scholarly journals Chromosome breakage in yeast caused by sister-chromatid recombination in an integrated 2-micron plasmid

1982 ◽  
Vol 47 (6) ◽  
pp. 355-369 ◽  
Author(s):  
Steen Holmberg ◽  
Torsten Nilsson-Tillgren ◽  
Morten C. Kielland-Brandt ◽  
Jens G. Litske Petersen
Genetics ◽  
1999 ◽  
Vol 153 (2) ◽  
pp. 621-641 ◽  
Author(s):  
Dawn A Thompson ◽  
Franklin W Stahl

AbstractMeiotic exchange occurs preferentially between homologous chromatids, in contrast to mitotic recombination, which occurs primarily between sister chromatids. To identify functions that direct meiotic recombination events to homologues, we screened for mutants exhibiting an increase in meiotic unequal sister-chromatid recombination (SCR). The msc (meiotic sister-chromatid recombination) mutants were quantified in spo13 meiosis with respect to meiotic unequal SCR frequency, disome segregation pattern, sporulation frequency, and spore viability. Analysis of the msc mutants according to these criteria defines three classes. Mutants with a class I phenotype identified new alleles of the meiosis-specific genes RED1 and MEK1, the DNA damage checkpoint genes RAD24 and MEC3, and a previously unknown gene, MSC6. The genes RED1, MEK1, RAD24, RAD17, and MEC1 are required for meiotic prophase arrest induced by a dmc1 mutation, which defines a meiotic recombination checkpoint. Meiotic unequal SCR was also elevated in a rad17 mutant. Our observation that meiotic unequal SCR is elevated in meiotic recombination checkpoint mutants suggests that, in addition to their proposed monitoring function, these checkpoint genes function to direct meiotic recombination events to homologues. The mutants in class II, including a dmc1 mutant, confer a dominant meiotic lethal phenotype in diploid SPO13 meiosis in our strain background, and they identify alleles of UBR1, INP52, BUD3, PET122, ELA1, and MSC1-MSC3. These results suggest that DMC1 functions to bias the repair of meiosis-specific double-strand breaks to homologues. We hypothesize that the genes identified by the class II mutants function in or are regulators of the DMC1-promoted interhomologue recombination pathway. Class III mutants may be elevated for rates of both SCR and homologue exchange.


PLoS Genetics ◽  
2017 ◽  
Vol 13 (5) ◽  
pp. e1006781 ◽  
Author(s):  
Sandra Muñoz-Galván ◽  
María García-Rubio ◽  
Pedro Ortega ◽  
Jose F. Ruiz ◽  
Sonia Jimeno ◽  
...  

1992 ◽  
Vol 7 (1_suppl) ◽  
pp. S79-S82 ◽  
Author(s):  
Pinar T. Ozand ◽  
Manjula Waghray ◽  
Jay D. Cook ◽  
Kirtikant Sheth ◽  
Generoso G. Gascon

A 20-month-old infant with "silvery-blond" hair color, widespread confettilike depigmentation of the skin, and mental retardation was found to have, in lymphocytes and fibroblast cultures, increased spontaneous chromosome breaks and breaks induced by both mitomycin and γ-irradiation. The sister chromatid exchange frequency was normal. This child probably represents a new chromosome breakage syndrome. (J Child Neurol 1992;7(Suppl):S79-S82.)


Genes ◽  
2019 ◽  
Vol 10 (3) ◽  
pp. 232 ◽  
Author(s):  
Benoît Falquet ◽  
Ulrich Rass

Complete genome duplication in every cell cycle is fundamental for genome stability and cell survival. However, chromosome replication is frequently challenged by obstacles that impede DNA replication fork (RF) progression, which subsequently causes replication stress (RS). Cells have evolved pathways of RF protection and restart that mitigate the consequences of RS and promote the completion of DNA synthesis prior to mitotic chromosome segregation. If there is entry into mitosis with underreplicated chromosomes, this results in sister-chromatid entanglements, chromosome breakage and rearrangements and aneuploidy in daughter cells. Here, we focus on the resolution of persistent replication intermediates by the structure-specific endonucleases (SSEs) MUS81, SLX1-SLX4 and GEN1. Their actions and a recently discovered pathway of mitotic DNA repair synthesis have emerged as important facilitators of replication completion and sister chromatid detachment in mitosis. As RS is induced by oncogene activation and is a common feature of cancer cells, any advances in our understanding of the molecular mechanisms related to chromosome underreplication have important biomedical implications.


Oncogene ◽  
2000 ◽  
Vol 19 (53) ◽  
pp. 6176-6183 ◽  
Author(s):  
Ralph Scully ◽  
Nadine Puget ◽  
Katerina Vlasakova

1981 ◽  
Vol 24 (11) ◽  
pp. 1409-1413 ◽  
Author(s):  
Glenn K. Sherer ◽  
Barbara B. Jackson ◽  
E. Carwile Leroy

1995 ◽  
pp. 41-62 ◽  
Author(s):  
Thomas D. Petes ◽  
Patricia J. Pukkila

Sign in / Sign up

Export Citation Format

Share Document