Studies on crossover-specific mutants and the distribution of crossing over in &lt;i&gt;Drosophila&lt;/i&gt; females

Bhagat, Rajal; Manheim, Elizabeth A.; Sherizen, Dalia; McKim, Kim S.

doi:10.1159/000080594

Cited by 37 publications

(43 citation statements)

References 29 publications

(49 reference statements)

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“…This is a lower frequency than that in previous studies, in which the frequency of PMS in NCOs from mei-9 mutants was 60-100% (Romans 1980b;Carpenter 1982;Bhagat et al 2004). We considered several possible explanations for the different results.…”

Section: Discussionmentioning

confidence: 54%

“…The average length of GC tracts among NCOs is lower in rec mutants than in wild type, suggesting that REC facilitates repair synthesis during meiotic recombination and that, as is thought to be the case in S. cerevisiae, most NCOs in Drosophila arise through SDSA. Mutations in mei-9 have a different effect on NCOs: they frequently exhibit postmeiotic segregation (PMS) (Romans 1980b;Hilliker and Chovnick 1981;Carpenter 1982Carpenter , 1984Bhagat et al 2004). PMS arises from a failure to repair heterologies in hDNA, resulting in sister chromatids containing different sequence information after the first round of postmeiotic replication.…”

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confidence: 99%

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Heteroduplex DNA in Meiotic Recombination in Drosophila mei-9 Mutants

et al. 2007

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Meiotic recombination gives rise to crossovers, which are required in most organisms for the faithful segregation of homologous chromosomes during meiotic cell division. Characterization of crossoverdefective mutants has contributed much to our understanding of the molecular mechanism of crossover formation. We report here a molecular analysis of recombination in a Drosophila melanogaster crossover-defective mutant, mei-9. In the absence of mei-9 activity, postmeiotic segregation associated with noncrossovers occurs at the expense of crossover products, suggesting that the underlying meiotic function for MEI-9 is in crossover formation rather than mismatch repair. In support of this, analysis of the arrangement of heteroduplex DNA in the postmeiotic segregation products reveals different patterns from those observed in Drosophila Msh6 mutants, which are mismatch-repair defective. This analysis also provides evidence that the double-strand break repair model applies to meiotic recombination in Drosophila. Our results support a model in which MEI-9 nicks Holliday junctions to generate crossovers during meiotic recombination, and, in the absence of MEI-9 activity, the double Holliday junction intermediate instead undergoes dissolution to generate noncrossover products in which heteroduplex is unrepaired.

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Section: Discussionmentioning

confidence: 54%

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confidence: 99%

Heteroduplex DNA in Meiotic Recombination in Drosophila mei-9 Mutants

et al. 2007

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“…Whether the amount of resection influences crossover formation as well is not yet clear (Keelagher et al 2010;Zakharyevich et al 2010); however, in the absence of mei-218 or rec, the frequency of crossovers is dramatically reduced and the residual crossovers exhibit an even distribution, suggesting pericentric suppression of crossovers is also disrupted. One possibility is that the change in distribution is an indirect consequence of the crossover reduction, similar to the interchromosomal effect (Bhagat et al 2004). Alternatively, shorter gene conversion tracts may preferentially result in a noncrossover repair product while also creating an equal, yet low likelihood of crossover formation along the entirety of chromosome arms.…”

Section: Blocks To Nhej: the Precondition Gene Mei-218mentioning

confidence: 99%

“…Mutations in these genes reduce the frequency of crossovers without affecting DSB formation or the timing of their repair, indicating a specific defect in the ability to repair DSBs as crossovers (Carpenter 1982(Carpenter , 1984Blanton et al 2005;Joyce and McKim 2009). As such, precondition gene products have been proposed to establish which DSBs will become crossovers rather than to be directly involved in the repair machinery (Carpenter and Sandler 1974;Bhagat et al 2004). In this article, we describe new genetic interactions between the precondition gene mei-218 and DSB repair genes spn-D and spn-B, which are important for the suppression of the NHEJ repair pathway during meiosis.…”

