Worm Breeder's Gazette 9(3): 29
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 wildtype strain of C. in Freiburg (Fbg 1A, available from the CGC as RC301) is a typical high-copy number strain with a mutator activity. I have been looking at its biology recently with the goal, shared with others, of obtaining transposon- insertion embryonic lethal mutations. Burrowing seen here appears to occur as a consequence of the accumulation of feeding animals of all ages on the thickened edge of the lawn (I call this propensity 'bordering'), followed by mechanical wearing down of the agar locally, leading finally to burrowing itself (and a tendency to stay under the surface). Bordering arises without any reduced motility, as compared to N2 on a lawn. N2 borders on an old lawn, where only the edge still has healthy, growing bacteria. On a very fresh, thin lawn Fbg does not prefer the border, as it is not thicker than the rest of the lawn, but like N2, chemotaxes nicely to such a lawn and disperses uniformly on it. Even just hatched Fbg worms tend to clump with each other, as N2 does in the swarm-stage on old plates, suggesting an enhanced sensitivity to some 'pheromone' as well. Both bordering and clumping are single-animal autonomous responses, as seen with morphologically marked mixed populations. Single-animal assays on 1/2' diameter day- old lawns show 90% of the tracks (and eggs if any) of mutant animals on the lawn s edge, vs 10% for N2. Jarring the plate may activate bordering animals to leave the edge briefly, while remaining on the lawn. Bordering is dominant in Fbg/N2 heterozygotes, suggesting N2 has lost this function (as proposed by Hodgkin et al, WBG 8, Nr. 3, 36). There are no maternal effects on bordering or nonbordering, nor is epistasis by other mutations detectable, as long as chemotaxis to the lawn is normal. Bordering is due to a single X-linked gene (proposed name:bor-l), mapping about 20% from lon-2 and 3% from unc-7 (maybe near osm-l?). Efforts are being made to isolate spontaneous non- burrowers. To reduce burrowing, besides using 3% agar, as recommended by Leon Avery (WBG 9, Nr.l, 88), retard bordering by using a richer medium (such as Avery s or 5x peptone), since the lawn edge thickens later, or by seeding a whole-plate lawn (no border!). Wildtype Fbg also has an autosomal dominant mating plug allele, presumably plg-1 ( Hodgkin et al, op.cit.). Plug formation depends only on the male genotype, showing no maternal effects (plg/N2 mutant males plug even if their mother was N2) or 'uxorial' effects (mutant males plug even if their mates are N2). Besides lots of somatic mutants and sick animals, many visible Fbg mutants have been found, roughly as frequently as with Bergerac B0. My screen for emb mutants involves looking for 'baggie' adults with unhatched eggs inside after leaving them in nicotine solution (without any vul- mutation). Screening single worms on plates (no nicotine) has revealed the complication that at a certain age a Fbg adult may begin to produce dead embryos, suggesting massive activation of Tc1 in the ovary, but give no mutants among the earlier, viable progeny. One of several real emb mutants isolated has slow embryonic cell divisions. So far, I have no revertant of any spontaneous Fbg mutant.