Altered Calmodulin Activity in Fluphenazine‐Resistant Mutant Strains: Pleiotropic Effect on Development and Cellular Organization in Volvox cavtevi

Nurith KURN*, Ben‐Ami ‐A SELA

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

Genetically altered calmodulin activity in spontaneously derived mutant strains, which were selected for resistance to the toxic effect of a specific inhibitor, the phenothiazine drug fluphenazine, is demonstrated. Partially purified calmodulin preparations from wild‐type and fluphenazine‐resistant strains of the multicellular alga Volvox carieri, were tested for the ability to activate Ca2+‐ATPase of the erythrocyte membranes, and the inhibition of this stimulatory activity by fluphenazine. Unlike the preparation obtained from wild‐type cells, mutant calmodulin is shown to be insensitive to fluphenazine inhibition, in one case, and calmodulin from another strain was found to be inactive in vitro, i.e. it did not activate Ca2+‐ATPase. The pleiotropic phenotype of the spontaneously derived mutant strains involved aberrant multicellular or‐ ganization and hormone‐independent committment of the multipotent asexual reproductive cells, gonodia, to sexual development. These results clearly implicate calmodulin in the control of development and morphogenesis in this simple multicellular eukaryote. In addition, intracellular inhibition of calmodulin in wild‐type cells is shown to block the morphogenic process of embryo inversion and to arrest motility. The availability of mutant calmodulin will facilitate further investigation of the role of this ubiquitous re‐ gulatory protein in the control of development and differentiation in multicellular eukarytes, as well as the fine structure/function relationship with regard to calmodulin modulation of a wide variety of cellular processes.

Original languageEnglish
Pages (from-to)53-57
Number of pages5
JournalEuropean Journal of Biochemistry
Volume121
Issue number1
DOIs
StatePublished - Dec 1981
Externally publishedYes

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