The complete absence of cytoplasmic γ-actin results in no discernible phenotype in mice or primary fibroblasts.

Abstract

Mice and primary fibroblasts derived from mouse embryos completely lacking cytoplasmic β-actin, because the Actb gene was engineered to instead express γ-actin protein, have previously been found to be virtually devoid of phenotype. Here, we report the characterization of mice and mouse embryonic fibroblasts homozygous for an Actg1 allele edited to translate β-actin instead of γ-actin (Actg1-coding beta; Actg1^c-b/c-b), which resulted in mice and fibroblasts that are devoid of γ-actin. We demonstrate that these Actg1^c-b/c-b mice present with no measurable phenotype in survival, body mass, activity, muscle contractility, or auditory function. Primary fibroblasts derived from Actg1^c-b/c-b mouse embryos were still proliferative, with several measured parameters of cell motility not different from wild type. From these and previous data, we conclude that β- and γ-actin proteins are redundant in primary embryonic fibroblasts and during normal mouse development.