Figure 9.

Working model for ArfA dependent secretion, actin ring positioning, hyphal growth, and morphology. (A) In wildtype hyphal tips, secretory vesicles containing cell end markers, wall synthesizing enzymes and other cargo move along microtubules and actin cables to the Spitzenkörper, and subsequently are fused to the plasma membrane by the exocyst/SNARE proteins, releasing hydrolytic/cell wall synthesizing enzymes. The actin ring is fixed a constant position of about 3 μm from the apex. Growth of the plasma membrane moves SNAREs/cell wall synthesizing enzymes to the posterior of the hypha (red arrows), which become endocytosed at the actin ring. Endosomes either recycle the contents back to the plasma membrane, presumably via the Spitzenkörper, or back to the anterior of the cell along microtubules as shown for A. nidulans (Taheri-Talesh et al., 2008). (B) Following a reduction or increase in ArfA levels, the secretory pathway is defective, disrupting supply of markers, enzymes, and other cargo. Either due to direct ArfA regulation, or due to this disruption of secretory cargo, the actin ring shifts an average of 0.6–1.2 μm toward the hyphal tip. Both defective vesicle formation, and actin ring position, may synergistically contribute to the pleiotropic phenotypic consequences of arfA mis-expression. For further discussion see main text.