Relevant bibliographies by topics / Suppressed recombination

Academic literature on the topic 'Suppressed recombination'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Suppressed recombination"

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Schild, D. "Suppression of a new allele of the yeast RAD52 gene by overexpression of RAD51, mutations in srs2 and ccr4, or mating-type heterozygosity." Genetics 140, no. 1 (May 1, 1995): 115–27. http://dx.doi.org/10.1093/genetics/140.1.115.

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Abstract The RAD52 gene of Saccharomyces cerevisiae is involved both in the recombinational repair of DNA damage and in mitotic and meiotic recombination. A new allele of rad52 has been isolated that has unusual properties. Unlike other alleles of rad52, this allele (rad52-20) is partially suppressed by an srs2 deletion; srs2 mutations normally act to suppress only rad6 and rad18 mutations. In addition, although haploid rad52-20 strains are very X-ray sensitive, diploids homozygous for this allele are only slightly X-ray sensitive and undergo normal meiosis and meiotic recombination. Because rad52-20 diploids homozygous for mating type are very X-ray sensitive, mating-type heterozygosity is acting to suppress rad52-20. Mating-type heterozygosity suppresses this allele even in haploids, because sir mutations, which result in expression of the normally silent mating-type cassettes, were identified among the extragenic revertants of rad52-20. A new allele of srs2 and alleles of the transcriptional regulatory genes ccr4 and caf1 were among the other extragenic revertants of rad52-20. Because other researchers have shown that the RAD51 and RAD52 proteins interact, RAD51 on a high copy number plasmid was tested and found to suppress the rad52-20 allele, but RAD54, 55 and 57 did not suppress. The RAD51 plasmid did not suppress rad52-1. The rad52-20 allele may encode a protein that has low affinity binding to the RAD51 protein. To test whether the selected revertants suppressed rad52-20 by elevating the expression of RAD51, an integrated RAD51-lacZ fusion was genetically crossed into each revertant. Because none of the revertants increased the level of RAD51-lacZ, the revertants must exert their effect by one or more mechanisms that are not mediated by RAD51.
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Milne, G. T., T. Ho, and D. T. Weaver. "Modulation of Saccharomyces cerevisiae DNA double-strand break repair by SRS2 and RAD51." Genetics 139, no. 3 (March 1, 1995): 1189–99. http://dx.doi.org/10.1093/genetics/139.3.1189.

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Abstract RAD52 function is required for virtually all DNA double-strand break repair and recombination events in Saccharomyces cerevisiae. To gain greater insight into the mechanism of RAD52-mediated repair, we screened for genes that suppress partially active alleles of RAD52 when mutant or overexpressed. Described here is the isolation of a phenotypic null allele of SRS2 that suppressed multiple alleles of RAD52 (rad52B, rad52D, rad52-1 and KlRAD52) and RAD51 (KlRAD51) but failed to suppress either a rad52 delta or a rad51 delta. These results indicate that SRS2 antagonizes RAD51 and RAD52 function in recombinational repair. The mechanism of suppression of RAD52 alleles by srs2 is distinct from that which has been previously described for RAD51 overexpression, as both conditions were shown to act additively with respect to the rad52B allele. Furthermore, overexpression of either RAD52 or RAD51 enhanced the recombination-dependent sensitivity of an srs2 delta RAD52 strain, suggesting that RAD52 and RAD51 positively influence recombinational repair mechanisms. Thus, RAD52-dependent recombinational repair is controlled both negatively and positively.
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Lewis, L. Kevin, G. Karthikeyan, James W. Westmoreland, and Michael A. Resnick. "Differential Suppression of DNA Repair Deficiencies of Yeast rad50, mre11 and xrs2 Mutants by EXO1 and TLC1 (the RNA Component of Telomerase)." Genetics 160, no. 1 (January 1, 2002): 49–62. http://dx.doi.org/10.1093/genetics/160.1.49.

