Table 2.
Maternal genotype | Zygotic genotype | Glp-1-like defects
|
Lin-12-like defect (two ACs*) | |
---|---|---|---|---|
Sterile | Mel | |||
hop-1/+; sel-12† | hop-1; sel-12 | Yes‡ | NA | 24/24 |
hop-1; sel-12/+§ | hop-1; sel-12 | No | Yes¶ | 0/25 |
hop-1/+; sel-12/+‖ | hop-1; sel-12 | No | Yes** | ND |
NA, not applicable; ND, not determined.
Number of hop-1; sel-12 animals with two ACs and the total number of animals scored are indicated. The number of ACs in non-Unc non-Dpy progeny of hop-1/unc-73 dpy-5; sel-12 parent animals or in non-Unc progeny of hop-1; sel-12/egl-17 unc-1 parent animals was determined in third- or fourth-larval stage animals by using differential interference contrast microscopy (see Fig. 2). After scoring, animals were allowed to develop to adulthood. Adult hop-1; sel-12 animals could be distinguished from their heterozygous siblings by their sterile or Mel phenotype. sel-12 single mutant animals have a single AC (ref. 6 and data not shown), indicating that in a hop-1(+) background, the absence of maternal and zygotic sel-12 activity does not cause defects in the AC/VU decision.
Complete genotype is hop-1(nr2003)/unc-73(e936) dpy-5(e61); sel-12(nr2011).
Non-Unc non-Dpy progeny (n = 147) of hop-1/+; sel-12 parent animals were cloned as L4 stage animals and incubated for 24–36 h. Of these, 60% were Egl and 40% were sterile. PCR analysis of 48 Egl and 44 sterile animals indicated that all of the Egl animals were heterozygous for the hop-1 deletion, whereas all of the sterile animals were hop-1 homozygotes. In a separate experiment, the germ-line phenotype of 59 young adult sterile animals was scored with differential interference contrast microscopy. Each gonad arm contained 50–100 sperm, no oocytes, and no undifferentiated germ cells (see Fig. 2), a phenotype resembling that of glp-1 reduction-of-function mutants (18).
Complete genotype is either hop-1(nr2003); sel-12(nr2011)/pha-2(ad472) dpy-3(e27) or hop-1(nr2003); sel-12(nr2011)/egl-17(e1313) unc-1(e538).
Non-Dpy progeny (n = 287) of hop-1; sel-12/pha-2 dpy-3 parent animals were cloned as L4 stage animals and incubated for 24–36 h. Of these, 64% were wild type, 29% were filled with dead eggs (the Mel phenotype), 5% were Egl with live progeny, and 2% were sterile. PCR analysis of 20 wild-type and 20 Mel animals indicated that all of the wild-type animals were heterozygous for the sel-12 deletion, whereas all of the Mel animals were sel-12 homozygotes. The Egl animals with live progeny were all sel-12 heterozygotes, indicating that, in a hop-1 mutant background, a single wild-type copy of sel-12 is not always sufficient for normal egg laying. The rare sterile animals did not appear to have a germ-like proliferation defect; the sterility was not characterized further.
Complete genotype is hop-1(nr2003)/unc-73(e936) dpy-5(e61); sel-12(nr2011)/+.
Twenty Egl, non-Unc non-Dpy progeny of hop-1/unc-73 dpy-5; sel-12/+ parent animals were cloned. Fourteen of these animals (presumed genotype hop-1/unc-73 dpy-5; sel-12) segregated both sterile animals with a germ-line proliferation defect and Unc Dpy animals. The remaining six animals had a Mel phenotype, producing only dead embryos; PCR analysis indicated that all of the Mel animals were of the genotype hop-1; sel-12.