A Balance of Capping Protein and Profilin Functions Is Required to Regulate Actin Polymerization inDrosophilaBristle

Abstract

Profilin is a well-characterized protein known to be important for regulating actin filament assembly. Relatively few studies have addressed how profilin interacts with other actin-binding proteins in vivo to regulate assembly of complex actin structures. To investigate the function of profilin in the context of a differentiating cell, we have studied an instructive genetic interaction between mutations in profilin (chickadee) and capping protein (cpb). Capping protein is the principal protein in cells that caps actin filament barbed ends. When its function is reduced in the Drosophila bristle, F-actin levels increase and the actin cytoskeleton becomes disorganized, causing abnormal bristle morphology. chickadee mutations suppress the abnormal bristle phenotype and associated abnormalities of the actin cytoskeleton seen in cpb mutants. Furthermore, overexpression of profilin in the bristle mimics many features of the cpb loss-of-function phenotype. The interaction between cpb and chickadee suggests that profilin promotes actin assembly in the bristle and that a balance between capping protein and profilin activities is important for the proper regulation of F-actin levels. Furthermore, this balance of activities affects the association of actin structures with the membrane, suggesting a link between actin filament dynamics and localization of actin structures within the cell.

Extrinsic and intrinsic mechanisms directing epithelial cell sheet replacement duringDrosophilametamorphosis

“…genes hold a tight balance between actin depolymerization and assembly (Hopmann and Miller, 2003). Loss of Cpb or excessive Profilin activity resulted in actin accumulations and abnormal bristles.…”

Cytoskeletal dynamics and cell signaling during planar polarity establishment in theDrosophilaembryonic denticle

“…EM studies, the use of cytoskeletal inhibitors, and FRAP, which proved informative in studies of wing hairs and bristles (Fei et al, 2002;Tilney et al, 1995;Tilney et al, 1996;Tilney et al, 2000a;Turner and Adler, 1998), may reveal how actin in denticles is assembled. Finally, it will be important to study in denticles additional actin regulators that regulate bristle development (Hopmann and Miller, 2003;Wahlstrom et al, 2001).…”

“…The core polarity proteins also regulate PCP of sensory bristles. Much is known about subsequent regulation of actin assembly there, revealing roles for actin cross-linkers and other actin regulators (Guild et al, 2003;Hopmann and Miller, 2003;Tilney et al, 1998;Tilney et al, 2000b;Wahlstrom et al, 2001).…”

The flare Gene, Which Encodes the AIP1 Protein of Drosophila, Functions to Regulate F-Actin Disassembly in Pupal Epidermal Cells

“…The hairs produced by both flr and tsr wing cells are far more abnormal than those seen due to mutations in genes that encode actin bundling proteins (Bryan et al 1993;Petersen et al 1994), capping protein (Hopmann et al 1996;Hopmann and Miller 2003;Frank et al 2006), cytoplasmic myosins such as myosin VII (Turner and Adler 1998;Kiehart et al 2004), or other proteins thought to modulate actin polymerization, such as profilin (Verheyen and Cooley 1994) or Arp2/3 (Hudson and Cooley 2002) . The reason for this is uncertain and leads to the question as to what is the basis for the extreme flr phenotype?…”