?-Actin specifically controls cell growth, migration, and the G-actin pool.

ABSTRACT: Ubiquitously expressed ?-actin and ?-actin isoforms play critical roles in most cellular processes; however, their unique contributions are not well understood. We generated whole-body ?-actin-knockout (Actb(-/-)) mice and demonstrated that ?-actin is required for early embryonic development. Lethality of Actb(-/-) embryos correlated with severe growth impairment and migration defects in ?-actin-knockout primary mouse embryonic fibroblasts (MEFs) that were not observed in ?-actin-null MEFs. Migration defects were associated with reduced membrane protrusion dynamics and increased focal adhesions. We also identified migration defects upon conditional ablation of ?-actin in highly motile T cells. Of great interest, ablation of ?-actin altered the ratio of globular actin (G-actin) to filamentous actin in MEFs, with corresponding changes in expression of genes that regulate the cell cycle and motility. These data support an essential role for ?-actin in regulating cell migration and gene expression through control of the cellular G-actin pool.

SUBMITTER: Bunnell TM 

PROVIDER: S-EPMC3204067 | biostudies-literature | 2011 Nov

REPOSITORIES: biostudies-literature