15)(16).…”

mentioning

confidence: 99%

Glucocorticoid Receptor Transcriptional Activation via the BRG1-Dependent Recruitment of TOP2β and Ku70/86

Trotter

King

Archer

2015

Molecular and Cellular Biology

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BRG1, the central ATPase of the human SWI/SNF complex, is critical for biological functions, including nuclear receptor (NR)-regulated transcription. Analysis of BRG1 mutants demonstrated that functional motifs outside the ATPase domain are important for transcriptional activity. In the course of experiments examining protein interactions mediated through these domains, Ku70 (XRCC6) was found to associate with a BRG1 fragment encompassing the conserved helicase-SANT-associated (HSA) and BRK domains of BRG1. Subsequent transcriptional activation assays and chromatin immunoprecipitation studies showed that Ku70/86 and components of the topoisomerase II␤ (TOP2␤)/poly(ADP ribose) polymerase 1 (PARP1) complex are necessary for NR-mediated SWI/SNF-dependent transcriptional activation from endogenous promoters. In addition to establishing Ku-BRG1 binding and TOP2␤/PARP1 recruitment by nuclear receptor transactivation, we demonstrate that the transient appearance of glucocorticoid receptor (GR)/BRG1-dependent, TOP2␤-mediated double-strand DNA breaks is required for efficient GR-stimulated transcription. Taken together, these results suggest that a direct interaction between Ku70/86 and BRG1 brings together SWI/SNF remodeling capabilities and TOP2␤ activity to enhance the transcriptional response to hormone stimulation.

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“…Examples of proteins involved in chromatin remodeling that were up-regulated by the overexpression of SMYD2 are the three proteins from the SWI/SNF complex (30,31). The SWI/SNF complex is recruited to chromatin to remodel nucleosomes using ATP hydrolysis as a source of energy (32). The SWI/SNF complex has been implicated in cancer through different mechanisms (30,33).…”

Section: Discussionmentioning

confidence: 99%

The Tale of Two Domains

Abu‐Farha

Lambert

Madhoun

et al. 2008

Molecular & Cellular Proteomics

174

105

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Very little is known about SET-and MYND-containing protein 2 (SMYD2), a member of the SMYD protein family. However, the interest in better understanding the roles of SMYD2 has grown because of recent reports indicating that SMYD2 methylates p53 and histone H3. In this study, we present a combined proteomics and genomics study of SMYD2 designed to elucidate its molecular roles. We report the cytosolic and nuclear interactome of SMYD2 using a combination of immunoprecipitation coupled with high throughput MS, chromatin immunoprecipitation coupled with high throughput MS, and co-immunoprecipitation methods. In particular, we report that SMYD2 interacted with HSP90␣ independently of the SET and MYND domains, with EBP41L3 through the MYND domain, and with p53 through the SET domain. We demonstrated that the interaction of SMYD2 with HSP90␣ enhances SMYD2 histone methyltransferase activity and specificity for histone H3 at lysine 4 (H3K4) in vitro. Interestingly histone H3K36 methyltransferase activity was independent of its interaction with HSP90␣ similar to LSD1 dependence on the androgen receptor. We also showed that the SET domain is required for the methylation at H3K4. We demonstrated using a modified chromatin immunoprecipitation protocol that the SMYD2 gain of function leads to an increase in H3K4 methylation in vivo, whereas no observable levels of H3K36 were detected. We also report that the SMYD2 gain of function was correlated with the upregulation of 37 and down-regulation of four genes, the majority of which are involved in the cell cycle, chromatin remodeling, and transcriptional regulation. TACC2 is one of the genes up-regulated as a result of SMYD2 gain of function. Up-regulation of TACC2 by SMYD2 occurred as a result of SMYD2 binding to the TACC2 promoter where it methylates H3K4. Furthermore the combination of the SMYD2 interactome with the gene expression data suggests that some of the genes regulated by SMYD2 are closely associated with SMYD2-interacting proteins. Molecular & Cellular Proteomics 7:560 -572, 2008.The mapping of protein-protein interaction helps us understand the function of proteins. In recent years, our group (1) and others (2, 3) have performed protein interaction experiments for large sets of human proteins. Our approach for the mapping of protein-protein interactions is based on immunoprecipitation coupled with high throughput MS (IP-HTMS). 1The SMYD protein family consists of five proteins (SMYD1-5) that are not fully characterized and are grouped based on the presence of two conserved domains (MYND and SET domains). The MYND domain is a zinc finger motif that is involved in protein-protein interaction. It is named after Myeloid, Nervy, and DEAF-1, which are the three most characterized proteins that contain the MYND domain (4). The SET domain is an evolutionarily conserved sequence motif consisting of 130 -140 amino acids. Its name is derived from the three proteins in which it was initially characterized: Su (var) 3-9, Enhancer-of-zeste, and Trithorax (5, 6). These enzymes a...

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Chromatin remodeling complexes: ATP-dependent machines in action

Cited by 69 publications

References 126 publications

IUGR increases chromatin-remodeling factor Brg1 expression and binding to GR exon 1.7 promoter in newborn male rat hippocampus

IUGR increases chromatin-remodeling factor Brg1 expression and binding to GR exon 1.7 promoter in newborn male rat hippocampus

Glucocorticoid Receptor Transcriptional Activation via the BRG1-Dependent Recruitment of TOP2β and Ku70/86

The Tale of Two Domains

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