Worm Breeder's Gazette 14(3): 22 (June 1, 1996)
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
Dept. of Genetics, Washington University School of Medicine, St. Louis, MO 63110.
We are interested in the regulation of meiotic maturation and ovulation. At maturation, the oocyte cell cycle progresses from prophase to metaphase. At ovulation, the oocyte exits the gonad arm. In many species, maturation and ovulation are coupled. In several characterized C. elegans mutants with the Emo phenotype, maturation is not followed by normal ovulation and the mature oocyte is trapped in the gonad arm where it endomitotically replicates its DNA (Emo = endomitotic oocytes in the gonad arm). Genes with mutant alleles where defective ovulation leads to the Emo phenotype include emo-1 (1), lin-3 (2), let-23 (2), mup-2 (3), and ceh-18 (4). Ablation of the somatic sheath or spermatheca can also disrupt ovulation and cause the Emo phenotype (5). Ablation of the proximal myoepithelial sheath eliminates the contractions necessary to expel the oocyte from the arm. Ablation of the narrow distal spermatheca allows the oocyte to 'slip-back' from the spermatheca into the gonad arm following ovulation. We have isolated and mapped additional mutants with the Emo phenotype. Mutants were isolated in screens for recessive steriles and include: Gene, Allele, Chromosome emo-2(oz136), LG III emo-3(oz138), LG IV emo-5(oz148), LG II emo-6(oz154), LG III Emo(oz196), LG III Emo(oz197), LG V Emo(oz198), LG IV Emo(oz199), LG III Emo(oz200) (6), LG IV Some of the new emo mutants, such as oz136, oz154, and oz196, appear similar in their terminal phenotype to the previously characterized ovulation defective mutants with the Emo phenotype. Endomitotic figures are most prominent in the very proximal portion of the gonad. However, in other new emo mutants, such as oz138, oz198, and oz200, endomitotic figures extend further distally. oz138 is also unusual in that its Emo phenotype is suppressed by feminization. In previously characterized mutants with the Emo phenotype, feminization delayed the onset of endomitosis (because it delays maturation and ovulation), but did not suppress the phenotype. Mating into oz138 females with wild type males results in a maternal effect embryonic lethality, but no Emo phenotype. The oz138 Emo phenotype is therefore dependent on oz138 sperm. In oz197, abnormalities are seen in chromosomal morphology in distal oocytes which are not yet endomitotic. This suggests a primary defects in meiotic prophase progression in this mutant rather than a defect in ovulation. In summary, initial characterization suggests at least three phenotypic categories for mutants with the Emo phenotype. These include 1) ovulation defective mutants, 2) sperm defective mutants, and 3) meiotic prophase defective mutants. Further characterization is in progress. 1 Iwasaki et al., (1996). JCB, In press. 2 McCarter et al., (1996). Midwest Worm Meeting Abstract. 3 Myers et al., (1996). JCB, 132:1061-1077. 4 Greenstein, et al., (1994). Genes & Dev., 8:1935-1948. 5 McCarter et al., (1996). In preparation. 6 We thank Eric Lambie for isolating oz200.