Chromatin Biology Definition

Chromatin Biology Definition Image link: https://en.wikipedia.org/wiki/Chromatin_remodeling
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  • The identification of CGI forests and prairies is robust over CGI definition ( Supplementary Figure S3 ).(More…)

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  • CDT1 (Chromatin licensing and DNA replication factor 1) is a protein that in humans is encoded by the CDT1 gene. 5 6 7 8 It is a licensing factor that functions to limit DNA from replicating more than once per cell cycle.(More…)

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The identification of CGI forests and prairies is robust over CGI definition ( Supplementary Figure S3 ). [1] To evaluate the robustness of the F-P definition over CGI identification, we defined CGI in an alternative way and examined the overlap between forests identified according to the canonical CGIs obtained from UCSC ( http://genome.ucsc.edu/cgi-bin/hgTables ) and the newly defined CGIs. [1] The alternative CGI F-P definition was based on the neighboring distances between these new CGIs using the same method described above. [1] The new definition of CGI was given based on the CpG density of each 200-bp window using a sliding window approach. [1]

We expanded the previous type A/B definition to the whole genome, with types A and B consist of 46.7% and 45.2% of the whole chromosome, respectively (Supplementary Table S4; Supplementary Materials). [1]

Genome Biology. 14 (R115): R115. doi : 10.1186/gb-2013-14-10-r115. [2]

Despite considerable new insights gained in the past few years into the localization and function of some cohesin proteins, and the recent identification of yet another meiosis-specific cohesin subunit, a plethora of open questions remains, which concern not only fundamental germ cell biology but also the consequences of cohesin impairment for human reproductive health. [3] Systems biology is the study of systems of biological components, which may be molecules, cells, organisms or entire species. [4]

Definition: Nucleosome is the fundamental repeating unit of eukaryotic chromosome, consisting of a length of DNA (200bp) coiled around a core of histones. [5]

That definition has stood the test of time because it emphasizes two major features of cancer: abnormal cell growth and the fact that abnormal growth occurs because of a malfunction in the mechanisms that control cell growth and differentiation (maturation). [6] Mapping such regions relies on surface markers and immunophenotypic definition of HSCs. [7]

POSSIBLY USEFUL

CDT1 (Chromatin licensing and DNA replication factor 1) is a protein that in humans is encoded by the CDT1 gene. 5 6 7 8 It is a licensing factor that functions to limit DNA from replicating more than once per cell cycle. [8] The enrichment of DHS open chromatin signal ( 47 ), typical transcription factors, and DNA binding protein modifier Ogt ( 48 ) in forests compared to neighboring prairies suggests that forests adopt a more open conformation with higher chromatin accessibilities and transcription factor binding affinity (Supplementary Figures S14 and S15). [1] Overall, the distributions of DNA methylation, histone marks, DHSs and TFBSs in forests and prairies all show that forests and prairies segregate the chromatin into distinct epigenetic domains, and the open and active chromatin is formed mainly by forests rather than prairies. [1] In the process to thermodynamic stable state, that is, phase separation, both structural and epigenetic properties of the chromatin become more consistent to sequential difference between forests and prairies, which in return may enhance the physical difference between the two sequential domains, accelerating the phase separation. [1] It was recently observed that HP1a protein which is characteristic of heterochromatin undergoes liquid-liquid demixing in vitro, and that heterochromatin exhibits liquid-phase separated dynamics ( 71 ), consistent with the segregation of prairie sequences which largely corresponds to repressive chromatin from forests being physically driven by a phase separation mechanism. [1] The spatial segregation of prairies from forest indicates a phase separation mechanism in chromatin structure formation and remodeling, and the lineage specific interaction between the two types of DNA domains in cellular processes provides a new view on how cellular functions are achieved through the control of chromatin 3D structures. [1] CGI forests and prairies largely improve the separation of the linear sequence into domains of different genetic properties, and the correspondence of sequential differences to the 3D chromatin structure differences in aspects including TADs and compartment types, providing possible sequence dependence on TAD structure formation and compartmentalization. [1]

