Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mapping the differential distribution of the cohesin subunit Scc1 in Trypanosoma brucei brucei.

ABSTRACT: Chromatin immunoprecipitation of genomic loci in Trypanosoma brucei where Scc1 is deposited. This was achieved by deletion of one Scc1 allele and N-terminal tagging of the second Scc1 allele with a Ty1-tag. During the ChIP experiment, the DNA was crosslinked and cells were permeabilized with digitonin. DNA was fragmented by sonication with a Covaris instrument. DNA bound to Ty1-Scc1 was pulled down by using a BB2 anti-Ty1 antibody. Cross links are reversed and the DNA was purified and prepared for Illumina sequencing.

ORGANISM(S): Trypanosoma brucei brucei

PROVIDER: GSE119071 | GEO | 2018/11/06

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Maps of histone variant H3.V deposition in Trypanosoma brucei brucei

Project description:Chromatin immunoprecipitation of genomic loci in Trypanosoma brucei where histone variant H3.V is deposited. This was achieved by deletion of one H3.V allele and N-terminal tagging of the second H3.V allele with a Ty1 tag. During the ChIP experiment, the DNA was digested with MNase to obtain mononucleosomes. Nucleosomes containing H3.V were pulled down by using a BB2 anti-Ty1 antibody. Cross links are reversed and mononucleosomal DNA is purified and prepared for Illumina sequencing.

2018-08-24 | GSE118917 | GEO

Maps of histone variant H4.V deposition in Trypanosoma brucei brucei

Project description:Chromatin immunoprecipitation of genomic loci in Trypanosoma brucei where histone variant H4.V is deposited. A previously generated cell line (Siegel et al., 2009) in which both endogenous H4.V alleles are knockout out and ectopic overexpression of a Ty1-tagged version of H4.V can be induced was used. During the ChIP experiment, the DNA was digested with MNase to obtain mononucleosomes. Nucleosomes containing H4.V were pulled down by using a BB2 anti-Ty1 antibody. Cross links are reversed and mononucleosomal DNA is purified and prepared for Illumina sequencing.

2018-08-24 | GSE118938 | GEO

Releasing activity disengages cohesin’s Smc3/Scc1 interface in a process blocked by acetylation

Project description:Sister chromatid cohesion conferred by entrapment of sister DNAs within a tripartite ring formed between cohesin’s Scc1, Smc1, and Smc3 subunits is generated during S and eventually destroyed at anaphase through cleavage of Scc1 by separase. Throughout the cell cycle, cohesin’s association with chromosomes is controlled by opposing activities: loading by the Scc2/4 complex and release by a separase independent releasing activity. Co-entrapment of sister DNAs during replication is accompanied by acetylation of Smc3 by Eco1, which blocks releasing activity and ensures that sisters remain stably connected. Because fusion of Smc3 to Scc1 prevents release and bypasses the requirement for Eco1, we suggested that release is mediated by disengagement of the Smc3/Scc1 interface. We now show that all mutations capable of bypassing Eco1, be they in cohesin’s Smc1, Smc3, Scc1,Wapl, Pds5, or Scc3 subunits, greatly reduce dissociation of N-terminal cleavage fragments of Scc1 (NScc1) from Smc3. We show that this process involves interaction between Smc ATPase heads and is inhibited by Smc3 acetylation

2016-02-18 | GSE76890 | GEO

Pectobacterium carotovorum strain:SCC1

Project description:Pectobacterium carotovorum SCC1 genome sequencing

| PRJNA379819 | ENA

Scc2 Is a Potent Activator of Cohesin's ATPase that Promotes Loading by Binding Scc1 without Pds5

Project description:In addition to sharing with condensin an ability to organize DNA into chromatids, cohesin regulates enhancer-promoter interactions and confers sister chromatid cohesion. Association with chromosomes is regulated by hook-shaped HEAT repeat proteins that Associate With its Kleisin (Scc1) subunit (HAWKs), namely Scc3, Pds5, and Scc2. Unlike Pds5, Scc2 is not a stable cohesin constituent but, as shown here, transiently displaces Pds5 during loading. Scc1 mutations that compromise its interaction with Scc2 adversely affect cohesin’s ATPase activity, loading, and translocation while Scc2 mutations that alter how the ATPase responds to DNA abolish loading despite cohesin’s initial association with loading sites. Lastly, Scc2 mutations that permit loading in the absence of Scc4 increase Scc2’s association with chromosomal cohesin and reduce that of Pds5. We suggest that cohesin switches between two states, one with Pds5 bound to Scc1 that is not able to hydrolyse ATP efficiently but is capable of release from chromosomes and another in which Scc2, transiently replacing Pds5, stimulates the ATP hydrolysis necessary for loading and translocation away from loading sites.

