Event Title

Characterizing Temperature-Sensitive Mutations in Caenorhabditis elegans Myosin (Unc-54)

Presenter Information

Amy Campbell, Oberlin College

Location

Science Center, Bent Corridor

Start Date

10-2-2015 12:00 PM

End Date

10-2-2015 1:20 PM

Poster Number

42

Abstract

Myosin 4, encoded by the gene unc-54, functions in the body wall muscle of the nematode C. elegans. In both nematode and human muscles, myosin is the motor in the force-generating powerstroke, which converts a chemical signal to mechanical energy. My research this summer aimed to characterize the genetic and physiological consequences of two temperature-sensitive mutations in the myosin head. More specifically, I explored whether the mutations’ phenotypic effects resulted from the reduced production of functional myosin or from the production of a poison myosin peptide, and whether the changes induced by an increase in temperature occurred developmentally or functionally. Using mechanical models for C. elegans movement, and polarized light microscopy of myosin filaments, I examined the phenotypic effects of the mutations e1301 and e1157 under different temperature conditions, and found evidence for dominant or semidominant behavior.

Major

Biology

Project Mentor(s)

Taylor Allen, Biology

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Oct 2nd, 12:00 PM Oct 2nd, 1:20 PM

Characterizing Temperature-Sensitive Mutations in Caenorhabditis elegans Myosin (Unc-54)

Science Center, Bent Corridor

Myosin 4, encoded by the gene unc-54, functions in the body wall muscle of the nematode C. elegans. In both nematode and human muscles, myosin is the motor in the force-generating powerstroke, which converts a chemical signal to mechanical energy. My research this summer aimed to characterize the genetic and physiological consequences of two temperature-sensitive mutations in the myosin head. More specifically, I explored whether the mutations’ phenotypic effects resulted from the reduced production of functional myosin or from the production of a poison myosin peptide, and whether the changes induced by an increase in temperature occurred developmentally or functionally. Using mechanical models for C. elegans movement, and polarized light microscopy of myosin filaments, I examined the phenotypic effects of the mutations e1301 and e1157 under different temperature conditions, and found evidence for dominant or semidominant behavior.