Worm Breeder's Gazette 10(3): 150
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.
The deg-1(u38) mutants have an unusual touch insensitive phenotype. The animals do not respond to the touch of a fine hair or the prodding of a worm pick when touched in the tail. This defect is the same as that seen when the PVC interneurons are ablated. Since the mec mutants and wild-type animals in which the touch receptor cells have been killed respond to the wire, but not the hair, I'll refer to this phenotype as Tab (for Touch abnormal). One interesting aspect of the deg-1(u38) Tab phenotype is that even though the PVC cells arise embryonically, the Tab phenotype is first detected during L2 (16 hrs post hatching at 25 C) and seen in virtually all animals by mid L3 (24 hrs). I have found that temperature, dosage of the wild-type gene, and partial intragenic reversion will affect the timing of the onset of the Tab phenotype and the PVC degeneration. The onset of the Tab phenotype is progressively more delayed when animals are grown at 20 C and 15 C. At 20 C animals become Tab between 24 and 48 hrs after hatching, although approximately 60% of the animals become Tab during the L4 stage (all times are given as 25 C equivalents; the L4 molt is at 36 hrs at this temperature). Animals grown at 15 C become Tab as egg-laying adults (between 40 and 72 hours). Many of these animals have deaths in the tail (presumably the PVC cells) at 72 hrs. This switch in the onset of the Tab phenotype suggests that a particular developmental event is not triggering the degeneration of the PVC cells. The deg-1 mutation is dominant, but increasing the dose of the wild- type gene delays the onset of the Tab phenotype. u38/u38/+ animals become Tab during the L4 stage, u38/+ animals become Tab a little later (at the time of the L4 molt), and u38/+/+ animals become Tab still later as young adults. These results indicate that the u38 dominant expression is not the result of overexpression or haplo- insufficiency. Instead the mutation appears to result in an antimorphic product whose effect can be competed away by the wild-type product. We have obtained a number of intragenic revertants of deg-1(u38) ( see past Newsletter contributions by Eve Wolinsky and myself). Two of these revertant mutations appear to suppress the Tab phenotype incompletely; their effect is to, once again, delay the onset of the PVC degenerations. deg-1(u38u354) animals become Tab between 40 and 56 hrs and deg-1(u38u352) animals become Tab between 48 and 72 hrs. The PVC degenerations are also appropriately delayed in these strains. These results demonstrate that different mutations in the same gene can affect the onset of the mutant phenotype. A similar result also appears to have occurred in Huntington's Disease (Folstein et al. Science 229: 776, 1985) [changes in the onset of expression of Huntington's is reported not to change, however, in putative homozygous individuals compared with heterozygous individuals (Wexler et al., Nature 326: 194, 1987)]. It is not clear how these various perturbations can alter the onset of the deg-1 degenerations. One possibility is that the deg-1(u38) product or a cellular component it interacts with must accumulate to a sufficient level before the degeneration can occur. The various perturbations may interfere with this accumulation.