Genetic screening for suppressor mutations of the hyper- or non-filamentous growth of the yeast osmotic signalling mutants

Conference poster, 2010

In certain yeast Saccharomyces cerevisiae strains, diploid cells develop pseudohyphae under nitrogen starvation, while haploid cells produce invasive filaments that penetrate the agar in rich medium. We have recently reported that these morphological developments are strongly inhibited under hyper-osmotic condition through the high-osmolarity glycerol (HOG) response MAPK pathway (Furukawa et al., 2009, Mol Microbiol). Deletion of the HOG1 MAPK gene enhances morphological developments, while expression of active Hog1 inhibits those even in the absence of hyper-osmotic stress. Moreover, it has been reported that HOG1 affects morphology and pathogenicity also in other fungal species. Candida albicans hog1 mutant cells form (pseudo)hyphae and show related transcriptome changes even in the absence of morphogenetic signals. Cryptococcus neoformans hog1 mutant cells enhance production of capsule and melanin, which are crucial virulence factors. Hence, fungal Hog1 orthologues are thought to be central negative regulators of many aspects of morphological developments and virulence, and studies on the underlying mechanisms are relevant for the identification of novel targets for antifungal therapy. In order to more deeply understand the inhibitory role of Hog1 in morphological developments, the proteins or signalling pathways affected by Hog1 need to be identified. In this study, we attempted to screen suppressor mutations of the hyper- or non-filamentous growth which are caused by HOG1 deletion or active Hog1, respectively. On the basis of the screening results, the mechanism by which Hog1 negatively regulates morphological developments will be discussed.