Table 2.

Genetic interactions with hop-1 and with lin-12^*

hop-1dependence
Relevant genotype	No. of Egl+/total, %
hop-1(ar179); sel-12(ar171)	0/28
hop-1(ar179); spr-2(ar199); sel-12(ar171)	0/30
hop-1(ar179); spr-2(ar211); sel-12(ar171)	0/40
No effect on the 0 AC defect caused by elevating lin-12 activity
Complete genotype	No. of 0 AC/total, %†
lin-12(n302)/unc-32; dpy-20/+	27/50 (54%)
lin-12(n302)/unc-32; spr-2(ar211) dpy-20	33/60 (55%)
lin-12(n302)/unc-32; spr-2(ar211)  dpy-20/spr-2(+) dpy-20	88/168 (52%)
No effect on the 2 AC defect caused by reducing lin-12 activity
Complete genotype	No. of 2 AC/total, %§
lin-12(ar170)‡ (25°C)	39/50 (78%)
lin-12(ar170); spr-2(ar211) (25°C)	25/39 (64%)
lin-12(ar170)‡ (20°C)	10/52 (19%)
lin-12(ar170); sel-12(ar171) unc-1 (20°C)	39/43 (91%)
lin-12(ar170); spr-2(ar211); sel-12(ar171)  unc-1 (20°C)	40/49 (82%)

^*Hermaphrodites of the relevant genotype shown segregated from parents that also carried the free duplication mnDp68 [sel-12(+)]. Maternal sel-12(+) activity provided by the duplication enables hop-1(−); sel-12(−) progeny to survive to adulthood and to produce progeny, which arrest as embryos (see ref. 18). spr-2 mutations do not suppress the maternal-effect lethality of embryos produced by hop-1(−); sel-12(−) mothers (data not shown). All strains also contained unc-1(e538). 

^† The 0 AC defect was scored by determining egg-laying ability; for lin-12(n302), the ability to lay eggs correlates absolutely with the presence of an AC (38). AC, anchor cell. 

^‡ lin-12(ar170) behaves as a partial loss-of-function allele at all temperatures but is most hypomorphic at 25°C (39). 

^§The number of ACs was scored directly using Nomarski microscopy.