2018-07-17 | GSE106182 | GEO

Mapping the differential distribution of the cohesin subunit Scc1 in Trypanosoma brucei brucei.

Project description:Mapping the differential distribution of the cohesin subunit Scc1 in Trypanosoma brucei brucei.

| PRJNA488057 | ENA

Releasing activity disengages cohesinâs Smc3/Scc1 interface in a process blocked by acetylation

Project description:Sister chromatid cohesion conferred by entrapment of sister DNAs within a tripartite ring formed between cohesinâs Scc1, Smc1, and Smc3 subunits is generated during S and eventually destroyed at anaphase through cleavage of Scc1 by separase. Throughout the cell cycle, cohesinâs association with chromosomes is controlled by opposing activities: loading by the Scc2/4 complex and release by a separase independent releasing activity. Co-entrapment of sister DNAs during replication is accompanied by acetylation of Smc3 by Eco1, which blocks releasing activity and ensures that sisters remain stably connected. Because fusion of Smc3 to Scc1 prevents release and bypasses the requirement for Eco1, we suggested that release is mediated by disengagement of the Smc3/Scc1 interface. We now show that all mutations capable of bypassing Eco1, be they in cohesinâs Smc1, Smc3, Scc1,Wapl, Pds5, or Scc3 subunits, greatly reduce dissociation of N-terminal cleavage fragments of Scc1 (NScc1) from Smc3. We show that this process involves interaction between Smc ATPase heads and is inhibited by Smc3 acetylation Effect of mutations QQ and EQ in Smc3 on cohesin loading onto chromosomes

2016-02-18 | E-GEOD-76890 | biostudies-arrayexpress

Wapl-mediated release of Scc1-cohesin regulates chromosome structure and segregation in mouse oocytes

Project description:Cohesin is essential for genome folding and chromosome inheritance through cell divisions. In somatic cells, both of these functions are mediated by Scc1-cohesin, which in mitosis is released from chromosomes by Wapl and separase. In mammalian oocytes, cohesion is mediated by Rec8-cohesin. Scc1 is also expressed but neither required nor sufficient for cohesion, and its function in oocytes is unknown. Likewise, it is unknown whether Wapl regulates one or both cohesin complexes and chromosome segregation in mature oocytes. Using conditional mouse mutagenesis, we show that in meiosis I Wapl is required for proper chromosome segregation, predominantly releases Scc1-cohesin from chromosomes and promotes production of euploid eggs. Using single-nucleus Hi-C, we found that Scc1 is essential for chromatin loops and topologically associating domains (TADs) in oocytes. Increasing Scc1 residence time on chromosomes by Wapl depletion leads to vermicelli formation and intra-loop structures but, unlike in mitotic cells, does not increase loop size. This implies that loop size has reached a maximum in oocytes, possibly because it is limited by barriers such as cohesive cohesin. We conclude that distinct cohesin complexes generate loops and cohesion in mammalian oocytes and propose that the same principle applies to all cell types and species.

2020-03-04 | GSE132264 | GEO

Capture-C experiments on auxin treated control (E14-Tir) and Scc1-AID, Ring1b-AID, Ring1b-AID-Scc1-AID and CTCF-AID (with and without a 6-hour auxin treatment) cells

Project description:The aim of the experiment was to gain a higher resolution for specific regions of interest to complement the Hi-C results. Capture-C experiments were performed on four-inducible degrons for Scc1, Ringb, Ring1b-Scc1 and CTCF, and Tir1 control, always in triplicates (three biological replicates per condition).

2020-01-23 | E-MTAB-7840 | biostudies-arrayexpress

TY1-H2A-ChIP-seq datasets of Trypanosoma brucei

Project description:Analysis of the genome-wide distribution of the histone H2A, using TY1-H2A as a Proxy

2020-02-21 | GSE145625 | GEO