| Many species of fungi undergo a dimorphic transition to switch from a unicellular yeast-like growth form to a filamentous growth form. Ustilago maydis undergoes such a transition, in response to successful mating events and subsequent host cues, to form a filamentous pathogenic form. U. maydis also undergoes haploid filamentous growth in response to several environmental cues including, but not limited to nutrient limitation, pH, lipids, among others.;Furthermore, I demonstrate the role of Ump2 in affecting filamentation depends on its expression levels. This study reveals that Ump2 as well as Ump1 expression alters the transcription of genes essential in the mating response pathway and in pathogenicity. Transcription of numerous other genes, some shown to be induced during filamentous growth and a few others, during growth of the fungus inside the host, are also affected by changes in the expression of U. maydis Amts. Interestingly, ump1ump2 double deletion strains are attenuated in their ability to infect the host. These results suggest Amts sense the external environment and transmit information by directly or indirectly affecting one or more signaling pathways to control the morphogenetic fate of U. maydis.;Ammonium transporter proteins (Amts) play an essential role in controlling the dimorphic transition in response to nutrient limitation, specifically nitrogen in the form of ammonium. I demonstrate a role for the U. maydis Amts in controlling filamentation under nitrogen limiting and nitrogen replete conditions via signal transduction pathways. I show a functional connection between Amts and the signaling protein, Rho1 GTPase, in U. maydis. These experiments suggest that both the high and low affinity ammonium transporters physically interact among themselves and also interact with Rho1 under low ammonium conditions. Epistasis experiments suggest that interaction of high affinity Amt, Ump2, with Rho1 is important for the filamentous growth response. Over-expression of rho1 reduced the filamentation by haploid cells under low ammonium conditions. Additionally, ump2 deletion further eliminated the filamentous growth by haploid cells over-expressing rho1 under low ammonium conditions. Inferring from these data and the known role of Rho1 in affecting filamentation, I propose a model for Ump2 and Rho1 function in U. maydis. |
