Worm Breeder's Gazette 8(2): 21
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.
lin-32(e1926) alters two aspects of embryonic neurogenesis. First, it changes the timing of the Q/V5 division. Second, it alters the differentiation of multiple sensory neurons. Q/V5 normally divides before hatching. However, in lin-32(e1926) animals the Q/V5 division is delayed, and occurs in the L1 just prior to the seam divisions. Q becomes a hypodermal cell that usually fuses with hyp-7 (see preceding note). This temporal shift appears to bring Q/V5 into the domain of the postembryonic heterochronic genes. At 25 C, the lin-14(n179) mutation causes the precocious expression of S2 lineage patterns during the L1 ( V. Ambros; see Newsletter. Vol. 6, No. 1). In lin- 32(e1926);lin-14( n179) double mutants, V(1-4,6) and Q/V5 behave identically, each expressing lineage patterns characteristic of V(1-4,6) in wild type L2 animals (see figure). Apparently, the Q/V5 seam cell itself (and not V5 its daughter) is now instructed to undergo the developmental sequence characteristic of S2 seam cells. The observation that e1926 delays the Q/V5 division raises the possibility that Q becomes a hypodermal cell instead of a neuroblast in the mutant because it is born at the wrong time. If the delayed division were responsible for the change in cell fate, then in e1926 the V5.p division (which generates a V5.pa seam cell instead of a postdeirid neuroblast) should also be delayed. However, we do not detect a consistent difference in the time of the V5.p division in e1926 animals compared to wild type. Thus delayed cell divisions per se cannot account for the conversion of neuroblasts into hypodermal cells in lin-32(e1926) mutants. The lin-32(e1926) mutation also alters the fates of certain sensory neurons produced during embryogenesis. The ALM cell body is does not complete its migration, and so is displaced anteriorly (its anterior process can run subdorsally or sublaterally). We are often unable to locate the male dorsal cephalic companion (CEMD) nuclei with Nomarski. The deirid neurons (ADE) and dorsal cephalic neurons (CEPD) are often undetectable in animals stained by FIF (Sulston and Kenyon). Additional sensory processes were found to be missing when the anterior sensilla of an adult male were examined by EM (with the help of Nichol Thomson. Eileen Southgate, and John White). These included certain IL1, IL2, OLL, CEP, CEM, BAG and FLP neurons. (The amphids appear to be normal.) In addition, e1926 animals often have a slight Notch phenotype. To determine whether the cell lineages generating the altered neurons were aberrant, we followed the lineages generated by AB. arpapaa. This cell normally produces both CEMDR and CEPDR neurons both of which are apparently absent in lin-32(e1926) animals. In each of 12 animals, CEMDR was produced normally (one of these was a male and, by Nomarski criteria, apparently lacked the CEMD nuclei). However the division that would normally generate CEPDR was either absent or substantially delayed in several animals. The observation that at least some altered neurons (CEMDR) are generated by a normal sequence of divisions suggests that lin-32 is necessary for aspects of neurogenesis that do not involve cell divisions. We are postponing further embryonic lineage analysis until the lin- 32 null phenotype is determined (the frequency of animals with altered embryonic neurons increases in lin-32(e1926)/eDf17 deficiency heterozygotes). To date, 4000 chromosomes have been examined in complementation screens, but no new alleles have been isolated. [see Figure 1]