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Relevant bibliographies by topics / Microhomology mediated recombination

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Academic literature on the topic 'Microhomology mediated recombination'

Author: Grafiati

Published: 31 August 2024

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Journal articles on the topic "Microhomology mediated recombination"

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Jiang, Yuning. "Contribution of Microhomology to Genome Instability: Connection between DNA Repair and Replication Stress." International Journal of Molecular Sciences 23, no. 21 (October 26, 2022): 12937. http://dx.doi.org/10.3390/ijms232112937.

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Microhomology-mediated end joining (MMEJ) is a highly mutagenic pathway to repair double-strand breaks (DSBs). MMEJ was thought to be a backup pathway of homologous recombination (HR) and canonical nonhomologous end joining (C-NHEJ). However, it attracts more attention in cancer research due to its special function of microhomology in many different aspects of cancer. In particular, it is initiated with DNA end resection and upregulated in homologous recombination-deficient cancers. In this review, I summarize the following: (1) the recent findings and contributions of MMEJ to genome instability, including phenotypes relevant to MMEJ; (2) the interaction between MMEJ and other DNA repair pathways; (3) the proposed mechanistic model of MMEJ in DNA DSB repair and a new connection with microhomology-mediated break-induced replication (MMBIR); and (4) the potential clinical application by targeting MMEJ based on synthetic lethality for cancer therapy.

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Xu, Yijiang, Hang Zhou, Ginell Post, Hong Zan, and Paolo Casali. "Rad52 mediates class-switch DNA recombination to IgD." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 112.17. http://dx.doi.org/10.4049/jimmunol.208.supp.112.17.

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Abstract While the biology of IgD begins to be better understood, the mechanism of expression of this phylogenetically old and highly conserved Ig remains unknown. In B cells, IgD is mainly expressed together with IgM through alternative splicing of primary VHDJH-Cμ-s-m-Cδ-s-m RNAs, but also independently through IgD class switch DNA recombination (CSR) via double-strand DNA breaks (DSBs) and synapse of Sμ with σδ. How such DSBs, however, are resolved is still unknown. Our previous demonstration of a novel role of Rad52 in a Ku70/Ku86-independent “short-range” microhomology-mediated synapsis of intra-Sμ region DSBs led us to hypothesize that this homologous recombination DNA annealing factor is also involved in short-range microhomology-mediated alternative endjoining (A-EJ) recombination of Sμ with σδ. We found that induction of IgD CSR downregulates Zfp318 and promotes Rad52 phosphorylation and recruitment to Sμ and σδ, leading to alternative end-joining (A-EJ)-mediated Sμ-σδ recombination of resected DSB ends with extensive microhomologies, VHDJH-Cδs transcription and sustained IgD secretion. Rad52 ablation in mouse Rad52−/− B cells aborted IgD CSR in vitro and in vivo and dampened the specific IgD antibody response to OVA. Rad52 knockdown in human B cells also abrogated IgD CSR. Finally, Rad52 phosphorylation was associated with high levels of IgD CSR and anti-nuclear IgD autoantibodies in lupus-prone mice and patients with lupus. Our findings thus show that Rad52 mediates IgD CSR through microhomology-mediated A-EJ in concert with Zfp318 downregulation. This is a previously unrecognized and critical role of Rad52 in mammalian DNA repair that provides a mechanistic underpinning to CSR A-EJ. Supported by NIH grants AI 079705, AI 105813, AAI 167416 and LRA grant 641363 to PC.

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Lee-Theilen, Mieun, Allysia J. Matthews, Dierdre Kelly, Simin Zheng, and Jayanta Chaudhuri. "CtIP promotes microhomology-mediated alternative end joining during class-switch recombination." Nature Structural & Molecular Biology 18, no. 1 (December 5, 2010): 75–79. http://dx.doi.org/10.1038/nsmb.1942.