These results show that CGI distribution (prairie and forest) is highly predictive for chromatin 3D structure formation. [1] Besides structure, CGI forests and prairies allow us to divide efficiently the genome into domains of markedly different epigenetic properties and establish a wide range of relations between DNA sequence and chromatin states. [1] Therefore, the vast majority of chromatin is surrounded by sequences of the same type, indicating that individual forests and prairies separately segregate in space. [1] Notably, as shown in previous study ( 45 ) as well as discussed later, the different methylation levels of forests and prairies across cell types also correlate to their differences in the spatial packing of the chromatin. [1] Tissue (or cell)-specific domains of the prairies remained in the open chromatin through mediators like tissue-specific TFs contribute to cell identity establishment. [1] TFs and other factors (e.g. RNA) mediated dynamic perturbation may be complement to thermodynamic driving force, influencing physical properties of their combined domains, thus regulating chromatin behavior in different cells. [1]

The growth of this phase is consistent with the observation that the chromatin of pluripotent cells tends to be relatively homogeneous with less heterochromatin which becomes more prevalent in differentiated cells ( 53, 54 ), as well as the spread of repressive H3K9me3 and H3K27me3 histone marks in differentiation ( 55, 56, 83 ). [1] This study, along with earlier analyses ( 11, 12 ), showed that the early embryonic chromatins are characterized by weak domain segregation, small heterochromatin, CpG demethylation, and less repressive histone marks. [1]

The type A and type B regions are regarded as different chromatin secondary structures and mainly comprise compartments A and B, respectively ( 7 ). [1] Eukaryotic chromatins possess highly complex structures which are of great biological importance. [1] Chromatin 3D structures are commonly partitioned into compartments. [1]

“The replicative regulator protein geminin on chromatin in the HeLa cell cycle”. [8] Though their specific function is largely under debate, noncoding DNAs are increasingly believed to play an architectural role in the formation of complex eukaryotic chromatin. [1] Methylated DNA immunoprecipitation (MeDIP), analogous to chromatin immunoprecipitation, immunoprecipitation is used to isolate methylated DNA fragments for input into DNA detection methods such as DNA microarrays (MeDIP-chip) or DNA sequencing (MeDIP-seq). [2] “Essential role of human CDT1 in DNA replication and chromatin licensing”. [8] Reciprocally, around 60-70% of human genes have a CpG island in their promoter region. 23 24 The majority of CpG islands are constitutively unmethylated and enriched for permissive chromatin modification such as H3K4 methylation. [2] In yeast at least, H3K36me3 recruits enzymes such as histone deacetylases to condense chromatin and prevent the activation of cryptic start sites. 34 In mammals, DNMT3a and DNMT3b PWWP domain binds to H3K36me3 and the two enzymes are recruited to the body of actively transcribed genes. [2]

The heterochromatin compaction and the cell- or tissue-specific genome activation together shape the chromatin. [1] It is thus reasonable to speculate that cancer chromatin associates with a large F-P separation. [1] The spatial packaging of chromatin also regulates gene expression. [1]

Gene Ontology (GO) analysis using DAVID ( https://david.ncifcrf.gov ) ( 33, 34 ) shows that HKGs in prairies are specifically enriched in GO terms of DNA damage and repair, chromatin remodeling, p53 signaling, and cellular response to oxidative stress compared to those in forests ( Supplementary Figure S5 ). [1] Their reconstructed 3D chromatin structures also exhibit strong domain segregation, in contrast to the structures with highly intermingled forests and prairies of normal somatic tissues (Figure 4J ). [1] The brain chromatin is characterized by strong F-P local interactions and weak domain segregation, with an open reconstructed chromatin structure (Figure 4J ). [1] Proliferating tissues and cell lines also possess segregated chromatin structures (Figure 6D ). [1] It is intriguing to examine in a more systematic way the roles of genomic information and phase separation in the chromatin structure formation for different species, at different cell and disease states, and under different environmental conditions, especially at different temperatures. [1] The mechanism, especially the sequence dependence for the formation of varied chromatin structures in different cells remains to be elucidated. [1] Our model explains the sequence-dependence and provides a more general and unified picture of chromatin structure formation and evolution in different biological events, such as differentiation and aging, and, more interestingly, a possible molecular mechanism for the change of cellular states. [1] As we have proposed, the chromatin structure change in differentiation and senescence resembles a “phase separation? mechanism that is characterized by the cell-specific removal of prairies from the active chromatin domains. [1] Based on these observations, we propose that chromatin structure change in cellular processes is characterized by the interplay between the global tendency of sequence based thermodynamic stabilization and the dynamic perturbation in differentiation provided at least partially by TFs. [1] Chromatin structure changes involving development, differentiation and disease were thus explained based on a rather simple theoretical framework. [1] Recent study on senescent cells suggests that epigenomic remodeling and chromatin structure changes could be discrete events ( 52 ). [1] The close but varied sequence-structure relation found in different cells led us to propose a sequence-based phase separation model which provided a possible explanation on how different chromatin structures are formed and how chromatin states are reached. [1] We propose that the phase separation of the 1D mosaic sequence in space serves as a potential driving force, and together with cell type specific epigenetic marks and transcription factors, shapes the chromatin structure in different cell types. [1] These factors along with epigenetic modifications shape the chromatin structure of different cell types via specific or non-specific binding to sequences. [1]

