J. Bahler et al., SACCHAROMYCES-CEREVISIAE CELLS LACKING THE HOMOLOGOUS PAIRING PROTEINP175(SEP1) ARREST AT PACHYTENE DURING MEIOTIC PROPHASE, Chromosoma, 103(2), 1994, pp. 129-141
Saccharomyces cerevisiae cells containing null mutations in the SEP1 g
ene, which encodes the homologous pairing and strand exchange protein
p175(SEP1), enter pachytene with a delay. They arrest uniformly at thi
s stage of meiotic prophase, probably revealing a checkpoint in the tr
ansition from pachytene to meiosis I. At the arrest point, the cells r
emain largely viable and are cytologically characterized by the duplic
ated but unseparated spindle pole bodies of equal size and by the pers
istence of the synaptonemal complex, a cytological marker for pachyten
e. In addition, fluorescence in situ hybridization revealed that in ar
rested mutant cells maximal chromatin condensation and normal homolog
pairing is achieved, typical for pachytene in wild type. A hallmark of
meiosis is the high level of homologous recombination, which was anal
yzed both genetically and physically. Formation and processing of the
double-strand break intermediate in meiotic recombination is achieved
prior to arrest. Physical intragenic (conversion) and intergenic (cros
sover) products are formed just prior to, or directly at, the arrest p
oint. Structural deficits in synaptonemal complex morphology, failure
to separate spindle pole bodies, and/or defects in prophase DNA metabo
lism might be responsible for triggering the observed arrest. The pach
ytene arrest in sep1 cells is likely to be regulatory, but is clearly
different from the RAD9 checkpoint in meiotic prophase, which occurs p
rior to the pachytene stage.