Worm Breeder's Gazette 11(2): 101
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.
Although the HSN neurons are born embryonically, they do not appear to differentiate fully until the L4 stage (Desai et al., 1988). How is the timing of HSN differentiation controlled? One possibility is that the HSNs contain an internal clock that is set to go off in L4 animals. Alternatively, the HSNs could differentiate in response to an external cue. The timing of many developmental events in C. elegans is controlled by the heterochronic genes (Ambros and Horvitz, 1984). Some mutations in these genes lead to precocious development, causing certain events to occur prematurely. Other mutations lead to retarded development, causing certain events to occur late. To determine if the heterochronic genes are important for HSN differentiation, we examined two aspects of HSN development in heterochronic mutants: the timing of hood formation and the timing of serotonin synthesis. The HSN hood is an eye-shaped structure that surrounds the HSN nucleus in L4 hermaphrodites and can be observed using Nomarski optics. Serotonin is an HSN neurotransmitter that becomes detectable immunocytochemically in young adult hermaphrodites. The timing of HSN differentiation is perturbed in heterochronic mutants. In the precocious mutants lin-14(n179) and lin-28(n719), the HSNs differentiate early. Hood formation occurs during the L3 stage, and the HSNs synthesize detectable serotonin in L4 animals. By contrast, the HSNs never differentiate in the retarded mutants lin-4( e912) and lin-14(e536sd). The HSNs appear normal in these mutants until the L4 stage, when either they fail to form a hood or they become indistinct and difficult to find. The lack of immunocytochemically detectable HSN serotonin in these mutants corroborates the Nomarski results. These HSN phenotypes are the same defects seen in the HSN maturation mutants, egl-45, t al., 1988; M. Basson, personal communication). In these mutants, the HSNs fail to differentiate. In contrast to the other retarded mutants, lin-29(n333) animals are normal for HSN hood formation; however, the HSNs often lack immunocytochemically-detectable serotonin. The only other event known to be affected by lin-29 mutations is the switch from larval to adult cuticle, which is blocked in this mutant (Ambros and Horvitz, 1984). Thus, lin-29 may be required specifically for late aspects of development, including late stages of HSN differentiation. What do these results say about HSN differentiation? Among the heterochronic genes, lin-14 plays a key role, with the level of lin-14 gene activity determining the timing of developmental events (Ambros and Horvitz, 1987). The postembryonic HSNs do not contain detectable lin-14 protein as determined by staining with anti-lin-14 antiserum ( Ruvkun and Guisto, 1989). This observation suggests that the time of onset of HSN differentiation is controlled by an external cue or cues, presumably presented to the HSNs by cells expressing the lin-14 protein.