Lineage-Specific Gene Expression in Caenorhabditis elegans 
the ges-1 gene and control its expression only in 
the gut and only at the correct embryonic stage. 
Here one of the few limitations of C. elegans as an 
experimental organism becomes apparent: it is 
essentially impossible to obtain large amounts of 
synchronized embryos on which to do biochemi- 
cal experiments. We are taking two routes past 
this'obstacle. 
The first route is to turn part of our efforts to 
Ascaris suum, the well-known parasite of pig in- 
testines. Ascaris adults are millions of times 
larger than adult C. elegans, yet their embryos are 
remarkably similar. Furthermore, Ascaris fe- 
males produce hundreds of thousands of ferti- 
lized eggs per day, which develop more-or-less 
synchronously. We hope to use this system to 
watch the arrival and departure of transcription 
factors during early nematode development. 
The second route is based on our finding that 
C. elegans embryos can be blocked in mid- 
development by exposure to the chemotherapeu- 
tic agent fluorodeoxyuridine. This has allowed us 
to produce nuclear extracts from these blocked 
embryos and to detect a number of protein factors 
(possibly as many as a dozen) that bind to the 
5'-flanking sequence of the ges-1 gene. We have 
concentrated on two such factors. 
The first factor binds to a DNA sequence that 
we have tentatively identified as a gut "activa- 
tor." The protein is not detectable in oocyte cyto- 
plasm and thus must be produced (transcribed or 
translated) sometime during early development. 
The second factor binds to a sequence that is com- 
pletely conserved between C. elegans and the re- 
lated nematode Caenorhabditis briggsae. Un- 
like the first factor, this second factor is present 
in the oocyte cytoplasm and must migrate at some 
point in early development into the embryonic 
nuclei. The second factor would thus be a candi- 
date for a classic cytoplasmic "determinant" pro- 
duced by the mother worm and then segregated 
into the gut lineage during early cell cycles. 
If we can indeed describe the constellation of 
transcription factors responsible for activating 
the ges-1 gene in the developing gut, will we re- 
ally be much further ahead in understanding its 
control? In some respects, all this work will only 
move the problem one step further back in devel- 
opment, to the question of how the transcription 
factors themselves got where they did. However, 
one of the main advantages of ges-1 as an experi- 
mental system is that we only have 3-5 cell cy- 
cles through which to regress, until we reach the 
oocyte. Thus it should be possible to describe the 
complete molecular logic that controls this sim- 
ple gene. 
This work was supported by the Medical Re- 
search Council of Canada and by the Alberta Heri- 
tage Foundation for Medical Research. 
A newly hatched larva of the nematode Caeno- 
rhabditis elegans. The dark red precipitate re- 
flects the esterase activity of the ges- 1 gene, ex- 
pressed in all 20 cells of the gut. 
From Edgar, L.G., and McGhee, J.D. 1986. 
DevBiol 114:109-118. 
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