scholarly journals DNA Recombination-Initiation Plays a Role in the Extremely Biased Inheritance of Yeast [rho−] Mitochondrial DNA That Contains the Replication Origin ori5

2006 ◽  
Vol 27 (3) ◽  
pp. 1133-1145 ◽  
Author(s):  
Feng Ling ◽  
Akiko Hori ◽  
Takehiko Shibata
Keyword(s):  
Mitochondrial Dna ◽  
Replication Origin ◽  
Excision Repair ◽  
Dna Recombination ◽  
Strand Break ◽  
Yeast Cells ◽  
Rolling Circle Replication ◽  
Rolling Circle ◽  
Mtdna Replication ◽  
Base Excision

ABSTRACT Hypersuppressiveness, as observed in Saccharomyces cerevisiae, is an extremely biased inheritance of a small mitochondrial DNA (mtDNA) fragment that contains a replication origin (HS [rho −] mtDNA). Our previous studies showed that concatemers (linear head-to-tail multimers) are obligatory intermediates for mtDNA partitioning and are primarily formed by rolling-circle replication mediated by Mhr1, a protein required for homologous mtDNA recombination. In this study, we found that Mhr1 is required for the hypersuppressiveness of HS [ori5] [rho −] mtDNA harboring ori5, one of the replication origins of normal ([rho +]) mtDNA. In addition, we detected an Ntg1-stimulated double-strand break at the ori5 locus. Purified Ntg1, a base excision repair enzyme, introduced a double-stranded break by itself into HS [ori5] [rho −] mtDNA at ori5 isolated from yeast cells. Both hypersuppressiveness and concatemer formation of HS [ori5] [rho −] mtDNA are simultaneously suppressed by the ntg1 null mutation. These results support a model in which, like homologous recombination, rolling-circle HS [ori5] [rho −] mtDNA replication is initiated by double-stranded breakage in ori5, followed by Mhr1-mediated homologous pairing of the processed nascent DNA ends with circular mtDNA. The hypersuppressiveness of HS [ori5] [rho −] mtDNA depends on a replication advantage furnished by the higher density of ori5 sequences and on a segregation advantage furnished by the higher genome copy number on transmitted concatemers.

scholarly journals DNA polymerase X from Deinococcus radiodurans implicated in bacterial tolerance to DNA damage is characterized as a short patch base excision repair polymerase

Microbiology ◽  
2009 ◽  
Vol 155 (9) ◽  
pp. 3005-3014 ◽  
Author(s):  
Nivedita P. Khairnar ◽  
Hari S. Misra
Keyword(s):  
Dna Damage ◽  
Dna Polymerase ◽  
Base Excision Repair ◽  
Deinococcus Radiodurans ◽  
Excision Repair ◽  
Strand Break ◽  
Klenow Fragment ◽  
E Coli ◽  
Base Excision

The Deinococcus radiodurans R1 genome encodes an X-family DNA repair polymerase homologous to eukaryotic DNA polymerase β. The recombinant deinococcal polymerase X (PolX) purified from transgenic Escherichia coli showed deoxynucleotidyltransferase activity. Unlike the Klenow fragment of E. coli, this enzyme showed short patch DNA synthesis activity on heteropolymeric DNA substrate. The recombinant enzyme showed 5′-deoxyribose phosphate (5′-dRP) lyase activity and base excision repair function in vitro, with the help of externally supplied glycosylase and AP endonuclease functions. A polX disruption mutant of D. radiodurans expressing 5′-dRP lyase and a truncated polymerase domain was comparatively less sensitive to γ-radiation than a polX deletion mutant. Both mutants showed higher sensitivity to hydrogen peroxide. Excision repair mutants of E. coli expressing this polymerase showed functional complementation of UV sensitivity. These results suggest the involvement of deinococcal polymerase X in DNA-damage tolerance of D. radiodurans, possibly by contributing to DNA double-strand break repair and base excision repair.

scholarly journals Distinct spatiotemporal patterns and PARP dependence of XRCC1 recruitment to single-strand break and base excision repair

2013 ◽  
Vol 41 (5) ◽  
pp. 3115-3129 ◽  
Author(s):  
Anna Campalans ◽  
Thierry Kortulewski ◽  
Rachel Amouroux ◽  
Hervé Menoni ◽  
Wim Vermeulen ◽  
...  
Keyword(s):  
Base Excision Repair ◽  
Excision Repair ◽  
Strand Break ◽  
Single Strand ◽  
Spatiotemporal Patterns ◽  
Single Strand Break ◽  
Base Excision

scholarly journals Role and Regulation of the RECQL4 Family during Genomic Integrity Maintenance

Genes ◽  
2021 ◽  
Vol 12 (12) ◽  
pp. 1919
Author(s):  
Thong T. Luong ◽  
Kara A. Bernstein
Keyword(s):  
Dna Repair ◽  
Excision Repair ◽  
Genetic Diseases ◽  
Genomic Stability ◽  
Strand Break ◽  
Developmental Defects ◽  
Dna Helicases ◽  
Nucleotide Excision ◽  
Evolutionarily Conserved ◽  
Base Excision

