“…Once settled along the Xi with the spreading Xist transcripts, PRC2 is responsible for marking the chromatin with H3K27 trimethylation (a repressive histone modification), which occurs in conjunction with the loss of active histone marks such as H4 acetylation, as well as H3K4 and H3K36 methylation [29,33]. In hnRNP U deficient cells, this H3K27 repressive mark is not established, leading to defects in XI formation [76,77]. After the deposition of these histone H3 marks, histone H2A is replaced with the variant macro -H2A [33].…”
Section: Xist and X-chromosome Inactivationmentioning
The field of long noncoding RNA (lncRNA) research has been rapidly advancing in recent years. Technological advancements and deep-sequencing of the transcriptome have facilitated the identification of numerous new lncRNAs, many with unusual properties, however, the function of most of these molecules is still largely unknown. Some evidence suggests that several of these lncRNAs may regulate their own transcription in cis, and that of nearby genes, by recruiting remodeling factors to local chromatin. Notably, lncRNAs are known to exist at many imprinted gene clusters. Genomic imprinting is a complex and highly regulated process resulting in the monoallelic silencing of certain genes, based on the parent-of-origin of the allele. It is thought that lncRNAs may regulate many imprinted loci, however, the mechanism by which they exert such influence is poorly understood. This review will discuss what is known about the lncRNAs of major imprinted loci, and the roles they play in the regulation of imprinting.
“…Once settled along the Xi with the spreading Xist transcripts, PRC2 is responsible for marking the chromatin with H3K27 trimethylation (a repressive histone modification), which occurs in conjunction with the loss of active histone marks such as H4 acetylation, as well as H3K4 and H3K36 methylation [29,33]. In hnRNP U deficient cells, this H3K27 repressive mark is not established, leading to defects in XI formation [76,77]. After the deposition of these histone H3 marks, histone H2A is replaced with the variant macro -H2A [33].…”
Section: Xist and X-chromosome Inactivationmentioning
The field of long noncoding RNA (lncRNA) research has been rapidly advancing in recent years. Technological advancements and deep-sequencing of the transcriptome have facilitated the identification of numerous new lncRNAs, many with unusual properties, however, the function of most of these molecules is still largely unknown. Some evidence suggests that several of these lncRNAs may regulate their own transcription in cis, and that of nearby genes, by recruiting remodeling factors to local chromatin. Notably, lncRNAs are known to exist at many imprinted gene clusters. Genomic imprinting is a complex and highly regulated process resulting in the monoallelic silencing of certain genes, based on the parent-of-origin of the allele. It is thought that lncRNAs may regulate many imprinted loci, however, the mechanism by which they exert such influence is poorly understood. This review will discuss what is known about the lncRNAs of major imprinted loci, and the roles they play in the regulation of imprinting.
“…Although this finding initially compromised the importance of observations demonstrating the role of this protein in the nuclear matrix, there are many examples that one protein can perform different functions. Indeed, SAF‐A/hnRNP‐U is involved in the regulation of transcription [109,110], alternative splicing [111] and Xist RNA positioning on the inactive copy of the female X chromosome [112,113]. In the latter case, SAF‐A/hnRNP‐U functions as a bona fide architectural protein.…”
Section: How the Functionally Dependent Architecture Of Interphase Chmentioning
a b s t r a c tThe most popular model of gene activation by remote enhancers postulates that the enhancers interact directly with target promoters via the looping of intervening DNA fragments. This interaction is thought to be necessary for the stabilization of the Pol II pre-initiation complex and/or for the transfer of transcription factors and Pol II, which are initially accumulated at the enhancer, to the promoter. The direct interaction of enhancer(s) and promoter(s) is only possible when these elements are located in close proximity within the nuclear space. Here, we discuss the molecular mechanisms for maintaining the close proximity of the remote regulatory elements of the eukaryotic genome. The models of an active chromatin hub (ACH) and an active nuclear compartment are considered, focusing on the role of chromatin folding in juxtaposing remote DNA sequences. The interconnection between the functionally dependent architecture of the interphase chromosome and nuclear compartmentalization is also discussed.
In female m ammals, one of the two X chromosomes in each cell is transcriptionally silenced in order to achieve dosage compensation between the genders in a process called X chromosome inactivation. The master regulator of this process is the long non-coding RNA Xist. During X-inactivation, Xist accumulates in cis on the future inactive X chromosome, triggering a cascade of events that provoke the stable silencing of the entire chromosome, with relatively few genes remaining active. How Xist spreads, what are its binding sites, how it recruits silencing factors and how it induces a specific topological and nuclear organization of the chromatin all remain largely unanswered questions. Recent studies have improved our understanding of Xist localization and the proteins with which it interacts, allowing a reappraisal of ideas about Xist function. We discuss recent advances in our knowledge of Xist-mediated silencing, focusing on Xist spreading, the nuclear organization of the inactive X chromosome, recruitment of the polycomb complex and the role of the nuclear matrix in the process of X chromosome inactivation.
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