Poster abstracts
Poster number 39 submitted by David Goich
The p38 MAPK Hog1 remodels the translatome of the fungal pathogen Cryptococcus neoformans.
David Goich (Microbiology and Immunology, University at Buffalo), Amanda L. M. Bloom (Microbiology and Immunology, University at Buffalo), John C. Panepinto (Microbiology and Immunology, University at Buffalo)
Abstract:
Cryptococcus neoformans is an environmental fungus that causes severe opportunistic infections in immunocompromised individuals, particularly people living with HIV/AIDS. Upon entry into the host, C. neoformans rapidly alters its proteome to accommodate a variety of stressors, including elevated temperature, reactive oxygen species (ROS) in phagocytes, nutrient deprivation, and more. Our preliminary data indicate that these processes are dependent in part on the p38 MAPK, Hog1, which couples the translational response to stress-sensing signal transduction. Using polysome profiling, translational output assays, and mRNA repression kinetics, we investigated whether two putative kinases downstream of Hog1, Hrk1 and Cmk2, are similarly defective in translatome reprogramming. We also investigated the role of these proteins in the translational response to fludioxonil, an antifungal with Hog1-dependent activity. We found that while hrk1∆ demonstated delayed recovery from translation repression, deletion of Cmk2 caused dysregulation of eIF2α. Our data suggests that both of these putative effectors of Hog1 play a role in translational adaptation to stress. Ongoing investigations will determine if these proteins play stress-specific roles, as well as the role of each in the translational response to fludioxonil.
Keywords: Translation