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display a highly disorganized arrangement of motor neuron processes along the ventral nerve cord (J. White et al., unpublished).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.