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confidence: 97%

Multiple Barriers to Nonhomologous DNA End Joining During Meiosis inDrosophila

Joyce¹,

Paul

Chen

et al. 2012

Genetics

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Repair of meiotic double-strand breaks (DSBs) uses the homolog and recombination to yield crossovers while alternative pathways such as nonhomologous end joining (NHEJ) are suppressed. Our results indicate that NHEJ is blocked at two steps of DSB repair during meiotic prophase: first by the activity of the MCM-like protein MEI-218, which is required for crossover formation, and, second, by Rad51-related proteins SPN-B (XRCC3) and SPN-D (RAD51C), which physically interact and promote homologous recombination (HR). We further show that the MCM-like proteins also promote the activity of the DSB repair checkpoint pathway, indicating an early requirement for these proteins in DSB processing. We propose that when a meiotic DSB is formed in the absence of both MEI-218 and SPN-B or SPN-D, a DSB substrate is generated that can enter the NHEJ repair pathway. Indeed, due to its high error rate, multiple barriers may have evolved to prevent NHEJ activity during meiosis.

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“…These data suggest that a defect often increased in this region in mutants that reduce crossing over in most other regions (Baker et al 1976; unrelated to homolog pairing should be considered as the cause of crossover suppression. Indeed, since Carpenter 1988; Bhagat et al 2004). Crossovers in proximal regions may also exhibit positive interference Drosophila homologs enter meiotic prophase already paired, there may be no need to propose the existence (Green 1975;Sinclair 1975;Denell and Keppy 1979).…”

Section: T(3;4)pmentioning

confidence: 99%

Meiotic Recombination in Drosophila Females Depends on Chromosome Continuity Between Genetically Defined Boundaries

et al. 2005

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In the pairing-site model, specialized regions on each chromosome function to establish meiotic homolog pairing. Analysis of these sites could provide insights into the mechanism used by Drosophila females to form a synaptonemal complex (SC) in the absence of meiotic recombination. These specialized sites were first established on the X chromosome by noting that there were barriers to crossover suppression caused by translocation heterozygotes. These sites were genetically mapped and proposed to be pairing sites. By comparing the cytological breakpoints of third chromosome translocations to their patterns of crossover suppression, we have mapped two sites on chromosome 3R. We have performed experiments to determine if these sites have a role in meiotic homolog pairing and the initiation of recombination. Translocation heterozygotes exhibit reduced gene conversion within the crossover-suppressed region, consistent with an effect on the initiation of meiotic recombination. To determine if homolog pairing is disrupted in translocation heterozygotes, we used fluorescent in situ hybridization to measure the extent of homolog pairing. In wild-type oocytes, homologs are paired along their entire lengths prior to accumulation of the SC protein C(3)G. Surprisingly, translocation heterozygotes exhibited homolog pairing similar to wild type within the crossover-suppressed regions. This result contrasted with our observations of c(3)G mutant females, which were found to be defective in pairing. We propose that each Drosophila chromosome is divided into several domains by specialized sites. These sites are not required for homolog pairing. Instead, the initiation of meiotic recombination requires continuity of the meiotic chromosome structure within each of these domains. M EIOTIC recombination usually occurs between sophila have supported the view that SC formation ocsimilar or identical sequences on homologous curs prior to DSB formation (Jang et al. 2003). chromosomes. In most organisms, at least part of the The presence of single-strand tails at DSB sites promeiotic recombination pathway occurs within the convides a mechanism for homology searching and chromotext of the synaptonemal complex (SC), which holds some alignment (Roeder 1997). In organisms like Droaligned homologous chromosomes together along their sophila and C. elegans, however, another mechanism entire lengths (von Wettstein et al. 1984). Surprisaside from recombination must exist to precisely align ingly, organisms can be classified into at least two types homolgous chromosomes during meiosis. Indeed, DSBon the basis of the relationship of double-strand-break independent mechanisms for aligning meiotic chromo-(DSB) formation to the SC. In Saccharomyces cerevisiae, somes appear to be widespread. Similar to Drosophila DSB formation occurs prior to, and is required for, SC and C. elegans, homolog pairing in fission yeast involves a formation (Padmore et al. 1991). A similar course of DSB-independent component (Ding et al. 2004). While events occurs in...

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Studies on crossover-specific mutants and the distribution of crossing over in <i>Drosophila</i> females

Cited by 37 publications

References 29 publications

Heteroduplex DNA in Meiotic Recombination in Drosophila mei-9 Mutants

Heteroduplex DNA in Meiotic Recombination in Drosophila mei-9 Mutants

Multiple Barriers to Nonhomologous DNA End Joining During Meiosis inDrosophila

Meiotic Recombination in Drosophila Females Depends on Chromosome Continuity Between Genetically Defined Boundaries

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