Worm Breeder's Gazette 10(3): 110

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Migratory Genes Seek Their Homes Across the Pond

Jim Manser

Figure 1

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 
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 
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]

Figure 1