The genes
clk-3 (abnormal function of biological clocks) and
mal-1 (maternal-effect morphological abnormal) were recovered in a screen for maternal-effect viable mutants (1). The restriction fragment length polymorphism (RFLP) mapping of each has begun.
clk-3 is defined by two alleles, qm-38 and
qm53, whose mutant phenotype is very similar to that of the extensively studied gene
clk-1 (2). These genes, when mutant, lengthen embryonic and post-embryonic development, lengthen the periods of various adult rhythmic behaviors, and increase mean and maximum life span.
clk-3 has been genetically mapped to the right arm of linkage group (LG) II, 1 cM to the left of the cloned gene
unc-52. This region has few cloned genes and therefore an RFLP mapping approach was chosen. There are only two known N2/AB2 RFLPs in the region (3), but we are presently identifying more. In anticipation of this, recombinants have been generated in an N2/AB2 background. Once the DNA of these recombinants has been isolated, the known polymorphisms, and any others detected, will be mapped with respect to
clk-3. The gene
mal-1 is defined by a single allele,
qm27, and is characterized by dorsal protrusions over the head and tail and a frequently twisted head. Genetic mapping has placed
mal-1 roughly 1 cM to the right of
unc-26, on the right arm of LGIV. N2/RW7000 polymorphisms in the region have previously been described during the cloning of
tra-3 (4). Therefore, 27 recombinants were generated in an N2/RW7000 background. The genetic mapping of 7 of the known RFLPs by Southern analysis indicates that
mal-1 lies between the two polymorphisms eP88 and eP87, which span approximately 150 kb. Injections of the cosmids from this region, which cover approximately 100 kb, are in progress. 1 Hekimi et al. 1995. Genetics 141:1351-1364. 2 Wong et al. 1995. Genetics 139: 1247-1259. 3 J. Simske, personal communication. 4 Barnes, T. 1991. Ph.D. Thesis. University of Cambridge, England.