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Role of BLM helicase in augmenting the phosphorylation of DNA damage response (DDR) proteins.

ABSTRACT: Assessing the importance of BLM helicase upon DNA damage in the phosphorylation enhancement of DNA damage response (DDR) proteins via phosphoproteomic profiling in the presence and absence of BLM.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

SUBMITTER: Ritu Agrawal

LAB HEAD: Dr. Sagar

PROVIDER: PXD048117 | Pride | 2025-05-06

REPOSITORIES: Pride

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			Action	DRS
	A1.raw	Raw
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Publications

Phosphorylated BLM peptide acts as an agonist for DNA damage response.

Agrawal Ritu R Agarwal Himanshi H Mukherjee Chetana C Chakraborty Baishali B Sharma Vandana V Tripathi Vivek V Kumar Nitin N Priya Swati S Gupta Nidhi N Jhingan Gagan Deep GD Bajaj Avinash A Sengupta Sagar S

Nucleic acids research 20250201 4

Upon exposure to ionizing irradiation, the MRE11-RAD50-NBS1 complex potentiates the recruitment of ATM (ataxia-telangiectasia mutated) kinase to the double-strand breaks. We show that the lack of BLM causes a decrease in the autophosphorylation of ATM in mice mammary glands, which have lost one or both copies of BLM. In isogenic human cells, the DNA damage response (DDR) pathway was dampened in the absence of BLM, which negatively affected the recruitment of DDR factors onto the chromatin, there ...[more]

PMID: 39997217

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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

BLM helicase negatively regulates a DNA damage dependent CDX2 inducible microRNA signature which targets BRCA1

Project description:In trying to understand how DNA damage modulates miR expression by high level of endogenous DNA damage, we carried out small RNA sequencing with two pairs of isogenic cell lines generated from two BS patients. For this, miRNA from immortalized cells from GM03509 complemented with either GFP-BLM (Clone 4.3.4) or GFP (Clone 100) or immortalized cells from another BS patient GM08505 complemented with either GFP-BLM or GFP were profiled by Next Generation Sequencing.

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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

Assessment of basal cell carcinoma and rhabdomyosarcoma tumorigenesis in Blm-deficient Ptch1+/- mice

Project description:Basal cell carcinomas (BCCs) have relative genomic stability and relatively benign clinical behavior but whether these two are related causally is unknown. To investigate the effects of introducing genomic instability into murine BCCs, we have compared ionizing radiation-induced tumorigenesis in Ptch1+/- mice vs. that in Ptch1+/- mice carrying mutant Blm alleles. We found that BCCs in Ptch1+/- Blmtm3Brd/tm3Brd mice had a trend towards greater genomic instability as measured by array CGH and that these mice developed significantly more microscopic BCCs than did Ptch1+/- Blm+/tm3Brd or Ptch1+/- Blm+/+ mice. The mutant Blm alleles also markedly enhanced the formation of rhabdomyosarcomas (RMS), another cancer to which Ptch1+/- mice and PTCH1+/- (basal cell nevus syndrome) patients are susceptible. Highly recurrent but different copy number changes were associated with the two tumor types and included losses of chromosomes 4 and 10 in all BCCs and gain of chromosome 10 in 80% of RMSs. Loss of chromosome 11 and 13, including the Trp53 and Ptch1 loci respectively, occurred frequently in BCCs, suggesting tissue-specific selection for genes or pathways that collaborate with Ptch deficiency in tumorigenesis. Despite the quantitative differences, there was no dramatic qualitative difference in the BCC or RMS tumors associated with the mutant Blm genotype.

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Assessment of basal cell carcinoma and rhabdomyosarcoma tumorigenesis in Blm-deficient Ptch1+/- mice

2010-05-15 | E-GEOD-19880 | biostudies-arrayexpress

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

BLM complex composition in unperturbed cells

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2022-02-15 | PXD018823 | Pride

BLM deficiency affects cytotoxicity of temozolomide and olaparib against human glioma cells and induces cellular senescence or polyploidy

Project description:BLM deficient cells responded differently to the temozolomide and olaparib treatment in comparison to the wild type cells. The double treatment evoked cell cycle arrest, cellular senescence or polyploidy in BLM KO LN229 and LN18 cells, respectively.

2023-05-17 | GSE214931 | GEO

BLM helicase protein negatively regulates stress granule formation through unwinding RNA G-quadruplex structures

Project description:Bloom’s syndrome (BLM) protein is a known nuclear helicase that is able to unwind DNA secondary structures such as G-quadruplexes. However, its role in the regulation of cytoplasmic processes that involve RNA G-quadruplexes (rG4s) has not been previously studied. Here, we demonstrate that BLM is recruited to stress granules (SGs), which are cytoplasmic biomolecular condensates composed of RNA-binding proteins and RNAs. BLM is enriched in SGs upon different stress conditions and in an rG4-dependent manner. We show that BLM unwinds rG4s efficiently, thus acting as a negative regulator of SG formation, potentially via its unwinding function. Altogether, our data expand the cellular activity of BLM and shed light on the function that helicases play in the dynamics of biomolecular condensates.

2023-10-24 | PXD039534 | 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