Inter-homolog crossing-over and synapsis in Arabidopsis meiosis are dependent on the chromosome axis protein AtASY3.
Inter-homolog crossing-over and synapsis in Arabidopsis meiosis are dependent on the chromosome axis protein AtASY3.
复制标题
拟南芥减数分裂中的血间交叉和突触取决于染色体轴蛋白ATASY3。
DOI:
10.1371/journal.pgen.1002507
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发表时间:
2012-02
期刊:
影响因子:
4.5
通讯作者:
Franklin FC
中科院分区:
文献类型:
--
作者:
Ferdous M;Higgins JD;Osman K;Lambing C;Roitinger E;Mechtler K;Armstrong SJ;Perry R;Pradillo M;Cuñado N;Franklin FC
In this study we have analysed AtASY3, a coiled-coil domain protein that is required for normal meiosis in Arabidopsis. Analysis of an Atasy3-1 mutant reveals that loss of the protein compromises chromosome axis formation and results in reduced numbers of meiotic crossovers (COs). Although the frequency of DNA double-strand breaks (DSBs) appears moderately reduced in Atasy3-1, the main recombination defect is a reduction in the formation of COs. Immunolocalization studies in wild-type meiocytes indicate that the HORMA protein AtASY1, which is related to Hop1 in budding yeast, forms hyper-abundant domains along the chromosomes that are spatially associated with DSBs and early recombination pathway proteins. Loss of AtASY3 disrupts the axial organization of AtASY1. Furthermore we show that the AtASY3 and AtASY1 homologs BoASY3 and BoASY1, from the closely related species Brassica oleracea, are co-immunoprecipitated from meiocyte extracts and that AtASY3 interacts with AtASY1 via residues in its predicted coiled-coil domain. Together our results suggest that AtASY3 is a functional homolog of Red1. Since studies in budding yeast indicate that Red1 and Hop1 play a key role in establishing a bias to favor inter-homolog recombination (IHR), we propose that AtASY3 and AtASY1 may have a similar role in Arabidopsis. Loss of AtASY3 also disrupts synaptonemal complex (SC) formation. In Atasy3-1 the transverse filament protein AtZYP1 forms small patches rather than a continuous SC. The few AtMLH1 foci that remain in Atasy3-1 are found in association with the AtZYP1 patches. This is sufficient to prevent the ectopic recombination observed in the absence of AtZYP1, thus emphasizing that in addition to its structural role the protein is important for CO formation. Homologous recombination (HR) during prophase I of meiosis leads to the formation of physical connections, known as chiasmata, between homologous chromosomes (homologs). Chiasmata are essential for accurate homolog segregation at the first meiotic division. HR is initiated by the formation of DNA double-strand breaks (DSBs). As DNA replication prior to meiosis results in the duplication of each homolog to form two identical sister chromatids, a DSB in one sister chromatid could potentially be repaired using the other as the repair template rather than one of the two non-sister chromatids of the homolog. If this route were predominant, the formation of chiasmata would be disfavored and chromosome segregation would be compromised. However, during meiosis there is a strong bias towards inter-homolog recombination (IHR). In this study we have identified AtASY3, a component of the proteinaceous axes that organize the chromosomes during meiosis in Arabidopsis. We find that AtASY3 interacts with AtASY1, a previously identified axis protein that is essential for crossover formation. We show that loss of AtASY3 disrupts the axis-organization of AtASY1. This results in a substantial reduction in chiasmata, and there is extensive chromosome mis-segregation. We propose that loss of AtASY3 affects the efficiency of the inter-homolog bias.
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