GENETIC-STUDIES OF MEI-1 GENE ACTIVITY DURING THE TRANSITION FROM MEIOSIS TO MITOSIS IN CAENORHABDITIS-ELEGANS

Genetic evidence suggests that the mei-1 locus of Caenorhabditis elega ns encodes a maternal product required for female meiosis. However, a dominant gain-of-function allele, mei-1(ct46), can support normal meio sis but causes defects in subsequent mitotic spindles. Previously iden tified intragenic suppressors of ct46 lack functional mei-1 activity; null alleles suppress only in cis but other alleles arise frequently a nd suppress both in cis and in trans. Using a different screen for sup pressors of the dominant ct46 defect, the present study describes anot her type of intragenic mutation that also arises at high frequency. Th ese latter alleles appear to have reduced meiotic activity and retain a weakened dominant effect. Characterization of these alleles in trans -heterozygous combinations with previously identified mei-1 alleles ha s enabled us to define more clearly the role of the mei-1 gene product during normal embryogenesis. We propose that a certain level of mei-1 activity is required for meiosis but must be eliminated prior to mito sis. The dominant mutation causes mei-1 activity to function at mitosi s; intragenic trans-suppressors act in an antimorphic manner to inacti vate multimeric mei-1 complexes. We propose that inactivation of meios is-specific functions may be an essential precondition of mitosis; fai lure to eliminate such functions may allow ectopic meiotic activity du ring mitosis and cause embryonic lethality.