Worm Breeder's Gazette 8(1): 10

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.

Expression of ace-1 in Genetic Mosaics

R.K. Herman

I have been studying the expression of ace-1 in animals made mosaic 
through the somatic loss of a free duplication.  Recall that ace-2- 
utants show a characteristic uncoordination (
Culotti et al.  1981 Genetics 97: 281-305), which I shall denote Ace-
Unc, and that one copy of either ace-1+ or ace-2+ is sufficient to 
confer normal movement.  Animals of genotype ace-2 I; unc-3 
ace-1 X; mnDp14 have a wildtype phenotype, since 
mnDp14 carries the wild type alleles of unc-3 
ogeny lacking mnDp14 are Unc-3 
r amphids and phasmids are not stained by 
fluorescein isothiocyanate (FITC), owing to the Daf-6 phenotype.  The 
Ace-Unc phenotype is difficult to discern when the animals are also 
Unc-3, but Ace-Unc by itself is easy to distinguish from Unc-3 (or 
semi-Unc-3, which is produced by loss of the duplication in certain 
cells descending from AB.p).  I have found six Ace-Unc non-Unc-3 self-
progeny of ace-2; daf-6 mnDp14 
hermaphrodites.  All six had no duplication in their germ lines, i.e., 
all of their self progeny were Unc-3.  Five of the six were stained 
with FITC and seen to be positive (wild type).  I previously showed 
that Unc-3 mosaics generated from unc-3 es 
are FITC-negative and that semi-Unc-3 mosaics generated from the same 
genotype usually show some lack of sensilla staining as well.  One 
AceUnc animal was assayed histochemically for acetylcholinesterase (
Culotti et al., ibid.).  By this method, we see the 
acetylcholinesterase activity in the region of the nerve ring (but not 
the ventral nerve cord) conferred by a single copy of ace-1+.  The Ace-
Unc animal was negative.  These results suggest that the uncoordinated 
phenotype and the absence of enzyme activity determined 
histochemically in the region of the nerve ring were the result of the 
absence of ace-1+ in descendants of P1.  The most reasonable 
interpretation would be that the ace-1+ gene is active in muscle cells.
This interpretation is consistent with the results obtained with two 
other mosaic animals found among the progeny of ace-2; 
daf-6 mnDp14 hermaphrodites.  
These were Unc-3 animals that gave some wild-type self-progeny.  As I 
have previously shown, such animals have lost the duplication at AB or 
AB.p.  Both were found to have normal acetylcholinesterase activity in 
the region of the nerve ring.
It should be obvious that these results are quite sketchy and that 
more data needs to be collected.  I am also constructing a strain of 
the following genotype: ace-2 I; unc-93 III; unc-3 
lication carries sup-10+, which 
is dominant to sup-10, the suppressor of unc-93.  The prediction to be 
tested is that all nonUnc-3 non-Unc-93 animals produced through 
duplication loss, which I have previously argued must occur at P1, 
will be Ace-Unc (and FITC-positive and acetylcholinesterase negative).