I am continuing studies that I initiated in Boulder of several cell migration mutants [Manser and Wood, manuscript in preparation; also, e. g., WBG 9(3), p.91 and 9(2), p.63, 1986]. To investigate how the corresponding genes are involved in cell movement, I would like to isolate and use DNA clones and perform mosaic analyses. At present, I am focusing on the
mig-10(
ct41)III and
mig-11(
ct78)III genes. In most
mig-10(
ct41) embryos, neurons ALM, CAN, and HSN migrate only partway toward their normal destinations (sometimes the ccL mother cells do likewise). In
mig-11(
ct78) embryos, CAN migration is rendered partially defective with high penetrance, while ALM and HSN migrations are affected at very low penetrance. Previously obtained genetic map data place both loci within the
lon-1 to
unc-32 cluster on LGIII, a region favorable for mosaic analysis (qDp3,
unc-36; see Austin and Kimble Cell 51: 589-599, 1987), and one that is partially covered by the current physical map (
lin-12, ibly
ced-4, contigs; see Coulson et.al., this issue). However, more precise map positions are required to construct strains for mosaic analyses and to determine whether the current physical map will be of use for cloning. Thus I have been doing some additional mapping. I have found that
mig-10(
ct41)III lies within the interval covered by both nDf16 and nDf20.
mig-10 thus maps within the
mab-5 to
dpy-19 interval (see Figure), which is completely spanned by the
lin-12 contig. More precise positioning of
mig-10 within this interval should allow me to select a small set of cosmids for use in transformation rescue experiments (Hope et.al., WBG 10(2) pp.97-98, 1988) or, if rescue cannot be achieved, to devise alternative cloning strategies that make efficient use of the physical map (e.g., searches for polymorphisms in mutants). Thus I am currently mapping
mig-10 relative to
mab-5,
unc-86,
dpy-19 have been placed on the current physical map). Results from the deficiency mapping experiments also suggest that the
ct41 allele is null or nearly null. Specifically, I examined several phenotypes of
ct41/nDf20 animals ( adult viability, adult dissecting microscope phenotypes, and cell migration phenotypes as determined by Nomarski microscopic examination of L1's), and found none to be more severe than what is observed for
ct41 homozygotes. Even if
ct41 is not a true null, it should be possible to isolate such an allele in a complementation screen with
ct41. I have positioned
mig-11(
ct78)III within the
lon-1 to
sma-3 interval in three-factor and deficiency (nDf16 and nDf20) mapping experiments ( see Figure; complementation tests with nDf16 indicate that
mig-11 maps to its left). Because
lon-1, genes between them (
daf-4 and
sma-4) have not yet been assigned to contigs, it is possible that
mig-11 is absent from the current physical map. Nevertheless, I am currently mapping
mig-11 relative to
lon-1,
sma-4, and
sma-3 in anticipation that the physical and genetic maps will eventually become better correlated in this region. I also plan to continue my studies of the
vab-8V gene (whose apparent null phenotype includes a highly penetrant CAN migration defect: Manser and Wood, op. cit.). The close proximity of
vab-8V to
myo-3V on the genetic map suggests that
vab-8 may be contained in the
myo-3 contig; if so, the physical map may prove useful for cloning. [See Figure 1]