Worm Breeder's Gazette 11(5): 93
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.
We wish to understand the development and the functioning of the nervous system. The phenotype of the unique allele e189 of unc-32 suggests that one or two classes of motoneurones (VA and perhaps VB) are specifically affected: L1 are wild type and adults are ventral coilers. However serial reconstruction of the first repeat in the ventral nerve cord behind the RVG failed to show any wiring defect in the motor neurons (John White, Eileen Southgate and Nichol Thomson, pers. comm.). So the function of unc-32 in the nervous system remains mysterious. There have been oral reports of failure to recover alleles of unc-32. This may hide interesting genetic features. Therefore, we performed a standard EMS mutagenesis that gave 16% lethals and 6% visible mutants on the X chromosome, and looked for new alleles of unc-32 and at the same time of unc-116. Out of 11115 dpy- 17 mes tested for non complementation of unc- 116(e2310)89), we found one new allele of unc-116( f121), which is a zygotic lethal presently under investigation, and three new alleles of unc-32, among which two are zygotic lethals. The pattern of complementation is complex (see table). The dosage studies indicate that both e189 and the new allele f120 are hypomorphs: for instance e189/e189/e189 is slightly less Unc than e189/e189, and can be unambiguously recognized. f121 and f123 are non-complementing zygotic lethal alleles. f123 could be the amorph. It has two zygotic effects, on embryonic viability and on coordination (as seen against uncoordinated alleles). In addition, when covered by the cosmid ZK637, which rescues lin-9 ( Beitel and Horvitz, WBG 11.2, page 29) and unc-32 (John Sulston, WBG 10.2 p97), both zygotic effects are removed, but a strict maternal effect early embryonic lethality is unmasked. f121 fails to complement the lethality of f123, but it complements almost fully the Unc phenotype of the Unc alleles. However, it cannot be a null allele of unc-32: if it were, we should recover, by mutagenising e189, around 1 in 3000 animals resembling f121/e189, i.e. almost wild type, ratchety in reverse 'pseudo revertants'. But, out of 68000 e189 chromosomes mutagenised (18% lethals on X), only one semi-dominant suppressor of e189, f125, mapping on chromosome I, was recovered. We are trying to rescue the maternal effect by injection of cosmids overlapping ZK637 to the right and to segregate it away from the unc- 32 locus. We wish to study the suppressor and the cell autonomy of the zygotic lethality, by using qDp3 and ncl-1, and also to get more alleles of unc-32.[See Figure 1]