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Abstract Rad50, Mre11, and Xrs2 form a nuclease complex that functions in both nonhomologous end-joining (NHEJ) and recombinational repair of DNA double-strand breaks (DSBs). A search for highly expressed cDNAs that suppress the DNA repair deficiency of rad50 mutants yielded multiple isolates of two genes: EXO1 and TLC1. Overexpression of EXO1 or TLC1 increased the resistance of rad50, mre11, and xrs2 mutants to ionizing radiation and MMS, but did not increase resistance in strains defective in recombination (rad51, rad52, rad54, rad59) or NHEJ only (yku70, sir4). Increased Exo1 or TLC1 RNA did not alter checkpoint responses or restore NHEJ proficiency, but DNA repair defects of yku70 and rad27 (fen) mutants were differentially suppressed by the two genes. Overexpression of Exo1, but not mutant proteins containing substitutions in the conserved nuclease domain, increased recombination and suppressed HO and EcoRI endonuclease-induced killing of rad50 strains. exo1 rad50 mutants lacking both nuclease activities exhibited a high proportion of enlarged, G2-arrested cells and displayed a synergistic decrease in DSB-induced plasmid:chromosome recombination. These results support a model in which the nuclease activity of the Rad50/Mre11/Xrs2 complex is required for recombinational repair, but not NHEJ. We suggest that the 5′–3′ exo activity of Exo1 is able to substitute for Rad50/Mre11/Xrs2 in rescission of specific classes of DSB end structures. Gene-specific suppression by TLC1, which encodes the RNA subunit of the yeast telomerase complex, demonstrates that components of telomerase can also impact on DSB repair pathways.
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Shammas, Masood A., Shujuan J. Xia, and Robert J. Shmookler Reis. "Induction of Duplication Reversion in Human Fibroblasts, by Wild-Type and Mutated SV40 T Antigen, Covaries With the Ability to Induce Host DNA Synthesis." Genetics 146, no. 4 (August 1, 1997): 1417–28. http://dx.doi.org/10.1093/genetics/146.4.1417.

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Intrachromosomal homologous recombination, manifest as reversion of a 14-kbp duplication in the hypoxanthine phosphoribosyl transferase (HPRT) gene, is elevated in human cells either stably transformed or transiently transfected by the SV40 (simian virus 40) large T antigen gene. Following introduction of wild-type SV40, or any of several T-antigen point mutations in a constant SV40 background, we observed a strong correlation between the stimulation of chromosomal recombination and induction of host-cell DNA synthesis. Moreover, inhibitors of DNA replication (aphidicolin and hydroxyurea) suppress SV40-induced homologous recombination to the extent that they suppress DNA synthesis. Stable integration of plasmids encoding T antigen also augments homologous recombination, which is suppressed by aphidicolin. We infer that the mechanism by which T antigen stimulates homologous recombination in human fibroblasts involves DNA replicative synthesis.
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Nanbu, Tomoko, Katsunori Takahashi, Johanne M. Murray, Naoya Hirata, Shinobu Ukimori, Mai Kanke, Hisao Masukata, Masashi Yukawa, Eiko Tsuchiya, and Masaru Ueno. "Fission Yeast RecQ Helicase Rqh1 Is Required for the Maintenance of Circular Chromosomes." Molecular and Cellular Biology 33, no. 6 (January 7, 2013): 1175–87. http://dx.doi.org/10.1128/mcb.01713-12.

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Protection of telomeres protein 1 (Pot1) binds to single-stranded telomere overhangs and protects chromosome ends. RecQ helicases regulate homologous recombination at multiple stages, including resection, strand displacement, and resolution. Fission yeastpot1and RecQ helicaserqh1double mutants are synthetically lethal, but the mechanism is not fully understood. Here, we show that the synthetic lethality ofpot1Δrqh1Δ double mutants is due to inappropriate homologous recombination, as it is suppressed by the deletion ofrad51+. The expression of Rad51 in thepot1Δrqh1Δrad51Δ triple mutant, which has circular chromosomes, is lethal. Reduction of the expression of Rqh1 in apot1disruptant with circular chromosomes caused chromosome missegregation, and this defect was partially suppressed by the deletion ofrad51+. Taken together, our results suggest that Rqh1 is required for the maintenance of circular chromosomes when homologous recombination is active. Crossovers between circular monomeric chromosomes generate dimers that cannot segregate properly inEscherichia coli. We propose that Rqh1 inhibits crossovers between circular monomeric chromosomes to suppress the generation of circular dimers.
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Charlesworth, Deborah, Roberta Bergero, Chay Graham, Jim Gardner, and Karen Keegan. "How did the guppy Y chromosome evolve?" PLOS Genetics 17, no. 8 (August 9, 2021): e1009704. http://dx.doi.org/10.1371/journal.pgen.1009704.

