We use the model fungus Ustilago maydis to study the role of the UPR in controlling development and adaptation to different environmental conditions. Cells need to re-adjust and modify their cellular programs in response to a wide range of biotic and abiotic stimuli. The UPR is a highly conserved cellular response to maintain homeostasis of the endoplasmic reticulum (ER). In situations of increased demands for protein production and secretion, potentially harmful un- or mis-folded proteins accumulate in the ER and activate the UPR pathway. Defects in UPR signaling are associated with a wide range of developmental, metabolic and neurodegenerative disorders.
The basidiomycete phytopathogen Ustilago maydis triggers plant tumor formation upon infection of its host plant corn. The infection process is dependent on the execution of defined developmental steps. These are controlled by the b-heterodimer, representing the master regulator of pathogenic and sexual development in U. maydis. Modification of the regulatory circuits controlled by the b-heterodimer is necessary to execute the developmental subprograms. Previous studies have shown that the Clp1 protein serves as the main factor to modify the b-regulatory circuit in order to align cell cycle control and the developmental program to the plant environment. The UPR pathway is directly connected to this regulatory module and required for pathogenic development of U. maydis.
We analyze the crosstalk of the UPR pathway and its role in controlling pathogenic development in U. maydis. We are currently investigating the role and principles of the UPR in controlling cellular behavior and developmental decisions using a wide range of genetic, biochemical and cell biological methods.