Abstract

During meiosis, the establishment of cohesion between sister chromatids and other meiotic events such as homologous chromosome pairing, synaptonemal complex formation and recombination are essential. A T-DNA insertional line (dsy10) was previously identified as a male and female sterile mutant that exhibited a desynaptic phenotype (Cai and Makaroff, 2001). We have isolated the gene associated with the dsy10 mutation and shown that it is allelic to the previously isolated swi1 and dyad mutations. Interestingly, the various mutations exhibit considerably different phenotypes. DAPI spreads and FISH studies demonstrate pairing of homologous chromosomes in the dsy10 mutant. However, ten univalent chromosomes were observed at diakinesis suggesting that no recombination occurred. This was confirmed by the absence of RAD51 foci in the dsy10 mutant. There was an early disassociation of the axial element protein, ASY1, consistent with a defect in the synaptonemal complex formation. We also observed the disassociation of the SYN1 and SMC3 cohesin proteins from the chromosomes at pachytene, indicating an early release of sister chromatid cohesin. We demonstrate through expression analysis the absence of SWI1 transcripts in the dsy10 mutant. Antibodies specific to the N- and the C-terminus of DSY10/SWI1, also failed to detect SWI1 in the dsy10 mutant. In contrast, we detected SWI1 in the swi1.2 mutant using the N-terminus antibody. This and other observations made by Mercier, et al, 2003, suggest that the swi1.2 mutation exhibits a recessive dominant effect. Based on these observations, we speculate that the DSY10 protein may be required for the establishment of sister chromatid cohesion that is essential for synapsis and recombination. This project was supported by a grant from NSF (MCB – 0322171).

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