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The sex chromosome pairs of many species do not undergo genetic recombination, unlike the autosomes. It has been proposed that the suppressed recombination results from natural selection favouring close linkage between sex-determining genes and mutations on this chromosome with advantages in one sex, but disadvantages in the other (these are called sexually antagonistic mutations). No example of such selection leading to suppressed recombination has been described, but populations of the guppy display sexually antagonistic mutations (affecting male coloration), and would be expected to evolve suppressed recombination. In extant close relatives of the guppy, the Y chromosomes have suppressed recombination, and have lost all the genes present on the X (this is called genetic degeneration). However, the guppy Y occasionally recombines with its X, despite carrying sexually antagonistic mutations. We describe evidence that a new Y evolved recently in the guppy, from an X chromosome like that in these relatives, replacing the old, degenerated Y, and explaining why the guppy pair still recombine. The male coloration factors probably arose after the new Y evolved, and have already evolved expression that is confined to males, a different way to avoid the conflict between the sexes.
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Poteete, Anthony R. "Modulation of DNA Repair and Recombination by the Bacteriophage λ Orf Function in Escherichia coli K-12." Journal of Bacteriology 186, no. 9 (May 1, 2004): 2699–707. http://dx.doi.org/10.1128/jb.186.9.2699-2707.2004.

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ABSTRACT The orf gene of bacteriophage λ, fused to a promoter, was placed in the galK locus of Escherichia coli K-12. Orf was found to suppress the recombination deficiency and sensitivity to UV radiation of mutants, in a Δ(recC ptr recB recD)::P tac gam bet exo pae cI ΔrecG background, lacking recF, recO, recR, ruvAB, and ruvC functions. It also suppressed defects of these mutants in establishing replication of a pSC101-related plasmid. Compared to orf, the recA803 allele had only small effects on recF, recO, and recR mutant phenotypes and no effect on a ruvAB mutant. In a fully wild-type background with respect to known recombination and repair functions, orf partially suppressed the UV sensitivity of ruvAB and ruvC mutants.
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Feng, Zichao, Ruina Ma, An Du, Yinan Zhang, Xue Zhao, Yongzhe Fan, and Xiaoming Cao. "Enhanced Performance of Near-Infrared-Absorption CdSeTe Quantum Dot-Sensitized Solar Cells Via Octa-Aminopropyl Polyhedral Oligomeric Silsesquioxane Modification." Nano 14, no. 07 (July 2019): 1950087. http://dx.doi.org/10.1142/s1793292019500875.

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The charge recombination caused by surface defects limits photovoltaic properties of quantum dot-sensitized solar cells (QDSSCs), which can be suppressed by modifying organic or inorganic molecules and atomic ligands. In this paper, octa-aminopropyl polyhedral oligomeric silsesquioxane (OA-POSS) connected and modified near-infrared absorption CdSeTe quantum dots (QDs) through coupling agent (1-ethyl-3-3-dimethylaminopropyl carbodiimide hydrochloride). The results suggest that OA-POSS reduces the surface defects of CdSeTe QDs and suppresses charge recombination. Therefore, the power conversion efficiency improves nearly 41%, which increases from 2.00% to 2.82%.
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Olson, M. V., A. Kas, K. Bubb, R. Qui, E. E. Smith, C. K. Raymond, and R. Kaul. "Hypervariability, suppressed recombination and the genetics of individuality." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 359, no. 1441 (January 29, 2004): 129–40. http://dx.doi.org/10.1098/rstb.2003.1418.

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We define ‘genetic individuality’ as intraspecies variation that has substantial heritability and involves traits that are sufficiently common that they can be observed in any modest–sized sampling of individuals. We propose that genetic individuality is largely shaped by the combinatory shuffling of a modest number of genes, each of which exists as a family of functionally and structurally diverged alleles. Unequivocal examples of such allele families are found at the O–antigen–biosynthetic locus in Pseudomonas aeruginosa and the human leucocyte antigen locus in humans. We examine characteristic features of these allele families and explore the possibility that genetic loci with similar characteristics can be recognized in a whole–genome scan of human genetic variation.
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Shulman, M. J., C. Collins, A. Connor, L. R. Read, and M. D. Baker. "Interchromosomal recombination is suppressed in mammalian somatic cells." EMBO Journal 14, no. 16 (August 1995): 4102–7. http://dx.doi.org/10.1002/j.1460-2075.1995.tb00082.x.

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Dissertations / Theses on the topic "Suppressed recombination"

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Straughen, Joel E. "BLM Is a Suppressor of DNA Recombination." University of Cincinnati / OhioLINK, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1022269717.

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Lohn, Zoe Roy. "A new role for the tumour suppressor LIN-35 during meiotic recombination in Caenorhabditis elegans." Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/27276.

