Background Caenorhabditis elegans is a nonparasitic, translucent roundworm that is commonly found in temperate soil ecosystems (Husson et al., 2009). Its length is approximately 1 millimeter even though adult worms can grow to a length of 1.5 millimeters. The worm is unsegmented and has a pseudocoelom. It does not have a respiratory and a circulatory system. The gut of C. elegans contains gut pellets that emanate a bright blue fluorescence, which is predominant when the animal dies. Most of these roundworms are hermaphrodites. However, the male worms possess dedicated tails for mating, which have spicules. C. elegans is an extensively investigated experimental prototypical organism that has led to great discoveries in the field of genetic analysis. Some of the features that contribute to its applicability in genetic studies include a short, three-day life cycle, small size, and an uncomplicated laboratory cultivation process (Andersen, Krichevsky, Leheste, & Moloney, 2008). Hundreds of these roundworms can be cultivated on one Petri dish containing a lawn of Escherichia coli as the source of food. In addition, the worm has been used to study molecular biology techniques such as RNA interference. Also, the worm is often used as a model to study physiological processes that occur in higher organisms (Benian & Epstein, 2011). The unc-22 gene codes for the production of a protein called twitchin, which is a gigantic intracellular protein with numerous fibronectin- and immunoglobulin-like realms. The protein also contains one protein kinase domain that resembles titin. The unc-22 gene is fundamental in tissues where it controls the actinomyosin contraction-relaxation cycle. The gene is also responsible for the sustenance of standard muscle morphology. Unc-22 interacts with the muscle protein myosin and is confined to A-bands of the worm’s striated muscles that make up the wall of the animal’s body. The unc-22 proteins can add phosphate groups to the light chain peptides that make up myosin and go through autophosphorylation outside a living organism. Twitchin influences muscle synchronization in C. elegans and controls muscular contraction. Interference with the unc-22 gene in C. elegans affects its function leading to compromised movement and the characteristic “twitcher” phenotype. Studies involving the manipulation of the unc-22 gene including the introduction of mutations and silencing various alleles of the gene have helped elucidate the structure and function of the gene, which is beneficial to the field of muscle physiology. Research Question Which alleles of the unc-22 gene elicit the strongest response in muscle movement when mutated? The unc-22 gene is fascinating because of its rare phenotype. Distorted alleles of the locus bring about different degrees of compromised movement and muscle incompetence. Weak alleles show a minimal effect on the motion or organization of the muscle. When strong alleles are affected, the result is almost complete paralysis of adult worms. Moreover, there may be aberrant muscle structure where the thick and thin filaments are available in the usual amounts, but their distribution is altered. However, all alleles result in a continuous, subcellular jerk in all the cells making up the muscles of the body wall. It has been reported that the alleles of the unc-5