93
views
0
recommends
+1 Recommend
0 collections
    1
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Mechanisms and Regulation of Mitotic Recombination in Saccharomyces cerevisiae

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Homology-dependent exchange of genetic information between DNA molecules has a profound impact on the maintenance of genome integrity by facilitating error-free DNA repair, replication, and chromosome segregation during cell division as well as programmed cell developmental events. This chapter will focus on homologous mitotic recombination in budding yeast Saccharomyces cerevisiae. However, there is an important link between mitotic and meiotic recombination (covered in the forthcoming chapter by Hunter et al. 2015) and many of the functions are evolutionarily conserved. Here we will discuss several models that have been proposed to explain the mechanism of mitotic recombination, the genes and proteins involved in various pathways, the genetic and physical assays used to discover and study these genes, and the roles of many of these proteins inside the cell.

          Related collections

          Most cited references447

          • Record: found
          • Abstract: found
          • Article: not found

          Comprehensive identification of cell cycle-regulated genes of the yeast Saccharomyces cerevisiae by microarray hybridization.

          We sought to create a comprehensive catalog of yeast genes whose transcript levels vary periodically within the cell cycle. To this end, we used DNA microarrays and samples from yeast cultures synchronized by three independent methods: alpha factor arrest, elutriation, and arrest of a cdc15 temperature-sensitive mutant. Using periodicity and correlation algorithms, we identified 800 genes that meet an objective minimum criterion for cell cycle regulation. In separate experiments, designed to examine the effects of inducing either the G1 cyclin Cln3p or the B-type cyclin Clb2p, we found that the mRNA levels of more than half of these 800 genes respond to one or both of these cyclins. Furthermore, we analyzed our set of cell cycle-regulated genes for known and new promoter elements and show that several known elements (or variations thereof) contain information predictive of cell cycle regulation. A full description and complete data sets are available at http://cellcycle-www.stanford.edu
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            RAD6-dependent DNA repair is linked to modification of PCNA by ubiquitin and SUMO.

            The RAD6 pathway is central to post-replicative DNA repair in eukaryotic cells; however, the machinery and its regulation remain poorly understood. Two principal elements of this pathway are the ubiquitin-conjugating enzymes RAD6 and the MMS2-UBC13 heterodimer, which are recruited to chromatin by the RING-finger proteins RAD18 and RAD5, respectively. Here we show that UBC9, a small ubiquitin-related modifier (SUMO)-conjugating enzyme, is also affiliated with this pathway and that proliferating cell nuclear antigen (PCNA) -- a DNA-polymerase sliding clamp involved in DNA synthesis and repair -- is a substrate. PCNA is mono-ubiquitinated through RAD6 and RAD18, modified by lysine-63-linked multi-ubiquitination--which additionally requires MMS2, UBC13 and RAD5--and is conjugated to SUMO by UBC9. All three modifications affect the same lysine residue of PCNA, suggesting that they label PCNA for alternative functions. We demonstrate that these modifications differentially affect resistance to DNA damage, and that damage-induced PCNA ubiquitination is elementary for DNA repair and occurs at the same conserved residue in yeast and humans.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Sgs1 helicase and two nucleases Dna2 and Exo1 resect DNA double-strand break ends.

              Formation of single-strand DNA (ssDNA) tails at a double-strand break (DSB) is a key step in homologous recombination and DNA-damage signaling. The enzyme(s) producing ssDNA at DSBs in eukaryotes remain unknown. We monitored 5'-strand resection at inducible DSB ends in yeast and identified proteins required for two stages of resection: initiation and long-range 5'-strand resection. We show that the Mre11-Rad50-Xrs2 complex (MRX) initiates 5' degradation, whereas Sgs1 and Dna2 degrade 5' strands exposing long 3' strands. Deletion of SGS1 or DNA2 reduces resection and DSB repair by single-strand annealing between distant repeats while the remaining long-range resection activity depends on the exonuclease Exo1. In exo1Deltasgs1Delta double mutants, the MRX complex together with Sae2 nuclease generate, in a stepwise manner, only few hundred nucleotides of ssDNA at the break, resulting in inefficient gene conversion and G2/M damage checkpoint arrest. These results provide important insights into the early steps of DSB repair in eukaryotes.
                Bookmark

                Author and article information

                Journal
                Genetics
                Genetics
                genetics
                genetics
                genetics
                Genetics
                Genetics Society of America
                0016-6731
                1943-2631
                November 2014
                1 November 2014
                1 November 2014
                : 198
                : 3
                : 795-835
                Affiliations
                [* ]Department of Microbiology and Immunology, Columbia University Medical Center, New York, New York 10032
                []Department of Genetics and Development, Columbia University Medical Center, New York, New York 10032
                []Department of Biology, University of Copenhagen, DK-2200 Copenhagen, Denmark
                Author notes
                [1 ]Corresponding authors: Department of Microbiology and Immunology, Columbia University Medical Center, New York, NY 10032. E-mail: lss5@ 123456columbia.edu ; Department of Genetics and Development, Columbia University Medical Center, New York, NY 10032. E-mail: rothstein@ 123456columbia.edu ; and Department of Biology, University of Copenhagen, DK-2200 Copenhagen, Denmark. E-mail: mlisby@ 123456bio.ku.dk
                Article
                166140
                10.1534/genetics.114.166140
                4224172
                25381364
                fb29b44e-6c98-4f34-b41c-cc643851a67b
                Copyright © 2014 by the Genetics Society of America

                Available freely online through the author-supported open access option.

                History
                : 12 May 2014
                : 15 August 2014
                Page count
                Pages: 41
                Categories
                YeastBook
                Genome Organization and Integrity

                Genetics
                recombination,repair,budding yeast
                Genetics
                recombination, repair, budding yeast

                Comments

                Comment on this article

                scite_
                0
                0
                0
                0
                Smart Citations
                0
                0
                0
                0
                Citing PublicationsSupportingMentioningContrasting
                View Citations

                See how this article has been cited at scite.ai

                scite shows how a scientific paper has been cited by providing the context of the citation, a classification describing whether it supports, mentions, or contrasts the cited claim, and a label indicating in which section the citation was made.

                Similar content544

                Cited by169

                Most referenced authors4,135