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Francis, Nigel J., Bairbre McNicholas, Atif Awan, Mary Waldron, Donal Reddan, Denise Sadlier, David Kavanagh, et al. "A novel hybrid CFH/CFHR3 gene generated by a microhomology-mediated deletion in familial atypical hemolytic uremic syndrome." Blood 119, no. 2 (January 12, 2012): 591–601. http://dx.doi.org/10.1182/blood-2011-03-339903.

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Abstract Genomic disorders affecting the genes encoding factor H (fH) and the 5 factor H related proteins have been described in association with atypical hemolytic uremic syndrome. These include deletions of CFHR3, CFHR1, and CFHR4 in association with fH autoantibodies and the formation of a hybrid CFH/CFHR1 gene. These occur through nonallelic homologous recombination secondary to the presence of large segmental duplications (macrohomology) in this region. Using multiplex ligation-dependent probe amplification to screen for such genomic disorders, we have identified a large atypical hemolytic uremic syndrome family where a deletion has occurred through microhomology-mediated end joining rather than nonallelic homologous recombination. In the 3 affected persons of this family, we have shown that the deletion results in formation of a CFH/CFHR3 gene. We have shown that the protein product of this is a 24 SCR protein that is secreted with normal fluid-phase activity but marked loss of complement regulation at cell surfaces despite increased heparin binding. In this study, we have therefore shown that microhomology in this area of chromosome 1 predisposes to disease associated genomic disorders and that the complement regulatory function of fH at the cell surface is critically dependent on the structural integrity of the whole molecule.

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Ahrabi, Sara, Sovan Sarkar, Sophia X. Pfister, Giacomo Pirovano, Geoff S. Higgins, Andrew C. G. Porter, and Timothy C. Humphrey. "A role for human homologous recombination factors in suppressing microhomology-mediated end joining." Nucleic Acids Research 44, no. 12 (April 29, 2016): 5743–57. http://dx.doi.org/10.1093/nar/gkw326.

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6

Chan, C. Y., M. Kiechle, P. Manivasakam, and R. H. Schiestl. "Ionizing radiation and restriction enzymes induce microhomology-mediated illegitimate recombination in Saccharomyces cerevisiae." Nucleic Acids Research 35, no. 15 (July 11, 2007): 5051–59. http://dx.doi.org/10.1093/nar/gkm442.

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Ling, Alexanda K., Clare C. So, Michael X. Le, Audrey Y. Chen, Lisa Hung, and Alberto Martin. "Double-stranded DNA break polarity skews repair pathway choice during intrachromosomal and interchromosomal recombination." Proceedings of the National Academy of Sciences 115, no. 11 (February 22, 2018): 2800–2805. http://dx.doi.org/10.1073/pnas.1720962115.

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Activation-induced cytidine deaminase (AID) inflicts DNA damage at Ig genes to initiate class switch recombination (CSR) and chromosomal translocations. However, the DNA lesions formed during these processes retain an element of randomness, and thus knowledge of the relationship between specific DNA lesions and AID-mediated processes remains incomplete. To identify necessary and sufficient DNA lesions in CSR, the Cas9 endonuclease and nickase variants were used to program DNA lesions at a greater degree of predictability than is achievable with conventional induction of CSR. Here we show that Cas9-mediated nicks separated by up to 250 nucleotides on opposite strands can mediate CSR. Staggered double-stranded breaks (DSBs) result in more end resection and junctional microhomology than blunt DSBs. Moreover, Myc-Igh chromosomal translocations, which are carried out primarily by alternative end joining (A-EJ), were preferentially induced by 5′ DSBs. These data indicate that DSBs with 5′ overhangs skew intrachromosomal and interchromosomal end-joining toward A-EJ. In addition to lending potential insight to AID-mediated phenomena, this work has broader carryover implications in DNA repair and lymphomagenesis.

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Chan, Cecilia Y., and Robert H. Schiestl. "Rad1, rad10 and rad52 Mutations Reduce the Increase of Microhomology Length during Radiation-Induced Microhomology-Mediated Illegitimate Recombination in Saccharomyces cerevisiae." Radiation Research 172, no. 2 (August 1, 2009): 141. http://dx.doi.org/10.1667/rr1675.1.

