The choice in meiosis - defining the factors that influence crossover or non-crossover formation

被引:119
作者
Youds, Jillian L. [1 ]
Boulton, Simon J. [1 ]
机构
[1] Canc Res UK, London Res Inst, DNA Damage Response Lab, S Mimms EN6 3LD, Herts, England
关键词
DSB repair; Meiosis; Crossover control; Homologous recombination; DOUBLE-STRAND BREAK; HOLLIDAY JUNCTION RESOLVASE; MEIOTIC RECOMBINATION HOTSPOTS; SYNAPTONEMAL COMPLEX-FORMATION; HOMOLOGOUS CHROMOSOME SYNAPSIS; STRUCTURE-SPECIFIC NUCLEASES; HELICASE-LIKE PROTEIN; CAENORHABDITIS-ELEGANS; CROSSING-OVER; SACCHAROMYCES-CEREVISIAE;
D O I
10.1242/jcs.074427
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Meiotic crossovers are essential for ensuring correct chromosome segregation as well as for creating new combinations of alleles for natural selection to take place. During meiosis, excess meiotic double-strand breaks (DSBs) are generated; a subset of these breaks are repaired to form crossovers, whereas the remainder are repaired as non-crossovers. What determines where meiotic DSBs are created and whether a crossover or non-crossover will be formed at any particular DSB remains largely unclear. Nevertheless, several recent papers have revealed important insights into the factors that control the decision between crossover and non-crossover formation in meiosis, including DNA elements that determine the positioning of meiotic DSBs, and the generation and processing of recombination intermediates. In this review, we focus on the factors that influence DSB positioning, the proteins required for the formation of recombination intermediates and how the processing of these structures generates either a crossover or non-crossover in various organisms. A discussion of crossover interference, assurance and homeostasis, which influence crossing over on a chromosome-wide and genome-wide scale - in addition to current models for the generation of interference - is also included. This Commentary aims to highlight recent advances in our understanding of the factors that promote or prevent meiotic crossing over.
引用
收藏
页码:501 / 513
页数:13
相关论文
共 148 条
[1]   BRC-1 acts in the inter-sister pathway of meiotic double-strand break repair [J].
Adamo, Adele ;
Montemauri, Paolo ;
Silva, Nicola ;
Ward, Jordan D. ;
Boulton, Simon J. ;
La Volpe, Adriana .
EMBO REPORTS, 2008, 9 (03) :287-292
[2]   Zip3 provides a link between recombination enzymes and synaptonemal complex proteins [J].
Agarwal, S ;
Roeder, GS .
CELL, 2000, 102 (02) :245-255
[3]   Differential timing and control of noncrossover and crossover recombination during meiosis [J].
Allers, T ;
Lichten, M .
CELL, 2001, 106 (01) :47-57
[4]   Drosophila MUS312 and the Vertebrate Ortholog BTBD12 Interact with DNA Structure-Specific Endonucleases in DNA Repair and Recombination [J].
Andersen, Sabrina L. ;
Bergstralh, Daniel T. ;
Kohl, Kathryn P. ;
LaRocque, Jeannine R. ;
Moore, Chris B. ;
Sekelsky, Jeff .
MOLECULAR CELL, 2009, 35 (01) :128-135
[5]  
Anderson LK, 1999, GENETICS, V151, P1569
[6]  
[Anonymous], 1988, NEMATODE CAENORHABDI
[7]   Competing crossover pathways act during meiosis in Saccharomyces cerevisiae [J].
Argueso, JL ;
Wanat, J ;
Gemici, Z ;
Alani, E .
GENETICS, 2004, 168 (04) :1805-1816
[8]   The Caenorhabditis elegans Homolog of Gen1/Yen1 Resolvases Links DNA Damage Signaling to DNA Double-Strand Break Repair [J].
Bailly, Aymeric P. ;
Freeman, Alasdair ;
Hall, Julie ;
Declais, Anne-Cecile ;
Alpi, Arno ;
Lilley, David M. J. ;
Ahmed, Shawn ;
Gartner, Anton .
PLOS GENETICS, 2010, 6 (07) :1-16
[9]   RTEL1 Maintains Genomic Stability by Suppressing Homologous Recombination [J].
Barber, Louise J. ;
Youds, Jillian L. ;
Ward, Jordan D. ;
McIlwraith, Michael J. ;
O'Neil, Nigel J. ;
Petalcorin, Mark I. R. ;
Martin, Julie S. ;
Collis, Spencer J. ;
Cantor, Sharon B. ;
Auclair, Melissa ;
Tissenbaum, Heidi ;
West, Stephen C. ;
Rose, Ann M. ;
Boulton, Simon J. .
CELL, 2008, 135 (02) :261-271
[10]   The mechanism of Mus81-Mms4 cleavage site selection distinguishes it from the homologous endonuclease Rad1-Rad10 [J].
Bastin-Shanower, SA ;
Fricke, WM ;
Mullen, JR ;
Brill, SJ .
MOLECULAR AND CELLULAR BIOLOGY, 2003, 23 (10) :3487-3496