The transcriptional
program of sporulation involves the sequential induction of temporally
distinct classes of genes. Genes induced when cells are exiting
meiotic prophase and entering the chromosomal divisions (middle genes)
are activated by the Ndt80 DNA binding protein that specifically
recognizes a promoter element termed the MSE. A subset of middle genes
are repressed in mitotic cells by the Sum1 DNA binding protein that
also specifically recognizes the MSE (Xie et al. 1999, EMBO J.
18:6448-54). Failure to complete meiotic recombination as observed in
a dmc1 mutant, blocks the nuclear divisions (the pachytene
checkpoint). Here we show that this block requires Sum1 as dmc1
sum1 double mutants undergo both nuclear divisions. In a sum1
dmc1 diploid, Sum1-repressible genes are expressed constitutively
throughout meiosis and middle gene induction does not occur. In
contrast, middle genes are induced when the dmc1 arrest is
relieved by deletion of the RAD17 cell cycle checkpoint
gene. Although the dmc1 sum1 and the dmc1 rad17 double
mutants complete both nuclear divisions, they fail to complete spore
morphogenesis. In contrast, a dmc1 sum1 rad17 triply mutant
strain undergoes meiosis and forms morphologically normal spores. The
results suggest that when recombination is blocked, Sum1 and Rad17
arrest meiotic progression by different pathways. Both pathways are
required to arrest the meiotic divisions; either pathway is sufficient
to prevent spore morphogenesis.
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