Worm Breeder's Gazette 11(3): 13

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.

Mosaic Expression of vit Transgene

Peg MacMorris, John Spieth, Susan Greenspoon, Sherryl Broverman and Tom Blumenthal

A critical part of our analysis of the importance of the sequence 
elements VPE1 and VPE2 for vit promoter function has been the 
verification of correctly regulated expression.  Stable transgenic 
lines containing a vit-2/6 fusion gene under the control of modified 
promoters have been tested for correct tissue, stage and sex 
specificity by in situ hybridization.  In the course of the analysis 
of strains containing mutant promoters, we have made two surprising 
observations.  (1) In strains in which most individuals have no 
detectable vit-2/6 RNA, there are occasional rare individuals (
approximately 5% in a strain with a point mutation in one of the two 
VPE2 elements) which have high levels of the RNA .  (2) Individual 
worms have expression levels which vary dramatically within a single 
intestine.
Since our initial discovery, we have looked at 13 strains with 11 
different modified promoters affecting 6 different elements within the 
promoter.  While 3 strains carrying the wild-type promoter region (247 
bp) show expression in all intestinal cells, all strains carrying 
mutant promoters exhibit mosaicism to varying degrees.  In each case 
the pattern is similar: the most anterior end of the intestine (int1 
cells) has no or low hybridization signal, the middle region (approx 
int5 cells) shows the highest signal and more posterior intestinal 
cells show lowered levels.  In strains that have mutant promoters with 
less drastically altered expression, the areas of positive signal 
extend farther anteriorly and posteriorly.  In the least extreme cases 
(i.e.  deletion of the most distal VPE1) the mosaicism is displayed 
only as a variable lack of signal in the first tier of intestinal 
cells.  The signal changes continuously from regions of high to low 
intensity in most cases, with the exception of the int1 cells.  The 
lack of expression in these cells is often delineated by an abrupt and 
distinct line of higher level expression beginning in the next set of 
cells.
If we look at strains with an unmodified promoter at very early time 
points relative to the onset of vitellogenin synthesis (late L4 to 
early post-lethargus adults) we sometimes find a similar pattern, 
consistent with Pepper Schedin's observations on wild-type worms 
examined with a vit-5 specific probe.
Our interpretation of the mosaic intestines is that the lowered 
affinity of binding for activator in these lines reveals an inherent 
spatial distribution of activator molecules within the worm intestine. 
The lowered level expression seen at the anterior and posterior ends 
of the intestine could be due to a single activator produced at the 
middle of the animal - creating a gradient in its distribution toward 
the head and tail, by gradients of two activators, both of which are 
required, one originating anteriorly and one posteriorly.  At the 
earliest times in wild-type strains we see evidence of the activator 
distribution pattern, but normally all cells in the intestine quickly 
reach threshold levels of activator sufficient for wild-type promoter 
function.  With debilitated promoters, higher thresholds are required 
and therefore mosaics can be found for an extended time.  We interpret 
the occurrence of rare expressing animals within negative populations 
as evidence that promoter function depends on the binding of proteins 
to several elements to build a complex.  Lowered levels of individual 
bound elements give a lowered chance of total complex function, yet 
once formed the complex gives 'normal' level expression.