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Meiosis is a fundamental biological process used by sexually reproducing species to ensure the faithful transmission of genetic material and to generate genetic diversity. In humans, failure to recombine properly during meiosis causes genetic conditions in the human conceptus such as aneuploidy and spontaneous abortion. An excellent model organism for the investigation of meiotic recombination is the nematode, Caenorhabditis elegans, which has many conserved meiotic processes. In this thesis, I have investigated the role of lin-35 in meiotic crossing over. LIN-35 is the C. elegans ortholog of the retinoblastoma (Rb) protein, well characterized with respect to its role in gene transcription and cell proliferation. My results show that mutation in the lin-35 gene alters recombination frequency differentially for several regions of the chromosome, causing increases in recombinationally suppressed regions and decreases in highly recombinogenic regions. In combination with Rec-1, a mutant known to alter crossover distribution, crossovers across the length of the entire chromosome, were decreased. In addition, other severely detrimental phenotypes were observed. For example, gametic viability was reduced dramatically in the double mutant, compared to either mutant alone. Thus, the Lin-35 and Rec-1 phenotypes were synergistic, indicating non-redundancy. In summary, lin-35 function plays a role in achieving normal levels of meiotic recombination, a role that may be related to its function in chromatin modification and gene transcription.
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Saberi, Alihossein. "RAD18 and poly〔ADP ribose〕polymerase independently suppress the access of nonhomologous end joining to double strand breaks and facilitate homologous recombination mediated repair." Kyoto University, 2007. http://hdl.handle.net/2433/135739.

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Jayatilake, Dimanthi Vihanga. "Fine mapping of nematode resistance genes Rlnn1 and Cre8 in wheat (Triticum aestivum)." Thesis, 2014. http://hdl.handle.net/2440/97789.

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The root lesion nematode Pratylenchus neglectus and the cereal cyst nematode Heterodera avenae cause significant yield damage to wheat (Triticum aestivum L.) and crops that are grown in rotation with wheat. The focus of this thesis is on two loci in wheat, Rlnn1and Cre8, which confer resistance against P. neglectus and H. avenae, respectively, with an overall scientific goal of characterizing these two resistance loci as an initiative towards isolation of the causal gene(s) and identification of diagnostic molecular markers for the use in marker-assisted selection in wheat breeding programmes. The thesis presents improvements to an existing Excalibur/Kukri linkage map of chromosome 7A by adding Lr20 (a gene for resistance against leaf rust caused by Puccinia triticina), Sr15 (a gene for resistance against stem rust caused by P. graminis), Psy-A1 (a phytoene synthase gene), Cat3-A1 (a catalase gene) and 59 new molecular markers. The genomic location of the Rlnn1 quantitative trait locus (QTL) was confirmed as the distal end of long arm of chromosome 7A (7AL). It coincides with the position of Lr20/Sr15, Psy-A1, Cat3-A1 and 34 molecular markers. Based on the findings that 1) some markers that collocate with the resistance genes Lr20/Sr15 and Rlnn1 are widely separated in mapping populations that do not segregate for these genes; 2) when anchored to a chromosome 7A syntenic build, these markers spanned a 0.9-Mb region; and 3) no recombinants were found in a large population of recombinant inbred lines, it is suggested that the clustering of molecular markers/genes/QTL at the distal end of 7AL is due to suppressed recombination. The suppressed recombination in Excalibur may be a result of a translocation. This suggestion is based on 1) phylogenetic analysis of Psy-A1 alleles; 2) marker amplification patterns that suggested that sequences at the distal end of 7AL in Excalibur are very different from those in Kukri and Chinese Spring; 3) amplicons observed for a normally 7B-specific marker that collocates with Rlnn1 on 7AL, and 4) FISH images that revealed an unknown putative translocation in Excalibur that is absent in Kukri. It seems likely that the Rlnn1-containing segment of 7AL may have been translocated from a 7B-like chromosome arm with an unknown ancestry. Such a translocation could have pre-dated hexaploidisation and occurred in a tetraploid or diploid ancestor. The thesis also presents a high-resolution genetic linkage map for a Trident/Molineux population. This map was used to confirm the locations of three previously reported QTL for H. avenae, including the Cre8 locus mapped as a large-effect QTL at the distal end of the long arm of chromosome 6B (6BL), with an estimated position 0.9 cM from the closest markers. A cross was designed and made to develop a population for future use in fine mapping. With these materials and with the closely-linked molecular markers developed here, Cre8 seems amenable to positional cloning. In the research conducted for this thesis, the Rlnn1 and Cre8 resistance loci were mapped at the distal ends of 7AL and 6BL, respectively and diagnostic markers were identified for the use in marker-assisted selection. A suppressed recombination at the end of 7AL impedes the prospects of cloning Rlnn1, while the research reported here have identified suitable markers and genetic resources for cloning the Cre8 gene with a forward genetics approach.
Thesis (Ph.D.) -- University of Adelaide, School of Agriculture, Food and Wine, 2014
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Savakis, Amie. "ClpXP-regulated Proteins Suppress Requirement for RecA in Dam Mutants of Escherichia coli K-12." 2018. https://scholarworks.umass.edu/masters_theses_2/697.