Important correlations have been identified between human and mouse DNA sequences and their 3D chromatin structures, epigenetics, as well as various biological functions. [1] These observations all promote us to propose that the segmented DNA sequence provides a more fundamental driving force for the formation of chromatin structure. [1]

The breakdown and reestablishment of TADs as well as the reshuffling of chromosome territory during mitosis in which factors like HP1 and polycomb proteins are excluded from the sequence ( 58, 59, 69, 70 ) also suggest a more intrinsic mechanism for chromatin structure sustainability than protein binding. [1] Similar to the importance of amino-acid sequence to protein structure and function, such a sequence dependence in chromatin structure provides a unified phase separation mechanism and information on the evolution of chromatin structures in various biological processes. [1] Although structural proteins are important for the formation of TADs and the CTCF binding sites can be used to predict Hi-C contact maps ( 67, 68 ), the loss of cohesin did not lead to the disruption of 3D chromatin structure ( 19 ), and a quarter of TAD boundaries show no evidence of CTCF binding ( 4 ). [1] Multiple factors contribute to the chromatin structure formation and functioning of organisms. [1] In the present study, we integrated various sources of genetic, epigenetic and 3D structural information to investigate the sequence dependence and cell-type specificity in the formation of 3D chromatin structure. [1]

The modelled chromatin structure of zygote in PN5 and IMR90 cell line is shown for (A) and (D), respectively. [1] Similar to embryonic and pluripotent cells, proliferating tissues and cell lines also possess segregated chromatin structures. [1]

The diversity of the dataset allows us to investigate the chromatin structure difference in different cell/tissue types and stages, obtaining information concerning early embryonic development, differentiation and senescence. [1] During early embryonic development, the magnitude of the F-index slightly increases from the early two-cell to the eight-cell stage (Figure 3A ), consistent with the re-establishment of TADs and high-order chromatin structures in early development ( 11, 12, 49, 50 ). [1] The change of local 3D chromatin structural properties during embryonic development and cell differentiation. ( A ) Average F-index of forests and prairies in different cells during mouse embryonic development. ( B ) Average F-index of forests (left) and prairies (right) in different stages during cell differentiation for four mouse cell types. ( C ) The box plot of F-indices in forest for three types of human cells. [1] Much progress has been made in the chromatin structural study of different cell types ( 8, 9 ) and different cellular processes like early embryonic development, cell differentiation, and cell senescence ( 10-15 ). [1]

In this way, the thermodynamic and dynamic regulation factors together shape the chromatin structures in varied cell types. [1] The chromatin structures can therefore be regarded as the result of the interplay between thermodynamic and dynamic factors. [1]

This link between DNA methylation and chromatin structure is very important. [2] Since F-P interactions appear to contribute to chromatin structure change in various processes and thus dynamic gene regulation, they provide a possible mechanism for cell-specific gene regulation. [1] Life might have evolved to cope with the irreversible chromatin structure segregation and the corresponding aging by introducing fertilization which yields globally F-P mixed and homogeneous chromatins. [1]

