Chromatin remodeling complexes (CRCs) are essential molecular machines that use ATP hydrolysis to move, destabilize, eject, or restructure nucleosomes. These complexes regulate multiple cellular processes, such as transcription and DNA repair, by controlling access to genomic DNA. They are large, multiprotein complexes that use the energy of ATP hydrolysis to mobilize and restructure nucleosomes.
Chromatin remodeling is crucial for the repair of DNA double-strand breaks (DSBs) and regulation of aging. The local chromatin environment is remodelled to facilitate the recruitment of DNA damage tolerance factors. As chromatin is condensed into the primary nucleosome structure, DNA becomes less accessible for transcription factors. A chromatin remodeling ATPase is required to unwrap the nucleosomal DNA or to ensure specific genomic sequences are accessible.
In summary, chromatin remodeling complexes facilitate nucleosome assembly and mobilization by breaking and reestablishing histone-DNA contacts. They are molecular machines that generate various chromatin landscapes, adjust nucleosome positioning, and alter DNA accessibility. Chromatin remodeling complexes are proteins powered by ATP that play a crucial role in sliding nucleosomes along DNA to ensure specific genomic sequences are accessible. Mutants of ino80 show hypersensitivity to agents that cause DNA damage, and their structure can be altered by modifying histone phosphorylation, ubiquitylation, and PARylation of DNA repair factors.
📹 Chromatin Remodeling in Eukaryotes
What is the use of chromatin remodeling complexes for transcriptional access of DNA?
Chromatin remodeling complexes (CRCs) are essential in regulating transcription by altering the composition and structure of chromatin. The nucleosome, the fundamental unit of eukaryotic chromatin, is the key component of these complexes. SWI2/SNF2-Related 1 Chromatin Remodeling Complex (SWR1-C) is a member of the INO80 chromatin remodeling family and primarily catalyzes the exchange of H2A-H2B with the H2A. Z-H2B dimer. The replacement of H2A. Z into nucleosomes affects nucleosome stability and chromatin structure.
The incorporation of H2A. Z into chromatin and its physiochemical properties play a crucial role in transcriptional regulation during developmental and environmental responses. In Arabidopsis, SWR1-C has been identified as pivotal in various developmental and physiological processes, including DNA damage repair, stress tolerance, and flowering time regulation. Recent discoveries have contributed to a better understanding of the function of the SWR1 complex in plants.
What is the DNA damage response of chromatin?
The structure of chromatin is subject to influence from histone modification and chromatin remodeling, with modifying enzymes increasing the accessibility of DNA lesions. The alterations in chromatin structure that result from DNA damage can facilitate the repair of damaged DNA and contribute to genomic stability. This process may offer new avenues for developing cancer therapies.
What are two forms of chromatin remodeling that affect transcription?
Chromatin is a complex formed by the DNA double helix and nuclear proteins called histones in the cell nucleus. This tightly wrapped structure prevents DNA from accessing regulatory proteins, leading to gene silencing. Chromatin has two forms: euchromatin, which is less condensed and can participate in transcription, and heterochromatin, which is highly condensed and cannot be transcribed. The basic unit of chromatin is the nucleosome, which is composed of 147 base pairs of DNA wrapped around 2 copies each of four histone proteins.
Chromatin remodeling depends on the three dynamic properties of nucleosomes: reconstruction, enzyme-induced covalent modification, and repositioning. Reconstruction involves compositional alteration using canonical histones or special histone variants, mediated by histone-exchange complexes like the SWR1 complex, which replaces canonical histones with a histone variant.
How does chromatin affect DNA?
Chromatin not only condenses DNA within the cellular nucleus but also controls its usage. This is evidenced by the observation that specific genes in eukaryotes only become expressed if they can be accessed by RNA polymerase and transcription factors.
How does chromatin accessibility regulate gene expression?
This review explores the dynamic nature of chromatin’s access to DNA, which is crucial for cellular identity. The organization of accessible chromatin across the genome is influenced by a network of interactions between enhancers, promoters, insulators, and chromatin-binding factors. This landscape changes dynamically in response to external stimuli and developmental cues. The review also suggests that homeostatic maintenance of accessibility is dynamically regulated through a competitive interplay between chromatin-binding factors and nucleosomes. The review aims to illustrate how chromatin accessibility defines regulatory elements within the genome and how these epigenetic features are dynamically established to control gene expression.
What are the mechanisms of chromatin remodeling?
Chromatin remodeling is a process that involves three dynamic properties of nucleosomes: reconstruction, enzyme-induced covalent modification, and repositioning. Reconstruction involves altering the composition of nucleosomes using canonical histones or special histone variants, which are mediated by histone-exchange complexes like the SWR1 complex. The newly formed variant recruits special regulators to regulate biological functions.
Covalent modification of histones by histone acetyltransferase, deacetylase, methyltransferase, and ATP-dependent protein complexes can also lead to chromatin remodeling. Repositioning of nucleosomes is also facilitated by remodeler complexes.
How is euchromatin made accessible for transcription?
Euchromatin, a relatively decondensed structure, allows for easy access to DNA by transcription-requiring proteins, unlike heterochromatin, which is more condensed and typically not transcriptionally active. This open structure allows for ready access to DNA by genes, while heterochromatin is more condensed, making genes less transcriptionally active. Copyright © 2024 Elsevier B. V., its licensors, and contributors. All rights reserved, including text and data mining, AI training, and similar technologies.
How does chromatin remodeling link metabolic signaling to gene expression?
Chromatin modifications enable responsive, rapid, and reversible gene expression. Chromatin remodelers regulate metabolic gene expression and cell division in response to changing nutrient environments. Metabolic signaling pathways, like the TOR pathway, cooperate with chromatin-remodeling. This information is sourced from ScienceDirect, a website that uses cookies and holds copyright for text and data mining, AI training, and similar technologies.
What are the examples of chromatin remodeling complexes?
The chromatin remodeling proteins are divided into four families: SWI/SNF, CHD, ISWI, and INO80. Mouse embryonic stem cells (ES) express a specific type of SWI/SNF complex called esBAF. This information was reported in a study by Elsevier B. V., which uses cookies and Creative Commons licensing terms for open access content. All rights are reserved for text and data mining, AI training, and similar technologies.
How does chromatin influence transcription?
The chromatin structure, which is regulated through a variety of mechanisms, including histone modification, chromatin remodeling, histone variant incorporation, and histone eviction, has a significant impact on transcription processes mediated by RNA polymerase II.
What are the effects of chromatin remodeling?
Chromatin remodeling factors not only facilitate nucleosome mobility but also enhance the accessibility of DNA-binding factors and nucleases to chromatin-packaged DNA, thereby disrupting histone-DNA interactions within the nucleosome.
📹 Chromatin Biology: Epigenetics and the Regulation of Gene Activity
This animation explains epigenetics, the study of changes in the pattern of gene expression that is regulated independently of the …
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