Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

BLM complex composition in unperturbed cells

ABSTRACT: The Bloom syndrome DNA helicase BLM contributes to chromosome stability through its roles in double-strand break repair by homologous recombination and DNA replication fork restart during the replication stress response. Loss of BLM activity leads to Bloom syndrome, which is characterized by extraordinary cancer risk and small stature. Here, we have analyzed the composition of the BLM complex in unperturbed cells and identified a direct physical interaction with the Mcm6 subunit of the minichromosome maintenance (MCM) complex by co-immunopecipitations using endogenous and recombinant proteins as well as two-hybrid analysis.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture, Skin, Fibroblast

SUBMITTER: Kristina Schmidt

LAB HEAD: Kristina Hildegard Schmidt

PROVIDER: PXD018823 | Pride | 2022-02-15

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	20161208_IP_0637-E1-1.mzXML	Mzxml
	20161208_IP_0637-E1-1.raw	Raw
	20161208_IP_0637-E1-2.mzXML	Mzxml
	20161208_IP_0637-E1-2.raw	Raw
	20161208_IP_0637-E1-3.mzXML	Mzxml

Items per page:

1 - 5 of 17

Publications

A novel cell-cycle-regulated interaction of the Bloom syndrome helicase BLM with Mcm6 controls replication-linked processes.

Shastri Vivek M VM Subramanian Veena V Schmidt Kristina H KH

Nucleic acids research 20210901 15

The Bloom syndrome DNA helicase BLM contributes to chromosome stability through its roles in double-strand break repair by homologous recombination and DNA replication fork restart during the replication stress response. Loss of BLM activity leads to Bloom syndrome, which is characterized by extraordinary cancer risk and small stature. Here, we have analyzed the composition of the BLM complex during unperturbed S-phase and identified a direct physical interaction with the Mcm6 subunit of the min ...[more]

PMID: 34370039

Similar Datasets

A POLD3/BLM dependent pathway handles DSBs in transcribed chromatin upon excessive RNA:DNA hybrids accumulation

Project description:Transcriptionally active loci are particularly prone to breakage and mounting evidence suggest that DNA Double-Strand Breaks arising in active genes are handled by a dedicated repair pathway, Transcription-Coupled DSB Repair (TC-DSBR), that entails R-loop accumulation and dissolution. Here, we uncovered a function for the Bloom RecQ DNA helicase (BLM) in TC-DSBR in human cells. BLM is recruited in a transcription dependent-manner at DSBs where it fosters resection, RAD51 binding and accurate Homologous Recombination repair. However, in an R-loop dissolution-deficient background, we found that BLM promotes cell death. We report that upon excessive R-loop accumulation, DNA synthesis is enhanced at DSBs, in a anner that depends on BLM and POLD3. Altogether our work unveils a role for BLM at DSBs in active chromatin, and highlights the toxic potential of RNA:DNA hybrids that accumulate at transcription-associated DSBs.

2022-04-13 | E-MTAB-11592 | biostudies-arrayexpress

Effect of TOPBEffect of TOPBP1 on BLM phosphosites

Project description:Identification of BLM phosphosites. The experiment is composed by 2 parts: i) identification of BLM phosphosites with DDA method ii) quantification of phosphosites with a targeted method.

2021-11-25 | PXD026460 | Pride

Identification BLM phosphosites in presence or absence of lambda phosphatase

Project description:Identification of BLM phosphosites in presence or absence of lambda phosphatase. DDA analysis of purified protein

2021-11-25 | PXD026452 | Pride

Bloom syndrome protein modulates protein-coding gene and miRNA expression as a function of G4 DNA content

Project description:Bloom syndrome is a rare autosomal recessive genetic instability and cancer predisposition syndrome caused by loss of function mutations in the BLM RECQ helicase gene. To ask if some of the distinctive pathological features of Bloom syndrome might reflect altered gene expression, we analyzed global mRNA and miRNA expression in fibroblasts from 16 patients and 15 matched normal controls, and in control primary diploid fibroblasts depleted of the BLM protein. We document significant differential expression of both protein-coding genes and miRNAs with well-characterized cancer associations in BLM-deficient cells. Differences in expression correlated significantly with G4 motifs, which are associated with potential to form G-quadruplex structures. These results indicate that BLM helicase may modulate gene expression by regulating the in vivo stability of G-quadruplex structures, and identify sets of genes and miRNAs whose expression, when altered, may drive the pathogenesis of Bloom syndrome and associated cancers. Global profiling of mRNA and miRNA expression was analyzed in primary fibroblasts from 16 patients and 15 matched normal controls, and in 9 primary diploid fibroblasts depleted of BLM protein by BLM-specific (3), control (3) and scrambled (3) shRNA.

2014-06-12 | E-GEOD-54502 | biostudies-arrayexpress

ChIP Sequencing of CRISPR/Cas9 corrected Bloom Syndrome patient cell line using antibody against BLM

Project description:BLM protein has been shown to play an important role in homologous recombination (HR) repair. We report that BLM interacts with RAD54 (another HR repair protein) to enhance its chromatin remodeling function. This experiment identifies that BLM gets recruited to different genetic loci even in the absence of damage, possibly along with RAD54 chromatin remodeler.