To further evaluate the chromatin states of forests and prairies, we investigated the F-P difference of histone marks. [1] Their correspondence to the chromatin state is also significantly weaker than the forests and prairies. [1]

They are useful for reconstructing chromatin structures and explaining chromatin states given certain cellular conditions. [1] Continuous mitosis resembles repeated annealing process for the chromatin structure to evolve towards stable states which probably adapt to the local cellular environment. [1]

Gene positioning and transcriptional activity represent major determinants of the microscopic chromatin structure that self-organizes in a rather predictable way. [1] We hope that more systematic Hi-C studies will shed light onto the chromatin structure change in oncogenesis. [1] Using Hi-C and ChIA-PET techniques, recent studies have shown that the 3D chromatin structure is important for gene regulation ( 1, 2 ). [1] The high-order chromatin structure plays a non-negligible role in gene regulation. [1] The genome can thus be regarded as an A-B block copolymer and the chromatin structure its assembly. [1] It also suggested possible links between chromatin structure and various phenomena such as the body temperature dependence in development and aging. [1] As temperature may affect the domain segregation, one would also expect the chromatin structure to vary with tissues of different temperatures. [1] Its reconstructed 3D chromatin structure shows a high degree of domain segregation. [1]

In mitosis, “mitotic bookmarking? transcription factors have been suggested to play a role in chromatin structure re-establishment ( 20 ). [1]

MBD proteins then recruit additional proteins to the locus, such as histone deacetylases and other chromatin remodeling proteins that can modify histones, thereby forming compact, inactive chromatin, termed heterochromatin. [2] This chromatin stability is consistent with the need of ATP associated chromatin remodeling factors in reprogramming ( 78-80 ). [1]

This current classification divides the genome into domains of more distinctly different genetic, epigenetic, and 3D chromatin structural properties. [1] In this way, we provide a bottoms-up theory to explain the chromatin structural and epigenetic changes in different processes. [1]

The methylation level of the open sea (defined as the genomic regions excluding CGIs, CGI shores and CGI shelves ( 44 )) lacks specificity and better reflects the environmental chromatin state. [1]

The structure of chromatin can be changed (remodeled) to alter how tightly DNA is packaged. [9] Chromatin is the network of DNA and proteins that packages DNA into chromosomes. [9] H1 histone attaches to the DNA near the nucleosome when a 10nm chromatin fiber undergoes the next level of packing. [5] In 1974, Roger Kornberg proposed that chromatin is made up of repeating units, each containing 200 bp of DNA and histone octamer. [5] The ARID1B subunit is able to attach (bind) to DNA and is thought to help target SWI/SNF complexes to the chromatin location that needs to be remodeled. [9] When DNA from MNase-treated chromatin is electrophoresed on an agarose gel, a number of bands will appear. [5] If a small amount of nuclease is added to chromatin mixture (partial digestion), the enzyme cleaves the string between the beads, leaving individual beads attached to about 200 bp of DNA. [5]

H1 is not a part of the nucleosome core particle but plays an important role in the nucleosome structure. (The H1 can be easily removed from chromatin without affecting the structure of the nucleosome, which suggests that its location is external to the nucleosome core particle). [5] When chromatin is isolated from the nucleus of a cell and viewed with an electron microscope, it frequently looks like beads on a string. [5] The CHD7 protein belongs to a family of proteins that are thought to play a role in the organization of chromatin. [10] Figure 1: a) An electron micrograph of chromatin isolated from interphase nuclei showing its “beads on a string” character b) general representation of beads on a string appearance of chromatin. [5] A chromosome is made up of tightly packed chromatin strands. [11]

The ARID1B gene mutations associated with ASD result in a reduced amount of the ARID1B protein or impair the protein’s function in chromatin remodeling. [9] The CHD7 protein regulates the activity (expression) of several other genes through a process known as chromatin remodeling. [10] Bouazoune K, Kingston RE. Chromatin remodeling by the CHD7 protein is impaired by mutations that cause human developmental disorders. [10] Shortage of this protein is thought to disrupt chromatin remodeling and the regulation of gene expression. [10] Chromatin remodeling is one way gene expression is regulated during development; when DNA is tightly packed, gene expression is lower than when DNA is loosely packed. [9]

