The Arabidopsis MutS homolog AtMSH5 is required for normal meiosis

Lu, Xiaoduo; Liu, Xiaolin; An, Lizhe; Zhang, Wei; Sun, Jian; Pei, Huijuan; Meng, Huaqing; Fan, Yanting; Zhang, Chunyi

doi:10.1038/cr.2008.44

Cited by 42 publications

(40 citation statements)

References 38 publications

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“…Copenhaver et al (2002) were able to fit Arabidopsis data to a counting model for interference (Foss et al 1993) if they assumed two types of crossovers: some that participate in interference and some that do not. Consistent with this prediction, experimental studies demonstrated that the residual crossovers in Arabidopsis and budding yeast msh4 and msh5 mutants do not display interference (Novak et al 2001;Argueso et al 2004;Higgins et al 2004;Lu et al 2008), as predicted by Zalevsky et al (1999). Conversely, Mus81-Mms4-independent crossovers in S. cerevisiae and Arabidopsis do exhibit interference (de los Santos et al 2003;Berchowitz et al 2007).…”

Section: Rise Of the Two-pathway Paradigmsupporting

confidence: 60%

Meiotic and Mitotic Recombination in Meiosis

Kohl

Sekelsky

2013

Genetics

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Meiotic crossovers facilitate the segregation of homologous chromosomes and increase genetic diversity. The formation of meiotic crossovers was previously posited to occur via two pathways, with the relative use of each pathway varying between organisms; however, this paradigm could not explain all crossovers, and many of the key proteins involved were unidentified. Recent studies that identify some of these proteins reinforce and expand the model of two meiotic crossover pathways. The results provide novel insights into the evolutionary origins of the pathways, suggesting that one is similar to a mitotic DNA repair pathway and the other evolved to incorporate special features unique to meiosis. MEIOSIS is essential to maintaining the proper complement of chromosomes in sexually reproducing organisms. By following one round of DNA replication with two rounds of cellular division, meiosis effectively halves the chromosome content of participating cells. Prior to the first meiotic division, homologous chromosomes pair and, in many organisms, undergo recombination. Both crossovers, characterized by the reciprocal exchange of flanking markers, and noncrossovers, in which flanking DNA remains unchanged, result from these recombination events. Crossovers can also occur in mitotically proliferating cells during repair of certain types of DNA damage, especially double-strand breaks. Meiotic crossovers likewise are initiated from double-strand breaks, and many of the proteins used in mitotic repair are also used in meiotic recombination. This has led to the suggestion that meiotic recombination evolved from mitotic recombination (Marcon and Moens 2005). However, several modifications were necessary to give rise to meiotic recombination in its current form (reviewed in Villeneuve and Hillers 2001). First, a mechanism of generating programmed double-strand breaks to initiate recombination was needed. This was achieved through the use of Spo11, a conserved protein that generates regulated meiotic double-strand breaks (Keeney et al. 1997). Second, whereas crossovers are avoided in mitotic cells to prevent loss of heterozygosity and chromosome rearrangement, crossover formation is emphasized in meiotic recombination to facilitate the segregation of homologous chromosomes and to increase genetic diversity. Third, the preferred repair template was changed from the sister chromatid in mitotic cells to the homologous chromosome in meiotic cells, since only crossovers between homologs give the aforementioned benefits. Finally, exquisite crossover control mechanisms arose to regulate the number and distribution of crossovers across the genome and relative to one another. In particular, every chromosome pair receives at least one crossover, sometimes called an obligate crossover (Jones 1984). Also, if additional crossovers occur, they tend not to be near one another, a phenomenon called crossover interference (reviewed in Berchowitz and Copenhaver 2010).A complication obscuring the relationship between the mitotic and meiot...

