ABSTRACT & LINKS
Franklin AE, Golubovskaya IN, Bass HW, and Cande WZ (2003).
Improper chromosome synapsis is associated with elongated
RAD51 structures in the maize desynaptic2 mutant
The RecA homolog, RAD51, performs a central role in catalyzing the DNA
strand exchange event of meiotic recombination. During meiosis RAD51
complexes develop on pairing chromosomes and then most disappear upon
synapsis. In the maize meiotic mutant desynaptic2 (dsy2), homologous
chromosome pairing and recombination are reduced by ~70% in male meiosis.
Fluorescent in situ hybridization studies demonstrate that a normal
telomere bouquet develops but the pairing of a representative gene locus
is still only 25%. Chromosome synapsis is aberrant as exemplified by
unsynapsed regions of the chromosomes. In the mutant we observed unusual
RAD51 structures during chromosome pairing. Instead of spherical single
and double RAD51 structures, we saw long thin filaments that extended
along or around a single chromosome or stretched between two widely
separated chromosomes. Mapping with simple sequence repeat (SSR) markers
places the dsy2 gene to near the centromere on chromosome 5, therefore it
is not an allele of rad51. Thus, the normal dsy2 gene product is required
for both homologous chromosome synapsis and proper RAD51 filament behavior
when chromosomes pair.
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