RAD51-dependent break-induced replication in yeast.

Mol Cell Biol

Department of Microbiology and Institute of Cancer Research, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA.

Published: March 2004

AI Article Synopsis

  • A chromosome fragmentation assay in Saccharomyces cerevisiae revealed high efficiency of break-induced replication (BIR) involving telomere generation and recombination over 100 kb of chromosomal sequences.
  • RAD51 plays a crucial role in over 95% of BIR events and is essential for creating chromosome fragments through single-end and two-event processes.
  • The study found that RAD52 is essential for BIR at unique sequences, while mutations in RAD50 or RAD59 did not significantly affect BIR efficacy in both RAD51 and rad51 strains.

Article Abstract

A chromosome fragmentation assay was used to measure the efficiency and genetic control of break-induced replication (BIR) in Saccharomyces cerevisiae. Formation of a chromosome fragment by de novo telomere generation at one end of the linear vector and recombination-dependent replication of 100 kb of chromosomal sequences at the other end of the vector occurred at high frequency in wild-type strains. RAD51 was required for more than 95% of BIR events involving a single-end invasion and was essential when two BIR events were required for generation of a chromosome fragment. The similar genetic requirements for BIR and gene conversion suggest a common strand invasion intermediate in these two recombinational repair processes. Mutation of RAD50 or RAD59 conferred no significant defect in BIR in either RAD51 or rad51 strains. RAD52 was shown to be essential for BIR at unique chromosomal sequences, although rare recombination events were detected between the subtelomeric Y' repeats.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC355873PMC
http://dx.doi.org/10.1128/MCB.24.6.2344-2351.2004DOI Listing

Publication Analysis

Top Keywords

break-induced replication
8
chromosome fragment
8
chromosomal sequences
8
bir events
8
essential bir
8
bir
6
rad51-dependent break-induced
4
replication yeast
4
yeast chromosome
4
chromosome fragmentation
4

Similar Publications

Mechanisms of tandem duplication in the cancer genome.

DNA Repair (Amst)

December 2024

Department of Data Science, Dana-Farber Cancer Institute, Boston, MA 02115, USA; Department of Pathology, Harvard Medical School, Boston, MA 02115,  USA; Broad Institute of Massachusetts Institute of Technology and Harvard, Cambridge, MA 02142, USA.

Tandem duplications (TD) are among the most frequent type of structural variant (SV) in the cancer genome. They are characterized by a single breakpoint junction that defines the boundaries and the size of the duplicated segment. Cancer-associated TDs often increase oncogene copy number or disrupt tumor suppressor gene function, and thus have important roles in tumor evolution.

View Article and Find Full Text PDF

Nonrecurrent Triplication of 5q21.3q23.3: A Case Report and Review of the Literature.

Am J Med Genet A

December 2024

Division of Medical Genetics and Genomics, Stead Family Department of Pediatrics, University of Iowa Health Care, Iowa City, Iowa, USA.

Triplications involving 5q21.3q23.3 are rare, and a phenotype has not been established.

View Article and Find Full Text PDF

Two-ended recombination at a Flp-nickase-broken replication fork.

Mol Cell

January 2025

Department of Medicine, Division of Hematology-Oncology and Cancer Research Institute, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA. Electronic address:

Replication fork collision with a DNA nick can generate a one-ended break, fostering genomic instability. The opposing fork's collision with the nick could form a second DNA end, enabling conservative repair by homologous recombination (HR). To study mechanisms of nickase-induced HR, we developed the Flp recombinase "step arrest" nickase in mammalian cells.

View Article and Find Full Text PDF

All cells are commonly exposed to DNA double-strand breaks (DSBs), which must be properly repaired to avoid genomic instability. Break-Induced Replication (BIR) is a Homologous Recombination subpathway, which repairs DSBs resulting in mutagenesis, chromosome translocations and loss of heterozygosity. In budding yeast, the Srs2 DNA helicase/translocase plays both anti- and pro-recombination roles.

View Article and Find Full Text PDF

DNA nicks in both leading and lagging strand templates can trigger break-induced replication.

Mol Cell

January 2025

Department of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, UK. Electronic address:

Article Synopsis
  • Replication forks encountering unrepaired single-strand breaks (SSBs) can lead to both single-ended (seDSBs) and double-ended double-strand breaks (deDSBs), which are significant in cancer development.
  • The study reveals that in fission yeast, SSBs typically result in deDSBs repaired by homologous recombination, but can also initiate break-induced replication (BIR).
  • The occurrence of BIR is more frequent when DNA replication fork convergence is delayed and the Ku70 protein, involved in non-homologous end joining, is absent.
View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!