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Section: Rise Of the Two-pathway Paradigmsupporting

confidence: 60%

Meiotic and Mitotic Recombination in Meiosis

Kohl

Sekelsky

2013

Genetics

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“…We next analyzed a fancm-1 msh4-1 double mutant. Although SC formation is normal, albeit delayed, in a msh4-1 mutant, loss of the gene results in a strong reduction in fertility due to a dramatic reduction in CO formation (Higgins et al, 2004(Higgins et al, , 2008bLu et al, 2008). Surprisingly, fancm-1 msh4-1 homozygous plants produced considerably more seeds per silique than msh4-1 (19.88 versus 4.0, respectively), although this was not as high as fancm-1 (41.36).…”

Section: Analysis Of At-fancm Function Within Meiotic Pathwaysmentioning

confidence: 78%

The Fanconi Anemia Ortholog FANCM Ensures Ordered Homologous Recombination in Both Somatic and Meiotic Cells in Arabidopsis

et al. 2012

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The human hereditary disease Fanconi anemia leads to severe symptoms, including developmental defects and breakdown of the hematopoietic system. It is caused by single mutations in the FANC genes, one of which encodes the DNA translocase FANCM (for Fanconi anemia complementation group M), which is required for the repair of DNA interstrand cross-links to ensure replication progression. We identified a homolog of FANCM in Arabidopsis thaliana that is not directly involved in the repair of DNA lesions but suppresses spontaneous somatic homologous recombination via a RecQ helicase (At-RECQ4A)-independent pathway. In addition, it is required for double-strand break-induced homologous recombination. The fertility of Atfancm mutant plants is compromised. Evidence suggests that during meiosis At-FANCM acts as antirecombinase to suppress ectopic recombination-dependent chromosome interactions, but this activity is antagonized by the ZMM pathway to enable the formation of interference-sensitive crossovers and chromosome synapsis. Surprisingly, mutation of At-FANCM overcomes the sterility phenotype of an At-MutS homolog4 mutant by apparently rescuing a proportion of crossover-designated recombination intermediates via a route that is likely At-MMS and UV sensitive81 dependent. However, this is insufficient to ensure the formation of an obligate crossover. Thus, At-FANCM is not only a safeguard for genome stability in somatic cells but is an important factor in the control of meiotic crossover formation.

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“…However, the functions of these proteins for SC assembly are divergent in other organisms. In Arabidopsis, no apparent defects in chromosome synapsis are observed in msh5 and zip4 mutants (Chelysheva et al, 2007;Higgins et al, 2008;Lu et al, 2008). In the msh4 mutant, chromosome synapsis might be incomplete but the defects are not severe (Higgins et al, 2004).…”

Section: Introductionmentioning

confidence: 97%

The Role of ZIP4 in Homologous Chromosome Synapsis and Crossover Formation in Rice Meiosis

Shen

Tang

Wang

et al. 2012

Journal of Cell Science

124

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SummaryIn budding yeast, the ZMM complex is closely associated with class I crossovers and synaptonemal complex (SC) formation. However, the relationship between the ZMM genes remains unclear in most higher eukaryotes. Here, we identify the rice ZIP4 homolog, a member of the ZMM gene group, and explore its relationship with two other characterized ZMM genes, MER3 and ZEP1. Our results show that in the rice zip4 mutant, the chiasma frequency is greatly reduced, although synapsis proceeds with only mild defects. Immunocytological analyses of wild-type rice reveal that ZIP4 presents as punctuate foci and colocalizes with MER3 in prophase I meiocytes. Additionally, ZIP4 is essential for the loading of MER3 onto chromosomes, but not vice versa. Double-mutant analyses show that zip4 mer3 displays a greater decrease in the mean number of chiasmata than either of the zip4 or mer3 single mutants, suggesting that ZIP4 and MER3 work cooperatively to promote CO formation but their individual contributions are not completely identical in rice. Although zep1 alone gives an increased chiasma number, both zip4 zep1 and mer3 zep1 show a much lower chiasma number than the zip4 or mer3 single mutants. These results imply that the normal functions of ZIP4 and MER3 are required for the regulation of COs by ZEP1.

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The Arabidopsis MutS homolog AtMSH5 is required for normal meiosis

Cited by 42 publications

References 38 publications

Meiotic and Mitotic Recombination in Meiosis

Meiotic and Mitotic Recombination in Meiosis

The Fanconi Anemia Ortholog FANCM Ensures Ordered Homologous Recombination in Both Somatic and Meiotic Cells in Arabidopsis

The Role of ZIP4 in Homologous Chromosome Synapsis and Crossover Formation in Rice Meiosis

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