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Double strand breaks (DSB) are a common source of DNA damage in both prokaryotes and eukaryotes. If they are not repaired or are repaired incorrectly, they can lead to cell death (bacteria) or cancer (humans). In Escherichia coli, repair of DSB are typically accomplished via homologous recombination and mediated by RecA. This repair pathway, among others, is associated with activation of the SOS response. DNA adenine methyltransferase (dam) mutants have an increased number of DSB and, therefore, are notorious for being RecA-dependent for viability. Here, we show that the synthetic lethality of Δdam/ΔrecA is suppressed when clpP is removed, suggesting that there is a protein, normally degraded by ClpXP, which is preventing DSB from occurring.
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Yu, Helen. "Caractérisation fonctionnelle du suppresseur de tumeurs BAP1." Thèse, 2015. http://hdl.handle.net/1866/12094.

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La déubiquitinase BAP1 (« BRCA1-Associated Protein1 ») a initialement été isolée pour sa capacité de promouvoir la fonction suppressive de tumeurs de BRCA1. BAP1 est muté de manière homozygote dans plusieurs cancers (tel que le cancer du rein, de la peau, de l’oeil et du sein) suggérant fortement que cette déubiquitinase est un suppresseur de tumeurs. Effectivement, la surexpression de BAP1 réduit la prolifération cellulaire et la croissance tumorale dans des modèles de xénogreffe de souris. Toutefois, la fonction biologique et le mécanisme d’action de cette déubiquitinase restent encore marginalement connus. Ainsi, les objectifs de cette thèse sont de caractériser la fonction biologique de BAP1 et de révéler les bases moléculaires de sa fonction suppressive de tumeurs. Pour déterminer la fonction biologique de BAP1, nous avons immuno-purifié et identifié les protéines associées à BAP1, qui s’avèrent être principalement des facteurs et co-facteurs de transcription. Ensuite, nous avons démontré que BAP1 est un régulateur de la transcription. Parallèlement, un autre groupe a montré que BAP1 chez la drosophile, Calypso, régule l’ubiquitination de H2A et la transcription génique. D’autre part, nos résultats d’analyse d’expression génique globale suggèrent que BAP1 jouerait un rôle important dans la réponse aux dommages à l’ADN. Effectivement, des expériences de gain et de perte de fonction (méthode de l’ARNi, modèle de cellules KO en BAP1 et de cellules déficientes en BAP1 re-exprimant BAP1) ont révélé que cette déubiquitinase régule la réponse aux bris double brin d’ADN par la recombinaison homologue. Nos résultats suggèrent que BAP1 exerce sa fonction suppressive de tumeurs en contrôlant la réparation sans erreur de l’ADN via la recombinaison homologue. En cas d’inactivation de BAP1, les cellules deviendront plus dépendantes du mécanisme de réparation par jonction d'extrémités non-homologues, qui est potentiellement mutagénique causant ainsi l’instabilité génomique. D’autres études seront nécessaires afin de déterminer le rôle exact de BAP1 dans la transcription et de comprendre comment la dérégulation de l’ubiquitination de H2A contribue au développement du cancer. Définir les mécanismes de suppression tumorale est de grand intérêt, non seulement pour comprendre la carcinogénèse mais également pour le développement de nouvelles thérapies contre cette maladie.
The deubiquitinase BAP1 (BRCA1-Associated Protein1) is a nuclear member of the ubiquitin C-terminal hydrolase (UCH) family, previously isolated for promoting the function of the tumor suppressor BRCA1. Importantly, homozygous inactivating mutations of BAP1 have been found in mesothelioma, renal, melanoma and breast cancers strongly suggesting that this deubiquitinase is a tumor suppressor. Indeed BAP1 overexpression reduces cell proliferation and tumor growth in xenograft models. Nonetheless, the biological function and the mechanism of action of this deubiquitinase remain poorly defined. The goals of this thesis are to characterize the biological function of BAP1 and to reveal the molecular basis of its tumor suppressive function. To provide insights into BAP1 biological function, we conducted a tandem affinity immunopurification of BAP1-associated proteins and found that most interacting partners are transcription factors and cofactors. Next, we demonstrated that BAP1 is indeed a transcription regulator. Concomitantly, another group showed that the drosophila BAP1, Calypso, is a Polycomb Group protein that regulates the ubiquitination levels of H2A and gene expression. Indeed, our global gene expression analysis suggests that BAP1 plays important role in DNA damage response. Consistently, loss- and gain- of function experiments (RNAi approach, DT40 chicken B cells KO model and re-introduction of BAP1 in BAP1 null-cells) revealed that BAP1 promotes homologous recombination-mediated DNA double strand break repair. Our data suggest that BAP1 exerts its tumor suppressor function by controlling error-free DNA repair by homologous recombination. Thus, in a situation of BAP1 inactivation, cells might become more reliant on non-homologous end joining, an error-prone DNA repair mechanism, which would result in the accumulation of mutations and chromosomal aberrations, causing genomic instability. Further studies are required to delineate the exact role of BAP1 in transcription and to define how deregulation of H2A ubiquitination pathway contributes to cancer. Defining the mechanisms of tumor suppression is of great interest, not only for understanding cancer development, but also for designing rational cancer therapies.
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Book chapters on the topic "Suppressed recombination"

