Worm Breeder's Gazette 11(4): 84

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.

mig-10 is Not Cell Autonomous

Jim Manser

The mig-10(ct41)III mutation affects embryonic migration of CAN, ALM,
HSN, and the ccL mother cells, as well as outgrowth of the posterior 
excretory canals [Manser and Wood Dev.  Genet.  11: 49-64 (1990)] .  
In a noncomplementation screen with ct41, I have isolated a second, 
phenotypically-less-severe, mig-10 allele (as well as several unc-36 
alleles, which are available upon request).
I am currently performing a mosaic analysis of mig-10 using ncl-1 
mig-10(ct41);qDp3 and sDp3(111,f) strains.  To 
date, I have focused on the incomplete outgrowth of the posterior 
excretory canals (pec's) exhibited by mig-10(ct41) because 1) unlike 
other ct41 phenotypes, it is completely penetrant and 2) both the 
excretory canal phenotype and the excretory (exc) cell genotype (i.e., 
Nc1 phenotype) can be reliably scored using DIC optics (the pec's are 
cytoplasmic processes of the exc cell).
Among 34 mosaics exhibiting mutant (shortened) pec's, 27 had mig-10(
ct41) [=mig-10(-)] exc cells, and 7 had mig-10(+) exc cells.  Thus mig-
10(+) activity within the exc cell is not sufficient to effect normal 
canal outgrowth, suggesting that gene activity is required 
extrinsically.  The high percentage of mosaics exhibiting mig-10(-) 
exc cells suggests that the putative extrinsic focus (or foci) may be 
closely related to the exc cell (ABplpappaap).  Alternatively, gene 
activity may be required in both the exc cell and external tissues.  
In nearly all of the 34 mosaics, Dp loss appeared to be confined to 
the AB lineage.
To investigate whether mig-10 activity is necessary within the exc 
cell, I am currently screening for mosaics with mig-10(-) cells that 
nevertheless exhibit normal pec outgrowth.  Identification of such 
mosaics would provide strong evidence against a role for mig-10 within 
the exc cell.  So far I have identified a single mosaic in which the 
outgrowth of pec's was significantly more extensive than in mig-10(
ct41), although still abnormal.  Identification of this mosaic 
confirms the existence of an extrinsic influence upon exc cell 
development in mig-10(ct41), but does not rule out the possibility 
that mig-10 activity might also be required within the exc cell.
In summary, my results suggest that mig-10 activity is required 
extrinsically for normal outgrowth of the pec's.  Current data suggest 
an AB-derived extrinsic focus, possibly hypodermis.  However, these 
data do not exclude the possibility that mig-10 activity within the 
exc cell might also be necessary.