RECQL4 is a member of the evolutionarily conserved RecQ family of 3’ to 5’ DNA helicases. RECQL4 is critical for maintaining genomic stability through its functions in DNA repair, recombination, and replication. Unlike many DNA repair proteins, RECQL4 has unique functions in many of the central DNA repair pathways such as replication, telomere, double-strand break repair, base excision repair, mitochondrial maintenance, nucleotide excision repair, and crosslink repair. Consistent with these diverse roles, mutations in RECQL4 are associated with three distinct genetic diseases, which are characterized by developmental defects and/or cancer predisposition. In this review, we provide an overview of the roles and regulation of RECQL4 during maintenance of genome homeostasis.

scholarly journals Role of Base Excision Repair Pathway in the Processing of Complex DNA Damage Generated by Oxidative Stress and Anticancer Drugs

2021 ◽  
Vol 8 ◽  
Author(s):  
Yeldar Baiken ◽  
Damira Kanayeva ◽  
Sabira Taipakova ◽  
Regina Groisman ◽  
Alexander A. Ishchenko ◽  
...  
Keyword(s):  
Dna Damage ◽  
Base Excision Repair ◽  
Genome Instability ◽  
Excision Repair ◽  
Chromosomal Rearrangements ◽  
Strand Break ◽  
Dna Lesions ◽  
Complex Nature ◽  
Base Excision

Chemical alterations in DNA induced by genotoxic factors can have a complex nature such as bulky DNA adducts, interstrand DNA cross-links (ICLs), and clustered DNA lesions (including double-strand breaks, DSB). Complex DNA damage (CDD) has a complex character/structure as compared to singular lesions like randomly distributed abasic sites, deaminated, alkylated, and oxidized DNA bases. CDD is thought to be critical since they are more challenging to repair than singular lesions. Although CDD naturally constitutes a relatively minor fraction of the overall DNA damage induced by free radicals, DNA cross-linking agents, and ionizing radiation, if left unrepaired, these lesions cause a number of serious consequences, such as gross chromosomal rearrangements and genome instability. If not tightly controlled, the repair of ICLs and clustered bi-stranded oxidized bases via DNA excision repair will either inhibit initial steps of repair or produce persistent chromosomal breaks and consequently be lethal for the cells. Biochemical and genetic evidences indicate that the removal of CDD requires concurrent involvement of a number of distinct DNA repair pathways including poly(ADP-ribose) polymerase (PARP)-mediated DNA strand break repair, base excision repair (BER), nucleotide incision repair (NIR), global genome and transcription coupled nucleotide excision repair (GG-NER and TC-NER, respectively), mismatch repair (MMR), homologous recombination (HR), non-homologous end joining (NHEJ), and translesion DNA synthesis (TLS) pathways. In this review, we describe the role of DNA glycosylase-mediated BER pathway in the removal of complex DNA lesions.

scholarly journals Identification of a cis-Acting Element Derived from Tomato Leaf Curl Yunnan Virus that Mediates the Replication of a Deficient Yeast Plasmid in Saccharomyces cerevisiae

Viruses ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 536 ◽  
Author(s):  
Fangfang Li ◽  
Xiongbiao Xu ◽  
Xiuling Yang ◽  
Zhenghe Li ◽  
Xueping Zhou
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Recombinant Plasmid ◽  
Tomato Leaf ◽  
Yeast Cells ◽  
Rolling Circle Replication ◽  
Yeast Plasmid ◽  
Rolling Circle ◽  
Shuttle Plasmid ◽  
Tomato Leaf Curl ◽  
Leaf Curl

Geminiviruses are a group of small single-stranded DNA viruses that replicate in the host cell nucleus. It has been reported that the viral replication initiator protein (Rep) and the conserved common region (CR) are required for rolling circle replication (RCR)-dependent geminivirus replication, but the detailed mechanisms of geminivirus replication are still obscure owing to a lack of a eukaryotic model system. In this study, we constructed a bacterial–yeast shuttle plasmid with the autonomous replication sequence (ARS) deleted, which failed to replicate in Saccharomyces cerevisiae cells and could not survive in selective media either. Tandemly repeated copies of 10 geminivirus genomic DNAs were inserted into this deficient plasmid to test whether they were able to replace the ARS to execute genomic DNA replication in yeast cells. We found that yeast cells consisting of the recombinant plasmid with 1.9 tandemly repeated copies of tomato leaf curl Yunnan virus isolate Y194 (TLCYnV-Y194, hereafter referred to as Y194) can replicate well and survive in selective plates. Furthermore, we showed that the recombinant plasmid harboring the Y194 genome with the mutation of the viral Rep or CR was still able to replicate in yeast cells, indicating the existence of a non-canonic RCR model. By a series of mutations, we mapped a short fragment of 174 nucleotides (nts) between the V1 and C3 open reading frames (ORFs), including an ARS-like element that can substitute the function of the ARS responsible for stable replication of extrachromosomal DNAs in yeast. The results of this study established a geminivirus replication system in yeast cells and revealed that Y194 consisting of an ARS-like element was able to support the replication a bacterial–yeast shuttle plasmid in yeast cells.

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