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Nonaka, Kenichi, Akihiko Horiuchi, Yuki Negoro, Kensuke Iwanaga, Seiichi Yokoyama, Hideki Hashimoto, Masashi Sato, Yusuke Maeyama, Masaaki Shimizu, and Hiroaki Iwakuro. "Suppressed Surface-Recombination Structure and Surface Passivation for Improving Current Gain of 4H-SiC BJTs." In Silicon Carbide, 445–65. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2011. http://dx.doi.org/10.1002/9783527629077.ch16.

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Lane, David P., Carol A. Midgley, Ted R. Hupp, Xin Lu, Borivoj Vojtesek, and Steven M. Picksley. "On the regulation of the p53 tumour suppressor, and its role in the cellular response to DNA damage." In DNA Repair and Recombination, 79–83. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0537-8_12.

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Huang, Henry V., Peter F. R. Little, and Brian Seed. "Improved Suppressor tRNA Cloning Vectors and Plasmid-Phage Recombination." In Vectors, 269–83. Elsevier, 1988. http://dx.doi.org/10.1016/b978-0-409-90042-2.50020-9.

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Kharaishvili, Gvantsa, Mariam Kacheishvili, and Giorgi Akhvlediani. "BRCA Gene Mutations and Prostate Cancer." In BRCA1 and BRCA2 Mutations - Diagnostic and Therapeutic Implications [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.108792.

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Prostate cancer remains the second most common cancer in men, with diverse courses from indolent cases to aggressive diseases. Among the key factors implicated in its pathogenesis are genomic alterations such as the TMPRSS2-ERG and related fusion oncogenes, loss of tumor suppressor PTEN, p53 or NKX3.1, inflammation, enhanced DNA damage, and chromosomal instability. Men with prostate cancer who carry BRCA1/2 mutations are at more risk of worse disease and poor prognosis. Cancer cells with mutant BRCA1 or BRCA2 repair genes with defects in homologous recombination are vulnerable to PARP inhibitors that target the genetic phenomenon known as synthetic lethality to exploit faulty DNA repair mechanisms. With relevance to prostate cancer, other features of cancer cells may also sensitize to PARP inhibitors, including aberrant transcription due to the androgen-driven fusion oncogene TMPRSS2-ERG or PTEN loss. Several models of synthetic lethality and potential biomarkers suggested up to date are also discussed. The chapter also highlights the importance of genetic screening of men with BRCA and shows diagnostic utility of plasma-derived circulating tumor DNA.
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"So FPTT is associated with two different types of D antigen and three different types of Ce antigens (Table IV). These results suggest that a similar amino acid sequence corresponding to the FPTT antigen is encoded by D genes and by CE genes. Since the genes are highly homologous and proteins very similar, it is possible that similar changes may have occurred. Several mechanisms could be involved: mutation, recombination or gene conversion have been invoked in other blood group systems to explain rare phenotypes. The large number of Rh antigens and their quantitative and qualitative variants will not be easy to explain. Variation in the Rh genes may explain some variants but we know that Rh expression is affected by suppressors unlinked to RH, homozygosity of one unlinked suppressor causes the regulator type of Rhnu|j. Mutation in one of the genes encoding a non-Rh protein required for formation of the Rh protein complex may affect the presentation of some Rh antigens at the cell surface. Rh groups will continue to be clinically and immunologically important until their genetic control is fully understood. Xga AND THE RELATED 12E7 ANTIGEN Unlike Rh antigens, Xga is not clinically significant but was a very valuable marker for studies of the X chromosome. Our interest in Xga and the related 12E7 antigen was rekindled recently by a report of PBDX, a candidate gene for XG [38], and by speculation of the role of 12E7 antigen as an adhesion molecule [39,40]. Xga is red cell specific; in contrast, 12E7 antigen is almost ubiquitous. 12E7 antigen, the MIC2 gene product, has been numbered CD99 at the fifth Leucocyte Workshop and this." In Transfusion Immunology and Medicine, 196. CRC Press, 1995. http://dx.doi.org/10.1201/9781482273441-14.

