Expression of chicken gizzard RLC complements the cytokinesis and developmental defects of Dictyostelium RLC null cells.

Dictyostelium RLC null cells have defects in cytokinesis and development that can be rescued by expression of either the wild type Dictyostelium RLC or an RLC mutant that cannot be phosphorylated by MLCK (S13A) (Ostrow et al., 1994). The wild type and S13A mutant LCs rescued the cells equally well, despite the fact that RLC phosphorylation increases purified Dictyostelium myosin's activity 5-fold.

Regulatory light chain mutations affect myosin motor function and kinetics.

The actin-based motor protein myosin II plays a critical role in many cellular processes in both muscle and non-muscle cells. Targeted disruption of the Dictyostelium regulatory light chain (RLC) caused defects in cytokinesis and multicellular morphogenesis. In contrast, a myosin heavy chain mutant lacking the RLC binding site, and therefore bound RLC, showed normal cytokinesis and development.

Utility of recombinant flagellar calcium-binding protein for serodiagnosis of Trypanosoma cruzi infection.

The protozoan Trypanosoma cruzi is the causative agent of Chagas' disease, a major public health problem in Latin America and of growing concern in the United States as the number of infected immigrants increases. There is currently no testing of U.S.