Worm Breeder's Gazette 8(3): 71
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.
In the last newsletter Donna Albertson (1) reported in situ hybridization data that localized myo-3 to a region of chromosome V encompassing the act 1,2,3 cluster and sup-3. The apparent effect of sup-3 on myo-3 activity (myosin A is elevated)(2) indicated the likelihood that these genes are in close proximity to each other. To test this possibility restriction digests of sup-3 deficiency DNA were probed on Southern blots with myo-3 cosmids. Two restriction fragment differences were detected. DNA was prepared from the semibalanced strain unc-15(e73);sup-3(eDf1)/sma-1(e30) for comparison with N2 DNA. (Homozygous eDf1 segregants die as L1's and e73;e30 homozygotes produce few progeny.)(3) Southern blots were hybridized with nick- translated myo-3 cosmids. The sup-3 DNA exhibits ~15 kb PstI and ~ 8 kb BclI fragments that are not present in N2 or homozygous e30 DNA. Control experiments have verified that the fragments are not partial digestion products nor do they hybridize with cosmid vector sequences. In addition the extra bands are significantly weaker than the wild type bands which is consistent with the approximate half molar amount of sup-3 DNA in this mutant. The precise location of the putative eDf1 deletion has not been determined as yet but it is clear that the myo-3 coding sequence is not altered. These results favor the hypothesis that sup-3 is a cis-acting DNA sequence that modulates the expression of the myo-3 gene.