Worm Breeder's Gazette 10(1): 40

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.

Transposon Tagging in Minnesota

W. Li, T. Starich, J. Shaw and B. Herman

Hedgecock et al.  (1985) have shown that mutations in unc-33 and unc-
44 affect the axonal growth of amphid and phasmid chemosensory neurons.
We have identified one unc-33 and two unc-44 spontaneous mutants in 
the famous TR679 mutator strain.  After many outcrosses to N2 and 
selection for recombination on each side of unc-33, we were unable to 
find an extra Tc1-containing band in Southern blots made from unc-33 
strains.  Using a probe kindly provided by Junying Yuan, however, we 
found that the unc-33 mutation appears to be an insertion of Tc4: 
Southern blots of EcoRI plus PstI digests showed two extra Tc4-
containing bands (Tc4 is itself cut by PstI), and the two bands were 
eliminated by reversion of the unc-33 mutation.  We hope to have unc-
33 cloned soon.  We have not yet clearly identified an extra 
transposon-containing band for unc-44, but both unc-44 mutations 
readily revert after outcrossing to TR679, so we have good reason to 
keep looking.
unc-3 mutants display a highly disorganized arrangement of motor 
neuron processes along the ventral nerve cord (J.  White et al., 
unpublished).  Genetic mosaic analysis indicates that the expression 
of unc-3(+) seems to be required only in the motor neurons themselves 
for normal neuronal development.  In an attempt to tag unc-3 with a 
transposon, N2 males were crossed to TR679 hermaphrodites, and the 
male progeny were used in a noncomplemention screen for spontaneous 
unc-3 alleles.  The unc-3 mutation carried by the hermaphrodite used 
in the screen was marked by a closely-linked daf-6 mutation.  One new 
unc-3 allele has been identified among 140,000 cross progeny.  We are 
now attempting to determine the nature of this mutation.
We are also generating a collection of TR679-derived mutants that 
are defective in uptake of FITC (Hedgecock et al.  1985).  To date, 
six mutants have been identified: one mutation maps on LGI, two on 
LGIV, one on LGV, and two on X.  One of the LGIV mutants fails to 
complement a daf-10 mutation and also retains a homozygous self-
sterile phenotype after repeated backcrossing; the homozygote is 
fertile when mated with N2 males.  One X-linked mutant was 
complemented in crosses to all other previously-identified X-linked 
genes affecting FITC uptake (che-2, 
et al.  1986) and may 
therefore identify a new gene.  The remaining FITC mutants have yet to 
be assigned to genes.