The organization of the actin cytoskeleton is essential for several cellular processes. Here we report the characterization of a Saccharomyces cerevisiae novel gene, SDA1, encoding a highly conserved protein, which is essential for cell viability and is localized in the nucleus. Depletion or inactivation of Sda1 cause cell cycle arrest in G 1 by blocking both budding and DNA replication, without loss of viability. Furthermore, sda1-1 temperature-sensitive mutant cells arrest at the non-permissive temperature mostly without detectable structures of polymerized actin, although a normal actin protein level is maintained, indicating that Sda1 is required for proper organization of the actin cytoskeleton. To our knowledge, this is the first mutation shown to cause such a phenotype. Recovery of Sda1 activity restores proper assembly of actin structures, as well as budding and DNA replication. Furthermore we show that direct actin perturbation, either in sda1-1 or in cdc28-13 cells released from G 1 block, prevents recovery of budding and DNA replication. We also show that the block in G 1 caused by loss of Sda1 function is independent of Swe1. Altogether our results suggest that disruption of F-actin structure can block cell cycle progression in G 1 and that Sda1 is involved in the control of the actin cytoskeleton.
The Saccharomyces cerevisiae SDA1 gene is required for actin cytoskeleton organization and cell cycle progression / G. Buscemi, F. Saracino, D. Masnada, M.L. Carbone. - In: JOURNAL OF CELL SCIENCE. - ISSN 0021-9533. - 113 ( Pt 7):7(2000 Apr), pp. 1199-1211.
The Saccharomyces cerevisiae SDA1 gene is required for actin cytoskeleton organization and cell cycle progression
G. BuscemiPrimo
;
2000
Abstract
The organization of the actin cytoskeleton is essential for several cellular processes. Here we report the characterization of a Saccharomyces cerevisiae novel gene, SDA1, encoding a highly conserved protein, which is essential for cell viability and is localized in the nucleus. Depletion or inactivation of Sda1 cause cell cycle arrest in G 1 by blocking both budding and DNA replication, without loss of viability. Furthermore, sda1-1 temperature-sensitive mutant cells arrest at the non-permissive temperature mostly without detectable structures of polymerized actin, although a normal actin protein level is maintained, indicating that Sda1 is required for proper organization of the actin cytoskeleton. To our knowledge, this is the first mutation shown to cause such a phenotype. Recovery of Sda1 activity restores proper assembly of actin structures, as well as budding and DNA replication. Furthermore we show that direct actin perturbation, either in sda1-1 or in cdc28-13 cells released from G 1 block, prevents recovery of budding and DNA replication. We also show that the block in G 1 caused by loss of Sda1 function is independent of Swe1. Altogether our results suggest that disruption of F-actin structure can block cell cycle progression in G 1 and that Sda1 is involved in the control of the actin cytoskeleton.File | Dimensione | Formato | |
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