Project description:We measured protein translation (by ribosome profiling) and RNA levels (by polyA-enriched RNA-seq) in Cryptococcus neoformans strain H99 and Cryptococcus neoformans strain JEC21. This is the first transcriptome-wide map of translation in this species complex.
Project description:Cryptococcus neoformans lab strain H99 was used to obtain tunicamycin adaptors. Transcriptome of one aneuploid adaptor, FY1381, was compared to parent.
Project description:Proper mitochondrial function is critical for the ability of the fungal pathogen Cryptococcus neoformans to cause disease. Mitochondrial dysfunction of WT cells treated with antimycin A or L-DOPA, or on cells lacking Cir1 is evident from this dataset. These experiments revealed influences on transcript levels of genes encoding Fe-S cluster assembly components and the response to oxidative stress in Cryptococcus neoformans.
Project description:In this study, H99 is a wild type Cryptococcus neoformans strain. TJ1854 is a chromosome 4 disomy strain derived from H99. Approximately 1 million cells of TJ1854 were spread on YPD plate supplemented with 6ug/ml amphtericin B. Randomlyh 27 adaptors (TJ2487-TJ2513) were chosen. These adaptors were sequenced.
Project description:We exposed Cryptococcus neoformans lab strain H99 to tunicamycin and obtained some adaptors. We did whole genome sequencing of these adaptors as well as the parent.
Project description:Log phase of Cryptococcus neoformans strain H99 was exposed to amphotericin B (1.5μg/ml) or vehicle (control) for 3h. Transcriptome of drug treated cells were compared to no treatment cells.
Project description:Thermotolerance, a key factor essential for the virulence of pathogenic fungi including Cryptococcus neoformans, remains largely unexplored in terms of its underlying mechanism. In this study, our findings demonstrate that Set3C, a widely distributed and conserved histone deacetylase complex, is required for thermotolerance in Cryptococcus neoformans. Specifically, the deletion of the core subunit Set302, responsible for the integrity of the complex, results in a significant reduction in the growth ability under high stress and the viability at extreme temperature. Moreover, the absence of Set302 leads to a decrease in the production of capsule and melanin. Transcriptomics analysis revealed that Set302 regulates a large number of genes compared to normal condition, and their expression is responsive to heat stress. Notably, we observed that Set302 positively influences the expression of genes related to ubiquitin-proteasome system (UPS) at high temperature. Using GFP-α-synuclein overexpression model, we observed a pronounced accumulation of misfolded proteins under heat stress, consequently inhibiting the thermotolerance of Cryptococcus neoformans. Furthermore, the loss of Set302 exacerbates this inhibition of thermotolerance. Interestingly, set302∆ strain exhibits a similar phenotype under proteasome stress as it does under high temperature. We also found that set302∆ strain displayed significantly reduced pathogenicity and colonization ability compared to the wild-type strain in the murine infection model. Collectively, our findings indicate that Set302 modulates the degradation of misfolded proteins through the UPS pathway, thereby affecting the thermotolerance and pathogenicity of Cryptococcus neoformans.
Project description:We investigated the effects of the hypoxia-mimetic CoCl2 on the gene expression of pathogenic fungus Cryptococcus neoformans. Keywords: compound treatment design
Project description:Cryptococcus neoformans lab strain H99 was used to obtain brefeldin A adaptors. Transcriptomes of 4 adaptors, each bearing a unique aneuploid, were compared to H99.
