mab-l 9 is required for the generation of the last three pairs of male tail peripheral sense organs, rays 7-9. Cell groups for rays 7-9 are derived from male-specific divisions of the lateral hypodermal blast cell, T.
bx38, an EMS-induced recessive allele of rnab-l 9, results in the variable loss of the T rays, but not rays 1-6 (derived from male-specific divisions of lateral hypodermal blast cells V5 and V6). Loss of rays is due to a lineage defect: any male-specific division of T may fail in
bx38 males, leading to ray loss. The mutation is pleiotropic:
bx38 males have gonad morphology defects and retained tail spikes at low penetrance, and exhibit low mating efficiency. Hermaphrodites are morphologically wild type, but brood sizes are reduced from 300 to approximately 100. Double mutants of mab- l 9
(bx38)X and other mutations that result in ray loss (mutant alleles of
mab-3, mab-S, pal-l ) are additive, and in double mutants of
bx38 and a mutation that causes ectopic T ray formation [
mab-21(
bx43)], formation of the ectopic ray is supressed by
bx38. Additionally, tra-l( elO99)111;
mab-19(
bx38)X doubly homozygous males (genotypically XX) are Mab, thus mab-l 9 does not act upstream of tra-l . The ray loss phenotype (Mab) of
bx38 males is suppressed by a number of mutations affecting body morphology (dpy or sqt but not lon or sma). Doubly homozygous combinations of
bx38 and all dpy alleles tested to date exhibit a greatly reduced Mab penetrance. This suppression is usually recessive, but
dpy-4 and
dpy-13 heterozygotes partially suppress the Mab phenotype. The Mab suppression is more general than two other reported Dpy suppression phenomena (glp-l, Maine, E. M. and Kimble, J. (1989) Development 105, 133-143;
bli4, Peters, K. and Rose, A. M. ( 1987) C. elegans meeting abstracts). Additionally, double homozygotes of
bx38 and most
unc-17 alleles [except the allele, el
l3 (see Rand, J. (1989) Genetics 122, 73-80)] arrest as twofold embryos. Thus, these allelic combinations are synthetic lethals.
unc-17 is one of many loci that can be mutated to aldicarb resistance, so other aldicarb- resistant mutant alleles were tested to ascertain whether these were also synthetic lethals in combination with
bx38. The synthetic lethality is restricted to
unc-17;
unc-36, cha-l, and
unc-18 aldicarb- resistant alleles are viable in combination with
bx38. By two-factor recombination, the lethality maps to within less than one map unit from
bx38, so it is likely that
bx38, instead of an additional X- linked mutation, is the cause of the synthetic lethality. Further characterization of mab-l 9 requires that additional alleles of mab-l 9 be isolated; progress on obtaining more alleles and a deficiency of mab-l 9 will be reported.