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spontaneous mitotic crossovers that occur when FANCM is missing are dependent on MUS312 and either MUS81 or SLX1.
did not find any role for MUS81-MMS4 in meiotic crossing over
A. thaliana TOP3alpha conserved zinc-finger domain (ZFD) T1 is specifically required for targeting the topoisomerase activity to Holliday junction like recombination intermediates to enable their processing. In the case of an inactivated enzyme, this leads to cell death due to the masking of these intermediates, hindering their resolution by MUS81.
SEND1 has at most a minor role in resolution of the Holliday junction but acts as an essential backup to MUS81 for resolution of toxic replication structures to ensure genome stability and to maintain telomere integrity.
Data show that DNA polymerase zeta catalytic subunit REV3 cooperates with ATP-dependent DNA helicase RECQ4A and e ndonuclease MUS81 to repair DNA interstrand cross links.
RECQ4A and MUS81 define RAD5A-independent pathways of DNA repair. RECQ4A and MUS81 act in parallel pathways presumably to resolve replication-associated DNA intermediates.
The role of AtMUS81 in meiotic and mitotic recombination.
AtMUS81 is involved in a secondary subset of meiotic crossovers that are interference insensitive.
The role of MUS81 in the reproduction and growth of A. thaliana, via its expression and metabolism during meiosis, is reported.
Both MUS81-EME1 endonuclease complexes are involved in DNA recombination and repair processes in Arabidopsis.
this study shows that immune rejection of prostate cancer cells relies on Mus81 and STING
Our study highlights the importance of the cooperation between Rad54 and Mus81 for mediating DNA DSB repair and restraining chromosome missegregation.
Mus81 knockdown improves the chemosensitivity of HCC cells by inducing S-phase arrest and promoting apoptosis through CHK1 pathway, suggesting Mus81 as a novel therapeutic target for HCC.
Using mice deficient in both Mus81 and the FA pathway protein FancC, we show both proteins cooperate in parallel pathways, as concomitant loss of FancC and Mus81 triggered cell-type-specific proliferation arrest, apoptosis and DNA damage accumulation in utero.
Data indicate that SLX1 and MUS81-EME1 nucleases act together to resolve Holliday junctions (HJs) in a manner that requires tethering to SLX4.
FBH1 helicase activity is required to eliminate cells with excessive replication stress through the generation of MUS81-induced DNA double-strand breaks.
data indicate that an important role for Chk2 is maintaining lymphocyte development and that dual inactivation of Chk2 and Mus81 remarkably inhibits cancer
studies demonstrate a critical role for the proper biallelic expression of the mammalian Mus81 in the maintenance of genomic integrity and tumor suppression
Mus81 acts at a late step in the repair of cross-link-induced lesions
Mus81-Eme1- and Rad54-mediated homologous recombination are involved in the same DNA replication-dependent interstrand crosslinks repair pathway
Data suggest that Mus81 suppresses chromosomal instability by converting potentially detrimental replication-associated DNA structures into intermediates that are more amenable to DNA repair.
Analysis of meiotic progression in Mus81-nullizygous mice, and our results implicate the MUS81 pathway as a regulator of crossover frequency and placement in mammals.
Fndings support a role for Mus81 in the resolution of replication-associated DNA damage associated with this genotoxic agent, by converting Cr[VI]-DNA lesions into a form more amenable for homologous recombination.
Replication fork progression in BRCA2-deficient cells requires MUS81. MUS81 nucleolytic activity is required to activate compensatory DNA synthesis during mitosis and to resolve mitotic interlinks, thus facilitating chromosome segregation.
Using RNAi or FA-P cells complemented with SLX4 mutants that abrogate interaction with MUS81 or SLX1, we show that SLX4 cooperates with MUS81 to introduce DSBs after replication stress but also counteracts pathological targeting of demised forks by GEN1.
The results showed that MUS81 modulates MCM2 levels as well as homologous recombination (HR) activity. Moreover, downregulation of MUS81 increased the sensitivity of epithelial ovarian cancer (EOC)cells to olaparib by inducing S phase arrest and promoting apoptosis through activation of MCM2. MUS81 may be a potential novel therapeutic target for EOC.
Mus81 knockdown improves the chemosensitivity of colon cancer cells by inducing S phase arrest and promoting apoptosis through activating CHK1 pathway
Low EZH2 or MUS81 expression levels predict chemoresistance.
RECQ5 removes RAD51 filaments stabilizing stalled replication forks at common fragile sites and hence facilitates CFS cleavage by MUS81-EME1.
The mitotic DNA synthesis is RAD52 dependent, and RAD52 is required for the timely recruitment of MUS81 and POLD3 to common fragile sites in early mitosis.
Data suggest that dimeric GEN1 binds with high affinity/selectivity to Holliday junctions, introducing two symmetrical hydrolytic cleavages of phosphodiester backbone; at present, less is known about SLX1-SLX4-MUS81-EME1 resolving enzyme complex. (GEN1 = Holliday junction 5' flap endonuclease; SLX = structure-specific endonuclease subunit; MUS81 = MUS81 endonuclease; EME1 = essential meiotic endonuclease 1) [REVIEW]
down-regulation of MUS81 expression in ovarian cancer cells inhibited cell proliferation and colony formation ability, and influenced cell cycle progression
SLX4-SLX1 Protein-independent Down-regulation of MUS81-EME1 Protein by HIV-1 Viral Protein R (Vpr).
Mus81 sumoylation is important for normal mitotic chromosome congression.
Data suggest that the ATM/Chk2 may promote the repair of DNA damage caused by cisplatin by sustaining methyl methanesulfonate and ultraviolet-sensitive gene clone 81, and the double-strand breaks generated by methyl methanesulfonate and ultraviolet-sensitive gene clone 81 may activate the ATM/Chk2 pathway.
Avoiding damage formation through invalidation of Mus81-Eme2 and Mre11, or preventing damage signaling by turning off the ATM pathway, suppresses the replication phenotypes of Chk1-deficient cells.
Mus81 regulates the rate of DNA replication during normal growth by promoting replication fork progression while reducing the frequency of replication initiation events.
Identification and characterization of MUS81 point mutations that abolish interaction with the SLX4 scaffold protein.MUS81 function in DNA interstrand crosslinks repair requires interaction with SLX4.
The data highlight the importance of Mus81 and Blm in DNA double-strand repair pathways, fertility, development and cancer.
Authors confirmed that HIV-1 Vpr induces degradation of Mus81 although, surprisingly, degradation is independent and genetically separable from Vprs ability to induce G2 arrest.
Results define distinct and temporal roles for MUS81-EME1 and MUS81-EME2 in the maintenance of genome stability.
Our findings reveal a novel RAD52/MUS81-dependent mechanism that promotes cell viability and genome integrity in checkpoint-deficient cells, and disclose the involvement of MUS81 to multiple processes after replication stress
Interacts with EME1 and EME2 to form a DNA structure- specific endonuclease with substrate preference for branched DNA structures with a 5'-end at the branch nick. Typical substrates include 3'-flap structures, replication forks and nicked Holliday junctions. May be required in mitosis for the processing of stalled or collapsed replication forks.
, crossover junction endonuclease MUS81
, MUS81 endonuclease homolog (S. cerevisiae)
, MUS81 endonuclease homolog
, MUS81 protein
, crossover junction endonuclease MUS81-like
, SLX3 structure-specific endonuclease subunit homolog
, hypothetical protein