Actin-Related Protein2/3 Complex Component ARPC1 Is Required for Proper Cell Morphogenesis and Polarized Cell Growth in Physcomitrella patens

• Published in: The Plant cell Vol. 17; no. 8; pp. 2327 - 2339
• Main Authors: Harries, Phillip A, Pan, Aihong, Quatrano, Ralph S
• Format: Journal Article
• Language: English
• Published: England American Society of Plant Biologists 01-08-2005
• Subjects: actin; Actin-Related Protein 2; Actin-Related Protein 3; Actins; Amino Acid Sequence; amino acid sequences; Animals; Bryopsida - cytology; Bryopsida - growth & development; Cell Division; Cell growth; Cell lines; Cell morphology; Cell walls; complementary DNA; Conserved Sequence; Cytoskeletal Proteins - genetics; Cytoskeletal Proteins - metabolism; gene expression; Gene Expression Regulation, Plant; genes; messenger RNA; Microfilaments; Molecular Sequence Data; Morphogenesis; Mosses; mosses and liverworts; mutants; nucleotide sequences; phenotype; Phenotypes; Physcomitrella patens; Plant cells; plant proteins; Plants; polarized cell growth; protein-protein interactions; Protoplasts; Reverse transcriptase polymerase chain reaction; Sequence Alignment; Sequence Homology, Amino Acid
• ISSN: 1040-4651; 1532-298X; 1532-298X
• DOI: 10.1105/tpc.105.033266

The actin-related protein2/3 (Arp2/3) complex functions as a regulator of actin filament dynamics in a wide array of eukaryotic cells. Here, we focus on the role of the Arp2/3 complex subunit ARPC1 in elongating tip cells of protonemal filaments of the moss Physcomitrella patens. Using RNA interference (RNAi) to generate loss-of-function mutants, we show dramatic defects in cell morphology manifested as short, irregularly shaped cells with abnormal division patterns. The arpc1 RNAi plants lack the rapidly elongating caulonemal cell type found in wild-type protonemal tissue. The absence of this cell type prevents normal bud formation even in response to cytokinin treatment and results in filamentous colonies lacking leafy gametophores. In addition, arpc1 protoplasts show an increased sensitivity to osmotic shock and are defective in their ability to properly establish a polarized outgrowth during regeneration from a single cell. This failure of arpc1 protoplasts to undergo proper tip growth is rescued by ARPC1 overexpression and is phenocopied in wild-type protoplasts treated with Latrunculin B, a potent inhibitor of actin polymerization. We show in moss that ARPC1, and by inference the Arp2/3 complex, plays a critical role in controlling polarized growth and cell division patterning through its regulation of actin dynamics at the cell apex.