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Nagai, Koki, Hirohito Shima, Miki Kamimura, Junko Kanno, Erina Suzuki, Akira Ishiguro, Satoshi Narumi, Shigeo Kure, Ikuma Fujiwara, and Maki Fukami. "Xp22.31 Microdeletion due to Microhomology-Mediated Break-Induced Replication in a Boy with Contiguous Gene Deletion Syndrome." Cytogenetic and Genome Research 151, no. 1 (2017): 1–4. http://dx.doi.org/10.1159/000458469.

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The Xp22.31 region is characterized by a low frequency of interspersed repeats and a low GC content. Submicroscopic deletions at Xp22.31 involving STS and ANOS1 (alias KAL1) underlie X-linked ichthyosis and Kallmann syndrome, respectively. Of the known microdeletions at Xp22.31, a common approximately 1.5-Mb deletion encompassing STS was ascribed to nonallelic homologous recombination, while 2 ANOS1-containing deletions were attributed to nonhomologous end-joining. However, the genomic bases of other microdeletions within the Xp22.31 region remain to be elucidated. Here, we identified a 2,735,696-bp deletion encompassing STS and ANOS1 in a boy with X-linked ichthyosis and Kallmann syndrome. The breakpoints of the deletion were located within Alu repeats and shared 2-bp microhomology. The fusion junction was not associated with nucleotide stretches, and the breakpoint-flanking regions harbored no palindromes or noncanonical DNA motifs. These results indicate that microhomology-mediated break-induced replication (MMBIR) can cause deletions at Xp22.31, resulting in contiguous gene deletion syndrome. It appears that interspersed repeats without other known rearrangement-inducing DNA features or high GC contents are sufficient to stimulate MMBIR at Xp22.31.

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Meyer, Damon, Becky Xu Hua Fu, and Wolf-Dietrich Heyer. "DNA polymerases δ and λ cooperate in repairing double-strand breaks by microhomology-mediated end-joining in Saccharomyces cerevisiae." Proceedings of the National Academy of Sciences 112, no. 50 (November 25, 2015): E6907—E6916. http://dx.doi.org/10.1073/pnas.1507833112.

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Maintenance of genome stability is carried out by a suite of DNA repair pathways that ensure the repair of damaged DNA and faithful replication of the genome. Of particular importance are the repair pathways, which respond to DNA double-strand breaks (DSBs), and how the efficiency of repair is influenced by sequence homology. In this study, we developed a genetic assay in diploid Saccharomyces cerevisiae cells to analyze DSBs requiring microhomologies for repair, known as microhomology-mediated end-joining (MMEJ). MMEJ repair efficiency increased concomitant with microhomology length and decreased upon introduction of mismatches. The central proteins in homologous recombination (HR), Rad52 and Rad51, suppressed MMEJ in this system, suggesting a competition between HR and MMEJ for the repair of a DSB. Importantly, we found that DNA polymerase delta (Pol δ) is critical for MMEJ, independent of microhomology length and base-pairing continuity. MMEJ recombinants showed evidence that Pol δ proofreading function is active during MMEJ-mediated DSB repair. Furthermore, mutations in Pol δ and DNA polymerase 4 (Pol λ), the DNA polymerase previously implicated in MMEJ, cause a synergistic decrease in MMEJ repair. Pol λ showed faster kinetics associating with MMEJ substrates following DSB induction than Pol δ. The association of Pol δ depended on RAD1, which encodes the flap endonuclease needed to cleave MMEJ intermediates before DNA synthesis. Moreover, Pol δ recruitment was diminished in cells lacking Pol λ. These data suggest cooperative involvement of both polymerases in MMEJ.

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Dissertations / Theses on the topic "Microhomology mediated recombination"

1

Chan, Cecilia Yuen-Ting. "The studies of double strand break-induced microhomology-mediated illegitimate recombination and its genetic control." Diss., Restricted to subscribing institutions, 2008. http://proquest.umi.com/pqdweb?did=1581660331&sid=1&Fmt=2&clientId=1564&RQT=309&VName=PQD.

