Program of the 2001 International Worm Meeting - Sternberg Lab ...

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with sys-1 to control cell polarity in the
hermaphrodite gonad. All six sys genes have
been carefully mapped, and to date, only
sys-2/pop-1 maps to a gene encoding a known
Wnt pathway component. The pop-1(RNAi)
phenotype suggests that pop-1 is part of a
common program that controls the asymmetric
first division of Z1 and Z4. We suggest that this
common program may have been modified
during evolution to generate critical regulatory
cells in distinct parts of the hermaphrodite and
male lineage. The mechanism by which POP-1
is differentially controlled in the two sexes is
not known, but may involve the two regions
altered by the pop-1/sys-2 missense mutations,
the β-catenin binding site and the HMG box.
1. Sternberg and Horvitz (1988) Developmental
Biology 130: 67-73.
2. Miskowski et al. (2000) Developmental
Biology 230: 61-73.
3. Lin, et al. (1995) Cell 83: 599-609.
4. Sawa et al. (1996) Genes & Development 10:
2189-97.
271. The presenilin SEL-12 is
required during vulva muscle
development for a normal egg laying
behaviour in C. elegans.
Stefan Eimer, Roland Donhauser,
Ralf Baumeister
Genzentrum/LMU, Feodor-Lynen-Strasse 25,
D-81377 Munich, Germany
271
The Caenorhabditis elegans SEL-12 protein was
shown to be not only structurally but also
functionally similar to the human presenilins
involved in Familial Alzheimer’s disease. sel-12
was initially identified as a suppressor of
gain-of-function alleles of lin-12/Notch in C.
elegans [1]. Animals mutant for sel-12 exhibit a
highly penetrant egg laying defect (egl) and
morphological abnormalities that lead to a
grossly abnormal protruding vulva (p-vul).
Anna Newman [2] has shown that some sel-12
animals fail to specify the p cell fate correctly
leading to a defective vulva uterine connection.
However strains containing weaker sel-12
alleles only show a weakly penetrant p-vul
defect and are able to lay eggs, but become Egl
and die of bagging later.This suggests that there
might be additional defects responsible for the
Egl defect.
We have previously identified a functional
defect of sel-12 loss-of-function mutants in
selected cholinergic neurons [3]. However,
sel-12 is broadly expressed both in neurons and
in a variety of muscles at all developmental
stages. Therefore we investigated whether the
inability of sel-12 animals to lay eggs is also
caused by a neuronal defect. Pharmacological
and epistasis tests revealed that sel-12 animals
behave like a muscle structure mutant. Using
different GFP expression constructs that stain
the vulva muscles, we are able to show that
sel-12 mutants indeed have several defects in
their vulva muscles. sel-12 mutant animals
display a range of defects. Most animals exhibit
misaligned, distorted vulva muscles but we also
see muscles which have mismigrated or
degenerated. Expression of the sel-12 cDNA
under the control of the myo-3 and unc-54
promoters does not rescue the Egl defect of
sel-12 which implies that sel-12 activity is not
required in mature vulva muscles but rather
during their development. In hermaphrodites,
the vulva muscles are derived from the