Worm Breeder's Gazette 16(5): 40 (February 1, 2001)
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.
S.L. Research Institute of Mt. Sinai Hospital, 600 University Ave., Toronto M5G 1X5 Canada
UNC-5 and UNC-40 receptors act together to mediate repulsive responses to the UNC-6 guidance cue. Attractive responses to UNC-6 also require UNC-40, but do not require UNC-5. Does UNC-40 require a co-receptor for attractive responses to UNC-6, the way it requires a co-recptor (namely UNC-5) to mediate repulsive responses to UNC-6? To look for mutations in such a hypothetical co-receptor for attraction or in mechanisms that act in parallel with UNC-6 and UNC-40, we searched for mutants specifically defective in ventralward guidance of the touch receptor axons AVM and PVM. The screen was carried out in a genetic background partially compromised for UNC-40 function. This screen yielded 12 mutations representing 6 genes. Two are unc genes previously identified as affecting axon guidance of a number of neurons (unc-44 and unc-51), while mutations in the other 4 genes are not Unc and only appear to affect certain ventrally oriented axons. avm-1 (allele ev755) is on LGIII, avm-2 (allele ev756) is on LGI, avm-3 (alleles ev740, ev741, ev742) is on LGX, and avm-4 (alleles ev750, ev751, ev752, ev753, ev754) is on LGI. We have rescued avm-3 with a fragment of cosmid C26G2 corresponding to the Slit gene (F40E10.4), which encodes an axon guidance ligand for the SAX-3 receptor. The laboratory of Dr. C. Bargmann (UCSF) is currently characterizing these mutations. We have also rescued avm-4 mutations with overlapping cosmids F14B11 and F32A7, and further localized the rescuing region to a single open reading frame. We have found that avm-4 mutations enhance AVM and PVM guidance defects of an unc-6 null allele, suggesting that AVM-4 functions in an axon guidance pathway that acts in parallel with UNC-5, UNC-6, and UNC-40. We are currently determining in which cells this gene must function by expression and mosaic analyses. We are also cloning and characterizing avm-1 and avm-2.