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Tichy, Elisia D. "Double-Strand DNA Break Repair By Homologous Recombination Contributes To The Preservation of Genomic Stability In Mouse Embryonic Stem Cells." University of Cincinnati / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1265989840.

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Kubilinskas, Rokas. "MitoTALENs to explore mitochondrial DNA repair and segregation." Electronic Thesis or Diss., Strasbourg, 2024. http://www.theses.fr/2024STRAJ014.

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Pendant longtemps, il n'était pas possible de manipuler le génome mitochondrial des plantes (mtDNA), jusqu'aux récentes avancées en édition des génomes utilisant des "Transcription Activator-Like Effector Nucleases" (TALEN). Dans ce travail, j'ai utilisé des TALENs spécifiquement ciblés sur les mitochondries (mitoTALENs) pour étudier la réparation et la ségrégation du mtDNA des plantes. Les constructions de mitoTALEN ont été introduites dans 10 lignées mutantes différentes d'Arabidopsis thaliana, déficientes en divers facteurs impliqués dans la réparation mitochondriale des plantes par recombinaison homologue. Les lignées résultantes ont eté analysées par séquençage Illumina et par des approches de qPCR. Chez les plantes de type sauvage, les cassures double brin (DSB) de l'ADN mitochondrial induites par les mitoTALENs ont été réparées par recombinaison homologue, entraînant le remplacement de la région contenant la DSB par une séquence distale, non-affectée, du mtDNA, flanquée par les mêmes séquences répétées. Chez les mutants déficients en facteurs de réparation, la réparation pourrait se dé placer vers des voies alternatives, telles que le "Single-Strand Annealing" (SSA) et "Microhomology-mediated recombination" (MHMR). De plus, chez certains mutants, les données n'ont révélé aucune trace de réparation des DSB, mais ont plutôt suggéré que les plantes déficientes en facteurs de réparation essentiels pourraient survivre en reconstituant un génome mitochondrial alternatif viable, à partir de sous- génomes pré existants se répliquant de manière autonome
For long, the plant mitochondrial genome (mtDNA) was not amenable to manipulation, until recent advancements in genome engineering using Transcription Activator-Like Effector Nucleases (TALEN). In this work I used TALENs specifically targeted to mitochondria (mitoTALENs) to study plant mtDNA repair and segregation. MitoTALEN constructs were transformed into the background of 10 different Arabidopsis thaliana mutant lines, deficient in various factors involved in plant mitochondrial repair by homologous recombination. The resulting lines were analysed by Illumina sequencing and qPCR approaches. In wild type plants, the mtDNA double-strand-break (DSB) induced by MitoTALENs was repaired by homologous recombination, resulting in the replacement of the region containing the DSB by a distal unaffected sequence of the mtDNA, flanked by the same set of repeated sequences. In mutants deficient in repair factors, repair could shift to alternative pathways, such as Single-Strand Annealing (SSA) and Microhomology-mediated recombination (MHMR). Furthermore, in some mutants, the data revealed no evidence of DSB repair, but rather suggested that plants deficient in key repair factors could survive by reconstituting an alternative viable mitochondrial genome, from pre-existing autonomously replicating sub-genomes

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Conference papers on the topic "Microhomology mediated recombination"

1

Chang, Ching-Chun. "TALEN-mediated chloroplast geme editing in tobacco generates an abundant subgemic DNA resulting from microhomology-mediated recombination." In ASPB PLANT BIOLOGY 2020. USA: ASPB, 2020. http://dx.doi.org/10.46678/pb.20.1048272.

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Barghouth, Paul, Jonathan Ollivier, Pierre Montay-Gruel, Billy W. Loo, Marie-Catherine Vozenin, Charles Limoli, and Richard Frock. "Abstract PO-012: Ultra-high dose rate (FLASH) irradiation does not alter microhomology mediated recombination under varying oxygen tension when compared to standard clinical dose rates." In Abstracts: AACR Virtual Special Conference on Radiation Science and Medicine; March 2-3, 2021. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1557-3265.radsci21-po-012.

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