Producing haploid gametes is essential to the sexual cycle of all eukaryotes, yet control of the reductional division of meiosis is still poorly understood. The autosomal (IV) gene
him-8 specifically affects X-chromosome disjunction, and its predominant effect is during oogenesis (Hodgkin et al., Genetics 91: 67,1979).
him-8 mutants produce about 40% male progeny and, unlike other hims, have no concommitant increase in embryonic lethality (0.8%). We have shown that the canonical allele
el489 probably represents the null phenotype. A second phenotype of
him-8 mutations is a 90% reduction in recombination on the X (Hodgkin et al., 1979). Thus
him-8 affects recombination and disjunction of the X-chromosome, perhaps through a single event. We have more fully characterized the canonical allele
el489. To determine whether the reduction reported by Hodgkin et al. for the intervals
dpy-3-10n-2 and
lon-2-
unc-3 would be seen for all regions of the X, recombination was examined in small intervals along the length of the X in
el489 and control strains. Strikingly, initial results show that in
el489 hermaphrodites recombination is wild type ( or slightly elevated) between
unc1 and
dpy-3 at the extreme left end of the X, but is greatly reduced in other intervals. To determine whether this effect on recombination is characteristic of all alleles, two other
him-8 alleles are being tested. Herman et al. (Genetics 102: 379,1982) initially postulated that there is a pairing site on the X near unc-l.
him-8 could be affecting processivity or maintanance of chromsome synapsis from this initial site. Failed or improper synapsis could lead to decreased recombination and subsequent nondisjunction of homologs. Recombination along the X will also be tested in
him-5 and him-l to see whether this is a general consequence of genes affecting the X or speciflc to
him8. Double mutant analyses of
him-8 and him-l suggest that they affect disjunction via different pathways. Hodgkin et al. found this to be true for him-l and
him-5. Double mutant analyses of
him-8 and
him-5 are underway. We have also isolated a dominant him that produces greater than 20% males, has a small brood, is not associated with increased embryonic lethality, and maps to IV near
him-8. Three factor mapping is underway to map this mutation more finely. A dominant Him might be a novel function or a hypermorph; it is being tested over a deletion to to see how this effects the Him phenotype. We have also recovered a small deficiency that fails to complement
him-8 and
unc43, but complements
unc-24 and
dpy-20.
him-8 maps 0.05 mu right of
mec-3, which is on the physical map.
him-8 should therefore reside within a cosmid fairly close to that which contains
mec-3. A walk has been initiated using the absence of males from an injected
him-8 hermaphrodite as the screen. We hope to use a molecular genetic analysis of the gene
him-8, and its interactions with other him genes, to determine how a chromosome-specific disjunction system is generated, and to elucidate the general process of chromosome transmission.