Worm Breeder's Gazette 8(1): 12
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.
Mutations in the genes lin-12 and lin-17 cause cells that normally differ instead to appear identical. In general, lin-12 mutations cause certain non-identical homologues (generated as lineally equivalent descendants from morphologically similar progenitors that undergo identical division patterns) to adopt the same fate [Greenwald et al., Cell 34, 435 (1983)], whereas lin-17 mutations appear to cause certain non-identical sisters to adopt the same fate (see below). lin- 12 and lin-17 mutations affect partially overlapping sets of cell lineages (including Z1, Z4, Pn.p, B and M) at different stages of development and are expressed independently in doubly mutant strains. Defects in the male B, Z1 and Z4 lineages in lin-17 mutants precede those in lin-12 mutants, while defects in the hermaphrodite P(3-8).p lineages in lin-12 mutants precede those in lin-17 mutants. Thus, lin- 12 and lin-17 may normally function sequentially within each of several different lineages to specify certain cell fates. The phenotypes resulting from, and interactions between, mutations in lin-12 and lin-17 are exemplified by the hermaphrodite and male Z1 and Z4 lineages. In wild-type hermaphrodites, Z1 and Z4 each produce a ventral uterine precursor cell (VU) and a cell (ac/VU) that becomes either a VU or an anchor cell (ac)(see Fig. 1). Similarly, in wild- type males, Z1 and Z4 each produce a vas deferens precursor cell (VD) and a cell (lc/VD) that becomes either a linker cell (lc) or a VD cell (see Fig. 2). In a given animal only one of the ac/VU's or lc/VD's become an ac or lc, respectively. In hermaphrodites carrying a null allele of lin-12 ['lin-12(0)'], the VU cells are sometimes transformed into ac's. (This transformation occurs in addition to that of both ac/VU's becoming ac's, which we have described previously [ibid.].) Thus, lin-12(0) hermaphrodites have up to four ac's, suggesting that normally there is a low level of lin-12 activity in ac's. In semidominant lin-12 mutants ['lin-12(d)'], all four cells are VU 's, suggesting that during wild-type development there is a high level of lin-12 activity in the VU's. This high level of lin-12 activity may be set intrinsically in Z1.ppa and Z4.aap (which normally are both VU's) and by cell-cell interactions in the ac/VU that becomes a VU. Thus, an intrinsically-set high level of lin-12 activity may exclude the VU cells from the ventral uterine 'equivalence group' (comprising those cells that can become ac's in the wild type). In males, the lc/VD's and VD's are similarly affected by lin-12(d) and lin-12(0) mutations: lin-12(d) males can have four VD's and lin-12(0) males can have four lc's. The persistence of some VU's or VD's in the two lin- 12(0) strains examined suggests either that these strains have residual lin-12 activity or that lin-12 is not absolutely required for the production of these cell types. The transformations in cell fates caused by lin-17 mutants can be exemplified by the male Z1 and Z4 lineages. In wild-type males, during the L1-L2 divisions, Z1 and Z4 each produce one daughter that becomes a distal tip cell (dtc) and another daughter that generates four cells, including a VD and an lc/VD (Fig. 2). In lin-17 males Z1 and Z4 each can generate eight progeny during the L1-L2 divisions. lin-17 males often have two lc's and no dtc's. In addition, the germ line nuclei undergo meiosis prematurely, consistent with Judith Kimble's dtc-ablation experiments [Develop. Biol. 81, 208], which demonstrated that the dtc is necessary for continued mitosis of germ nuclei. If lin-17 causes both daughters of Z1 and Z4 to be identical, then lin-17 males should have four lc/VD's instead of two as in wild- type. However, only one (or two) of the lc/VD's would become a lc if the cell-cell interactions responsible for allowing only a single lc in the wild type are still functioning in lin-17 males. To test for the presence of multiple lc/VD's, we used a lin-12(0) mutation, which transforms lc/VD's (as well as VD's) into lc's. While lin-17 males have one or two lc's and lin-12(0) males have from two to four lc's, males carrying both mutations have from two to seven lc's. These results establish that there are indeed additional lc/VD's in lin-17 males, which indicates that the fates of both Z1 and both Z4 daughters are identical and reveals that the lin-17 and lin-12(0) mutations are expressed independently.