Cla4, but not Rac1, regulates the filamentous response of Ustilago maydis to low ammonium conditions.

Ustilago maydis, the fungal pathogen of maize, undergoes a dimorphic transition from budding yeast-like growth to filamentous growth, both as part of its program for pathogenesis and distinctly, in response to environmental cues, such as acid pH or low nitrogen availability. Smu1 is a p21-activated protein kinase (PAK) with roles in both the mating response required for the former function, as well as for the nutrient response. Hsl7 may be a negative regulator of Smu1 and appears to play a role in cell length and cell cycle.  Additional proteins that participate in cell polarity and filamentation pathways include the small G protein, Rac1, and its effector PAK kinase, Cla4. Here we describe further experiments that explore the roles of Cla4 and Rac1 in the response to nitrogen availability. While deletion of rac1severely delays filamentous growth on solid media low in ammonium (SLAD), we found that deletion of cla4 does not abolish filamentous cell morphology on solid SLAD. Unexpectedly, however, the Dcla4 mutants also filament in liquid SLAD. The filamentous cell morphology of the cla4 mutant in liquid SLAD has only been seen previously for one other mutant, a strain deleted for hsl7 that simultaneously over-expresses smu1.