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Conference papers on the topic "Suppressed recombination"

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Li, Cong, Qiang Guo, Tai Cheng, Wenyuan Qiao, Fuzhi Wang, Songyuan Dai, and Zhan’ao Tan. "Efficient perovskite/fullerene planar heterojunction solar cells with enhanced charge extraction and suppressed charge recombination." In Photonics for Energy. Washington, D.C.: OSA, 2015. http://dx.doi.org/10.1364/pfe.2015.pt4a.5.

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García-Santamaría, F., S. Brovelli, R. Viswanatha, J. A. Hollingsworth, H. Htoon, S. A. Crooker, and V. I. Klimov. "Highly Efficient Optical Gain Media Based on Thick-Shell CdSe/CdS Nanocrystals with Suppressed Auger Recombination." In Nonlinear Optics: Materials, Fundamentals and Applications. Washington, D.C.: OSA, 2011. http://dx.doi.org/10.1364/nlo.2011.nthd5.

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Brovelli, Sergio, Florencio García-Santamaría, Ranjani Viswanatha, Bhola N. Pal, Scott A. Crooker, and Victor I. Klimov. "Wavefunction engineering in core-shell semiconductor nanocrystals: from fine-tuned exciton dynamics and suppressed Auger recombination to dual color electroluminescence." In SPIE NanoScience + Engineering, edited by Jenny Clark, Carlos Silva, John B. Asbury, Oleg V. Prezhdo, and Sergei Tretiak. SPIE, 2012. http://dx.doi.org/10.1117/12.959441.

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Hoon Park, Hyunseock Jie, Ho-bum Lee, Keun-Hwa Chae, Jong-Ku Park, and Dok-Yol Lee. "Direct observation of suppressed recombination of electron-hole pairs in the TiO2 nanopowders with anatase-rutile interface: in-situ NEXAFS study under UV irradiation." In 2006 IEEE Nanotechnology Materials and Devices Conference. IEEE, 2006. http://dx.doi.org/10.1109/nmdc.2006.4388962.

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Leidy-Davis, Tiffany, Kai Cheng, Leslie Goodwin, Judith Morgan, Wen Chun Juan, Xavier Roca, Sin-Tiong Ong, and David E. Bergstrom. "Abstract 5097: Knock-in of a human tumor suppressor (25-kilobase pairs) by traditional and CRISPR/Cas9-stimulated homologous recombination." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5097.

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Sulkowski, Parker S., Sebstian Oeck, Jing Li, Brian Shuch, Megan C. King, Ranjit S. Bindra, and Peter M. Glazer. "Abstract SY21-02: Oncometabolites suppress homologous recombination DNA repair by inhibition of chromatin remodeling at the DNA double-strand break." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-sy21-02.

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Sulkowski, Parker S., Sebstian Oeck, Jing Li, Brian Shuch, Megan C. King, Ranjit S. Bindra, and Peter M. Glazer. "Abstract SY21-02: Oncometabolites suppress homologous recombination DNA repair by inhibition of chromatin remodeling at the DNA double-strand break." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-sy21-02.

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Ogiwara, Hideaki, Jun Yokota, and Takashi Kohno. "Abstract B65: Curcumin, a novel inhibitor of ATR-CHK1 pathway, suppresses homologous recombination and DNA damage checkpoint and enhances the sensitivity to PARP inhibitors." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-b65.

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Reports on the topic "Suppressed recombination"

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Schild, David, and Claudia Wiese. Overexpressed of RAD51 suppresses recombination defects: a possible mechanism to reverse genomic instability. Office of Scientific and Technical Information (OSTI), October 2009. http://dx.doi.org/10.2172/983266.

