Worm Breeder's Gazette 11(5): 93

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In Search of the Amorph Phenotype of unc-32

Danielle Thierry-Mieg and Andrew Spence

Figure 1

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]

Figure 1