Santen GW, Aten E, Sun Y, Almomani R, Gilissen C, Nielsen M, Kant SG, Snoeck IN, Peeters EA, Hilhorst-Hofstee Y, Wessels MW, den Hollander NS, Ruivenkamp CA, van Ommen GJ, Breuning MH, den Dunnen JT, van Haeringen A, Kriek M. Mutations in SWI/SNF chromatin remodeling complex gene ARID1B cause Coffin-Siris syndrome. [9]

The means of assessing outcome in the clinic are inaccurate, and there is a pressing need to more precisely identify men at risk of aggressive PC. We previously identified HIST1H1A as a susceptibility gene for aggressive PC. HIST1H1A encodes H1.1, a member of the linker histone family that is involved in chromatin organization and compaction. [7] We present scABC, an R package for the unsupervised clustering of single-cell epigenetic data, to classify scATAC-seq data and discover regions of open chromatin specific to cell identity. [7] Assays such as single cell ATAC-seq (scATAC-seq) offer an opportunity to interrogate cellular level epigenetic heterogeneity through patterns of variability in open chromatin. [7]

Genetic determinants of co-accessible chromatin regions in activated T cells across humans. [7] We found that regions of accessible chromatin (ATAC-peaks) are co-accessible at kilobase and megabase resolution, consistent with the three-dimensional chromatin organization measured by in situ Hi-C in T cells. [7] We investigated age-dependent, genome-wide alterations in the chromatin accessibility of primary human adipose-derived stem cells (ASCs) in comparison to age-matched fibroblasts via ATAC-seq technology. [7] BACKGROUND: Variation in chromatin organization across single cells can help shed important light on the mechanisms controlling gene expression, but scale, noise, and sparsity pose significant challenges for interpretation of single cell chromatin data. [7] Within each cell, chromatin is arranged in specific patterns to expose the repertoire of CREs required for optimal spatiotemporal regulation of gene expression. [7] During the prophase of mitosis, the chromatin in a cell compacts to form condensed chromosomes; this condensation is required in order for the cell to divide properly. [12] Although conventional methods such as MNase-seq, DNase-seq, and ChIP-seq have been used effectively to assess chromatin and locus accessibility at the genome level, these techniques generally require large numbers of input cells. [7] The DNA of eukaryotic genomes is packaged into chromatin by nucleosomes. [7] We develop BROCKMAN (Brockman Representation Of Chromatin by K-mers in Mark-Associated Nucleotides), an approach to infer variation in transcription factor (TF) activity across samples through unsupervised analysis of the variation in DNA sequences associated with an epigenomic mark. [7] The nucleus (plural nuclei) houses the cell’s DNA in the form of chromatin and directs the synthesis of ribosomes and proteins. [13] Background: Assay for Transposase-Accessible Chromatin (ATAC)-cap-seq is a high-throughput sequencing method that combines ATAC-seq with targeted nucleic acid enrichment of precipitated DNA fragments. [7] To identify regulatory regions in the parasite genome, we performed genome-wide profiling of chromatin accessibility in two culture-adapted isogenic subclones at four developmental stages during the intraerythrocytic cycle by using the Assay for Transposase-Accessible Chromatin by sequencing (ATAC-seq). [7] Assay for Transposase Accessible Chromatin with high-throughput sequencing (ATAC-seq) is a powerful genomic technology that is used for the global mapping and analysis of open chromatin regions. [7] To further understand the complex mechanisms that modulate transcription in the brain, we used frozen postmortem samples to generate the largest human brain and cell-type-specific open chromatin data set to date. [7] An atlas of chromatin accessibility in the adult human brain. [7]

BACKGROUND: Chromatin accessibility profiling assays such as ATAC-seq and DNase1-seq offer the opportunity to rapidly characterize the regulatory state of the genome at a single nucleotide resolution. [7] To understand chromatin, it is helpful to first consider chromosomes. [13] At the onset of prophase, chromatin fibers become tightly coiled, condensing into discrete chromosomes. [12]

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6. (4) CHD7 gene – Genetics Home Reference – NIH

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11. (1) Chromatid – an overview | ScienceDirect Topics

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