2024-04-03 | E-MTAB-11372 | biostudies-arrayexpress

Bloom syndrome protein modulates protein-coding gene and miRNA expression as a function of G4 DNA content

2014-06-12 | GSE54502 | GEO

The Bloom Syndrome Complex Senses RPA-Coated Single-Stranded DNA to Restart Stalled Replication Forks

Project description:The Bloom syndrome helicase BLM interacts with topoisomerase IIIa (TOP3A), RMI1 and RMI2 to form the BTR complex, which dissolves double Holliday junctions to produce non-crossover products during homologous recombination (HR). BLM also promotes DNA-end resection and stalled replication fork restart. However, it is still unclear how the activities of the BTR complex are regulated in cells. Here, we identify multiple highly conserved short linear peptide motifs within the BTR complex that interact cooperatively with RPA. Furthermore, we demonstrate that RPA-binding is essential for stable recruitment of BLM to DNA damage sites and for stalled fork restart, but not for its roles in HR. Disruption of RPA-binding thus constitutes a novel separation-of-function mutation of the BTR complex, and suggest a model in which BTR contains the intrinsic ability to measure levels of RPA-ssDNA at replication forks, which controls its recruitment and activation in response to replication stress.

2021-01-05 | PXD018322 | Pride

aCGH analyses of DSB-induced LOH in Blm-deficient mESCs

Project description:Genome modification in mouse embryonic stem cells (mESCs) has provided the versatile platform to analyzing gene functions in mammalian cells. Bloom helicase-deficient mESCs showed elevated rate of loss of heterozygosity (LOH) through mitotic recombination. By utilizing this characteristic of Blm deficiency, we established an efficient method to introduce homozygous mutations into mESCs, which can be used for phenotype-driven recessive screen. It is generally thought that mitotic recombination is initiated by double-strand break. DNA repair machinery, however, possesses mechanisms that suppress deleterious crossovers between homologous chromosomes. Bloom helicase plays a central role to suppress such crossover; hence its deficiency causes elevated frequency of mitotic recombination. To directly answer if DSB can initiate mitotic recombination, we established a reporter cell line, in which the recognition site of I-SceI endonuclease was introduced in the Aprt gene in Blm-deficient mESCs. We used two types of I-SceI expression vectors; one expresses a mammalian codon-optimized I-SceI (ISceIo) and the other expresses I-SceIo fused with N-terminal 110-amino acids of Geminin (Gemi). Geminin-fused I-SceI can be stabilized only in lateS/G2 phase. After I-SceI transfection and subsequent selection, we isolated Aprt-deficient mutants. Half of the mutants showed LOH in the whole telomeric region from I-SceI site, but the other half showed local LOH near the I-SceI site. Further analyses suggested that large deletion was introduced and caused LOH, which was not seen in spontaneous LOH. We designed CGH probes in 300-bp resolution in 8Mb telomeric region of chr 8 (The Aprt gene locates 7Mb from the telomere) to map the deleted regions in these mutants.

2012-11-30 | E-MTAB-1116 | biostudies-arrayexpress

TFIP11 competes with the Bloom syndrome helicase for binding to stalled replication forks to preserve genome stability

Project description:Replication fork reversal is a key protective mechanism against replication stress in higher eukaryotic cells and occurs via a series of coordinated enzymatic reactions. The Bloom syndrome gene product, BLM, is a member of the highly conserved RecQ helicase family and has been implicated in this process, but its precise regulation and role remain poorly understood. Here, we show that, upon replication stress, the GCFC domain-containing protein TFIP11 competes with the BLM helicase for association with stalled replication forks, thereby facilitates RAD51-mediated stalled fork reversal. Consequently, loss of TFIP11 results in aberrant accumulation of BLM at stalled forks, which in turn compromises RAD51 recruitment, impairs replication stress-induced fork reversal and slowing, hypersensitizes cells to replication stress-inducing agents, and enhances chromosomal instability. These findings reveal a previously unidentified regulatory mechanism that modulates the activities of BLM and RAD51 at stalled forks and thus genome integrity.

2024-05-24 | PXD042222 | Pride

DNA-damaging agent and immune inducer synergistically induced defence gene expression in Arabidopsis

Project description:We used microarrays to identify differentially expressed genes after DNA-damaging agent bleomycin (BLM) and/or immune inducer 2, 6-dichloroisonicotinic acid (INA) treatment. We focused on those genes that were synergistically induced by co-treatment (BLM+INA). Arabidopsis seedlings were treated with 4 μg/ml BLM and/or low INA (10 μM). There are 4 treatments: control (CK), INA, BLM and BLM+INA. Each treatments have three biological replicates. There are 12 samples in total.

2013-11-14 | E-GEOD-44793 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data