Official websites use. Share sensitive information only on official, secure websites. Caenorhabditis elegans strains mutant for the unc gene show abnormal locomotion and muscle structure. Experiments revealed that unc is one of four C. Assays of in vivo muscular performance at high and low loads indicated that su sd is most deleterious, with e least and su sd 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 filaments 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 filaments.
The exacerbated deficits of su sd 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 su sd highlights importance of the extreme C-terminus in the protein's inhibitory function.
Nearly a century ago, A. Hill drew attention to a problem that remains incompletely solved, namely how muscular performance is varied from one striated muscle to the next despite considerable similarity in structure.
