Mutations in many different genes result in an unusually high incidence of male self-progeny due to meiotic loss of the X-chromosome. Of these, the most extreme are mutations in
him-8 (40% male self-progeny) and
him-5 (up to 35% male self-progeny). Genetic and cytological evidence indicates that
him-8 affects the X chromosome exclusively during meiosis, whereas
him-5 affects the X much more strongly than the autosomes, but does affect the autosomes. Both
him-5 and
him-8 greatly reduce the number of crossovers on the X chromosome, and affect the location of the residual crossovers. In other organisms, these have been termed "pre-condition" mutants or "crossover control" mutants but the molecular mechanism is obscure. We have been carrying out a molecular analysis of the
him-8 and
him-5 loci, beginning with transformation rescue experiments, and including cDNA isolation, RT-PCR, northerns, sequencing wild-type and mutant strains, and most recently RNAi experiments (which we hope to have done by the meeting). The molecular structure of the
him-8 locus is complex, frustrating, and unresolved at this point. Although much less studied than
him-8, the
him-5 locus appears to be much simpler, and the predicted protein is very small (143 amino acids) and very basic (predicted pI of 10.5) with no homology to other known proteins. Some models for genes involved in crossover control predict that they might affect the structure of meiotic chromosomes, and the putative HIM-5 protein would not discourage such speculation.