Worm Breeder's Gazette 14(5): 49 (February 1, 1997)

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.

exc Gene Interactions

Matthew Buechner1, Ed Hedgecock2

1 Dept. of Microbiology, University of Kansas, Lawrence, KS, 66045
2 Dept. of Biology, Johns Hopkins University, Baltimore, MD, 21218

        We have continued genetic studies on exc mutants, in 
which the long hollow processes (canals) of the excretory 
cell form large fluid-filled cysts.  We previously 
classified these mutants into five groups based on cyst 
morphology:  exc-2, exc-4, let-4, and let-653 mutants form 
large septate cysts near the excretory cell body;  exc-1 and 
exc-5 mutants form extremely large septate cysts (often 
visible via dissecting microscope) predominantly at the 
shortened canal termini; exc-3, exc-6, and exc-8 mutants 
show regional canal widenings and meanderings, and 
occasional inappropriate extra branchings to form multiple 
canal lumena; alleles of sma-1 exhibit a short, very wide, 
unseptate canal.  Finally, the lone exc-7 allele rh252 
exhibits small cysts along the length of the canal, 
terminating in a large group of tiny cysts.
        We have now made double mutants of several of the genes 
from various groups.  Double mutants made of genes from 
within any one group showed no increase in severity in canal 
phenotype.  For example, exc-2 (rh90) exc-4 (rh133) animals 
showed no changes in cyst size or morphology compared to 
rh90 or rh133 alone, and no increase in larval lethality. 
Similarly, exc-6 (rh103) exc-8 (rh210) canals appeared no 
shorter or more meandering than those of the single mutants, 
and exc-1 (rh26) exc-5 (rh232) mutant canals had similar 
cyst size and placement as the single mutants alone.
        Doubles constructed with exc-7 (rh252) showed 
interesting effects, however.  exc-7 is epistatic to exc-6; 
the double mutants showed no abnormal branchings, only a 
series of small cysts along the entire canal length.  
Perhaps not surprisingly, the large cysts of exc-2 and exc-4 
are epistatic to exc-7.  Most strikingly, the doubles exc-7 
(rh252) sma-1 (e30) and especially exc-7 (rh252) exc-3 
(rh207) show canal phenotypes different from that of the 
single mutants; instead, these animals show large cysts near 
the excretory cell body, like those of exc-4 mutants.  
Finally, we have been unable so far to isolate doubles of 
exc-7 (rh252) and either exc-1 (rh26) or exc-5 (rh232); this 
could indicate that these mutants are lethal in combination.
        Our previous ultrastructural data, along with 
sequencing results from the labs of David Baillie (Jones & 
Baillie, Mol. Gen. Genet. 248, 719-726, !95) and Judith 
Austin (see McKeown, Patel, Praitis, and Austin, WBG 14 (2), 
p. 83) suggest that the exc genes encode proteins necessary 
for the proper placement of structural elements, both 
extracellular and cytoskeletal, at the apical epithelial 
surface.  We believe that these new genetic results indicate 
that the differing morphologies of the various groupings of 
exc genes reflect different elements that interact with each 
other to shape this surface; Exc-7 may play a central 
position in these interactions.