Functions of
vab-3 and
lin-17 in the male B lineage Helen M. Chamberlin and Paul W. Sternberg Division of Biology and HHMI. Caltech, Pasadena, CA 91125. The initial division of the C. elegans male B cell is asymmetric: the anterior daughter of B (B.a) is the precursor to all of the cells of the copulatory spicules, whereas B.p produces no spicule fates (Sulston, et al. (1980) Dev. Biol. 78, 542-576). In addition, B.a is larger, divides earlier, and produces more progeny than B.p. Iin-17 is required for the initial unequal division of the B cell as well as for fate specification (Sternberg and Horntz, (1988) Dev. Biol. 130, 67-73). In
lin-17 mutants the initial division of B is equal, and both B.a and B.p behave like a normal B.a cell. In genetic screens for mutants with male B lineage defects we recovered two
vab-3 mutations (
sy66 and
sy281; e.g., WBG 11(3), pg. 56).
vab-3 has many functions in development (A. Chisholm, WBG 11(4), pg. 83). We have found that in the B lineage
vab-3 uncouples the unequal cell division from fate specification. In
vab-3 mutants, B divides unequally, and B.a divides to produce a left and a right daughter as in wild type. However, lineages in two
vab-3(
sy66) and six vab- 3
(e648J males suggest that both B.al and B.ar behave like a normal B.p cell (although there is some lineage variability in the mutants). In addition to a transformation of the axis and timing of divisions of the B.a(Vr) cells some differentiated fates are also transformed. B.ppaa normally undergoes a programmed cell death, and in the
vab-3 mutants the corresponding cells in the B.a(Vr) lineages can also die. Thus
vab-3 is necessary for normal B.a or B.a(Vr) fates. We constructed
lin-17;
vab-3 double mutants. While the lineage defect in
vab-3 mutants results in a distinctive pattern of six progeny in the L3 larval stage rather than the normal ten progeny, in
lin-17 mutants there can be sixteen. In lin-17fn677);
vab-3(
e648) males there can be eight progeny. The defects are additive: the initial division of B is equal because
lin-17 is mutant, but both B.a and B.p behave like the abnormal B.a of
vab-3 mutants. Thus
lin-17 might be necessary for both the unequal cell division and the asymmetric distribution of fate potential, whereas
vab-3 acts downstream to specify B.a or B.a(Vr) fate. In contrast, Mike Herman's analysis of
lin-44 and
lin-17 suggests that
lin44 acts upstream of
lin-17 in the B lineage (Herman and Horvitz (1994) Deu. in press). Lineage analysis of
lin-17;
vab-3 double mutants suggests that
lin-17 may have additional functions in the B lineage. Specifically, predicted B.p like lineages are abnormal, and the cells generally divide synchronously (two animals followed). To identify additional functions of
lin-17 in the B.a and B.p lineages, we followed the B lineage in four lin- 17 mutants that had escaped the initial defect at the division of B, and the B.a lineage in two lin 17 animals in which B.p was ablated. The results suggest (1)
lin-17 functions in the B.p lineage to mediate the asymmetric division of B.pp, (2)
lin-17 functions in the B.a lineage to mediate the asymmetric cell division of B.aa/r)ap and possibly B.a(Vr)pa, and (3)
lin-17 does not appear to play a role in the divisions of B.a(Vr) or B.a(Vr)(a/p). Thus
lin-17 functions at multiple, but not all, asymmetric cell divisions in the B lineage.