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Pawlowski, Wojtek P., and Avraham A. Levy. What shapes the crossover landscape in maize and wheat and how can we modify it. United States Department of Agriculture, January 2015. http://dx.doi.org/10.32747/2015.7600025.bard.

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Meiotic recombination is a process in which homologous chromosomes engage in the exchange of DNA segments, creating gametes with new genetic makeup and progeny with new traits. The genetic diversity generated in this way is the main engine of crop improvement in sexually reproducing plants. Understanding regulation of this process, particularly the regulation of the rate and location of recombination events, and devising ways of modifying them, was the major motivation of this project. The project was carried out in maize and wheat, two leading crops, in which any advance in the breeder’s toolbox can have a huge impact on food production. Preliminary work done in the USA and Israeli labs had established a strong basis to address these questions. The USA lab pioneered the ability to map sites where recombination is initiated via the induction of double-strand breaks in chromosomal DNA. It has a long experience in cytological analysis of meiosis. The Israeli lab has expertise in high resolution mapping of crossover sites and has done pioneering work on the importance of epigenetic modifications for crossover distribution. It has identified genes that limit the rates of recombination. Our working hypothesis was that an integrative analysis of double-strand breaks, crossovers, and epigenetic data will increase our understanding of how meiotic recombination is regulated and will enhance our ability to manipulate it. The specific objectives of the project were: To analyze the connection between double-strand breaks, crossover, and epigenetic marks in maize and wheat. Protocols developed for double-strand breaks mapping in maize were applied to wheat. A detailed analysis of existing and new data in maize was conducted to map crossovers at high resolution and search for DNA sequence motifs underlying crossover hotspots. Epigenetic modifications along maize chromosomes were analyzed as well. Finally, a computational analysis tested various hypotheses on the importance of chromatin structure and specific epigenetic modifications in determining the locations of double-strand breaks and crossovers along chromosomes. Transient knockdowns of meiotic genes that suppress homologous recombination were carried out in wheat using Virus-Induced Gene Silencing. The target genes were orthologs of FANCM, DDM1, MET1, RECQ4, and XRCC2.
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Wisniewski, Michael E., Samir Droby, John L. Norelli, Noa Sela, and Elena Levin. Genetic and transcriptomic analysis of postharvest decay resistance in Malus sieversii and the characterization of pathogenicity effectors in Penicillium expansum. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7600013.bard.

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Blue mold of apple caused by Penicilliumexpansumis a major postharvest disease. Selection for postharvest disease resistance in breeding programs has been ignored in favor of fruit quality traits such as size, color, taste, etc. The identification of postharvest disease resistance as a heritable trait would represent a significant accomplishment and has not been attempted in apple. Furthermore, insight into the biology of the pathogenicity of P. expansumin apple could provide new approaches to postharvest decay management. Hypothesis: Postharvest resistance of apple to P. expansumcan be mapped to specific genetic loci and significant quantitative-trait-loci (QTLs) can be identified that account for a major portion of the population variance. Susceptibility of apple fruit to P. expansumis dependent on the ability of the pathogen to produce LysM effectors that actively suppress primary and/or secondary resistance mechanisms in the fruit. Objectives: 1) Identify QTL(s) and molecular markers for blue mold resistance in GMAL4593 mapping population (‘Royal Gala’ X MalussieversiiPI613981), 2) Characterize the transcriptome of the host and pathogen (P. expansum) during the infection process 3) Determine the function of LysM genes in pathogenicity of P. expansum. Methods: A phenotypic evaluation of blue mold resistance in the GMAL4593 mapping population, conducted in several different years, will be used for QTL analysis (using MapQTL 6.0) to identify loci associated with blue mold resistance. Molecular markers will be developed for the resistance loci. Transcriptomic analysis by RNA-seq will be used to conduct a time course study of gene expression in resistant and susceptible apple GMAL4593 genotypes in response to P. expansum, as well as fungal responses to both genotypes. Candidate resistance genes identified in the transcriptomic study and or bioinformatic analysis will be positioned in the ‘Golden Delicious’ genome to identify markers that co-locate with the identified QTL(s). A functional analysis of LysM genes on pathogenicity will be conducted by eliminating or reducing the expression of individual effectors by heterologous recombination and silencing technologies. LysMeffector genes will also be expressed in a yeast expression system to study protein function. Expected Results: Identification of postharvest disease resistance QTLs and tightly-linked genetic markers. Increased knowledge of the role of effectors in blue mold pathogenic
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