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

824
824. Structural and Functional
Disruption of Muscle Caused by
Troponin I Mutation
James Priest 1 , Angie Burkeen 2 ,
Krystina Rybicka 3 , Clara
Franzini-Armstrong 3 , Taylor Allen 1
1 Biology, Oberlin College, Oberlin, OH
44074-1082
2 Molecular Genetics & Cell Biology, U. of
Chicago, Chicago, IL 60637
3 Cell & Developmental Biology, U. of
Pennsylvania, Philadelphia, PA 19104-6058
Muscular performance varies enormously
among animals, as well as even within a single
organism, and some of the variation is
speculated to arise from adaptations of troponin,
which regulates tension development in striated
muscle. Like vertebrates, C. elegans has
multiple genes coding for troponin I (TnI), the
inhibitory subunit within the ternary troponin
complex. Phylogenetic analysis of the four C.
elegans TnIs suggested that diversification of
TnI isoforms occurred independently in
vertebrates and invertebrates. Nonetheless, the
domain architecture of TnI is preserved in all
isoforms. RNA interference (RNAi) of TnI-1
(F42E11.4), expressed in embryonic body wall
muscle and hermaphroditic gonad, led to no
discernible defect. Similar results were obtained
following RNAi of TnI-4 (W03F8.1), expressed
in the pharyngeal muscle. RNAi of the larval
and adult body wall muscle TnI, Unc-27/TnI-2
(ZK721.2), produced rigid paralysis mimicking
that of unc-27 mutants. Elimination of TnI-3
(T20B3.2) yielded constipated and egg-laying
defective worms, consistent with detection of
TnI-3 mRNA in vulval muscles and intestine.
Three mutant alleles of unc-27 exist: e155
(Gln10stop), a presumed null; su142sd
(Gln122stop), which lacks the domain thought
necessary for inhibition at sub-micromolar
Ca 2+ ; and su195sd (Glu207stop), which
eliminates only the C-terminus. Each of the
mutant alleles severely compromised swimming
behavior of adult homozygous hermaphrodites
(p