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

• Published in: Molecular biology of the cell Vol. 22; no. 21; pp. 4047 - 4058
• Main Authors: Bunnell, Tina M, Burbach, Brandon J, Shimizu, Yoji, Ervasti, James M
• Format: Journal Article
• Language: English
• Published: United States The American Society for Cell Biology 01.11.2011
• Series: A Highlights from
• Subjects: Actins - deficiency; Actins - genetics; Actins - metabolism; Animals; Brain - metabolism; CD4-Positive T-Lymphocytes - metabolism; CD4-Positive T-Lymphocytes - physiology; Cell Movement; Cell Proliferation; Cells, Cultured; Female; Fibroblasts; Gene Expression Profiling; Gene Expression Regulation; Gene Knockout Techniques; Heterozygote; Kaplan-Meier Estimate; Kidney - metabolism; Liver - metabolism; Lung - metabolism; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Organ Specificity; Primary Cell Culture
• ISSN: 1059-1524; 1939-4586
• DOI: 10.1091/mbc.E11-06-0582

Ubiquitously expressed β-actin and γ-actin isoforms play critical roles in most cellular processes; however, their unique contributions are not well understood. We generated whole-body β-actin-knockout (Actb(-/-)) mice and demonstrated that β-actin is required for early embryonic development. Lethality of Actb(-/-) embryos correlated with severe growth impairment and migration defects in β-actin-knockout primary mouse embryonic fibroblasts (MEFs) that were not observed in γ-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 β-actin in highly motile T cells. Of great interest, ablation of β-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 β-actin in regulating cell migration and gene expression through control of the cellular G-actin pool.