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.
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.