Meiotic crossovers are limited in number and are prevented from occurring close to each other by crossover interference. In many species, crossover number is subject to sexual dimorphism, and a lower crossover number is associated with shorter chromosome axes lengths. How this patterning is imposed remains poorly understood. Here, we show that overexpression of the Arabidopsis pro-crossover protein HEI10 increases crossovers but maintains some interference and sexual dimorphism. Disrupting the synaptonemal complex by mutating ZYP1 also leads to an increase in crossovers but, in contrast, abolishes interference and disrupts the link between chromosome axis length and crossovers. Crucially, combining HEI10 overexpression and zyp1 mutation leads to a massive and unprecedented increase in crossovers. These observations support and can be predicted by, a recently proposed model in which HEI10 diffusion along the synaptonemal complex drives a coarsening process leading to well-spaced crossover-promoting foci, providing a mechanism for crossover patterning.

Radiation sensitive 51 (RAD51) recombinases play crucial roles in meiotic double-strand break (DSB) repair mediated by homologous recombination (HR) to ensure the correct segregation of homologous chromosomes. In this study, we identified the meiotic functions of ZmRAD51C, the maize homolog of Arabidopsis and rice RAD51C. The Zmrad51c mutants exhibited regular vegetative growth but complete sterility for both male and female inflorescence. However, the mutants showed hypersensitivity to DNA damage by mitomycin C. Cytological analysis indicated that homologous chromosome pairing and synapsis were rigorously inhibited, and meiotic chromosomes were often entangled from diplotene to metaphase I, leading to chromosome fragmentation at anaphase I. Immunofluorescence analysis showed that although the signals of the axial element absence of first division (AFD1) and asynaptic1 (ASY1) were normal, the assembly of the central element zipper1 (ZYP1) was severely disrupted. The DSB formation was normal in Zmrad51c meiocytes, symbolized by the regular occurrence of γH2AX signals. However, RAD51 and disrupted meiotic cDNA 1 (DMC1) signals were never detected at the early stage of prophase I in the mutant. Taken together, our results indicate that ZmRAD51C functions crucially for both meiotic DSB repair and homologous recombination in maize.

The dual roles of the topoisomerase-encoding MTOPVIB in meiotic double-strand break formation and bipolar spindle assembly and are evolutionarily conserved in m

CtIP/Ctp1/Sae2/Com1, a highly conserved protein from yeast to higher eukaryotes, is required for DNA double-strand break repair through homologous recombination. In this study, we identified and characterized the COM1 homolog in maize. The ZmCom1 gene is abundantly expressed in reproductive tissues at meiosis stages. In ZmCom1-deficient plants, meiotic chromosomes are constantly entangled as a formation of multivalents and accompanied with chromosome fragmentation at anaphase I. In addition, the formation of telomere bouquet, homologous pairing and synapsis were disturbed. The immunostaining assay showed that the localization of ASY1 and DSY2 was normal, while ZYP1 signals were severely disrupted in Zmcom1 meiocytes, indicating that ZmCom1 is critically required for the proper SC assembly. Moreover, RAD51 signals were almost completely absent in Zmcom1 meiocytes, implying that COM1 is required for RAD51 loading. Surprisingly, in contrast to the Atcom1 and Oscom1 mutants, Zmcom1 mutant plants exhibited a number of vegetative phenotypes under normal growth condition, which may be partly attributed to mitotic aberrations including chromosomal fragmentation and anaphase bridges. Taken together, our results suggest that although the roles of COM1 in homologous recombination process seem to be primarily conserved，the COM1 dysfunction can result in the marked dissimilarity in mitotic and meiotic outcomes in maize compared to Arabidopsis and rice. We suggest that this character may be related to the discrete genome context.

Sexual dysmorphism in the number and distribution of meiotic crossovers is seen across species but is poorly understood. Here, we disrupt multiple anti-crossover pathways in hermaphrodite Arabidopsis and analyze thousands of female and male progeny genomes. The greatest crossover increase is seen in zyp1 recq4 mutants, with a 12-fold rise in females and 4.5-fold in males. Additional manipulation of crossover regulators does not further increase crossovers but shifts the balance between crossover pathways, suggesting competition for a shared, limited precursor pool. While wild-type crossover patterns differ between sexes, mutant crossover landscapes converge on a unique distinct profile, which we term Crossover Potential (CO_P). CO_P can be accurately predicted using only sequence and chromatin features. We propose that CO_P reflects the density of eligible recombination precursors, which is determined by genomic features and is thus identical across sexes, with sexual dimorphism resulting solely from differential regulation of their maturation into crossovers.