Caenorhabditis elegans strains mutant for the
unc-27 gene show abnormal locomotion and muscle structure. Experiments revealed that
unc-27 is one of four C. elegans troponin I genes and that three mutant alleles truncate the protein: recessive and presumed null allele
e155 terminates after nine codons; semidominant
su142sd eliminates the inhibitory and C-terminal regions; and semidominant
su195sd abbreviates the extreme C-terminus. Assays of in vivo muscular performance at high and low loads indicated that
su142sd is most deleterious, with
e155 least and
su195sd intermediate. Microscopy revealed in mutant muscle a prevalent disorder of dense body positioning and a less well defined sarcomeric structure, with small islands of thin. laments interspersed within the overlap region of A bands and even within the H zone. The mutants' rigid paralysis and sarcomeric disarray are consistent with unregulated contraction of the sarcomeres, in which small portions of each myofibril shorten irregularly and independently of one another, thereby distorting the disposition of. laments. The exacerbated deficits of
su142sd worms are compatible with involvement in vivo of the N-terminal portion of troponin I in enhancing force production, and the severe impairment associated with
su195sd highlights importance of the extreme C-terminus in