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.