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Transcript profiling of Candida albicasn gtr1/gtr1 mutant

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https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE104160
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The Target of Rapamycin complex (TORC1) is an essential regulator of metabolism in eukaryotic cells and in the fungal pathogen C. albicans regulates morphogenesis and nitrogen acquisition. Gtr1 encodes a highly conserved GTPase which in S. cerevisiae regulates nitrogen sensing and TORC1 activation. Here, were characterize the role of C. albicans GTR1 in TORC1 activation and compare with the previously characterized GTPase Rhb1. A homozygous gtr1/gtr1 mutant exhibited impaired TORC1-mediated phosphorylation of Ribosomal Protein S6 and increased susceptibility to rapamycin. Overexpression of GTR1 impaired nitrogen starvation induced filamentous growth, MEP expression and growth in BSA as the sole nitrogen source. Both GTR1 and RHB1 were shown to regulate genes involved in ribosome biogenesis, amino acid biosynthesis and expression of biofilm-growth induced genes. The rhb1/rhb1 mutant exhibited a different pattern of expression of Sko1 regulated genes and increased susceptibility to Congo Red and Calcofluor white. The homozygous gtr1/gtr1 mutant exhibited enhanced flocculation phenotypes and similar to the rhb1/rhb1 mutant exhibited enhanced biofilm formation on plastic surfaces. In summary, Gtr1 and Rhb1 link nutrient sensing and biofilm formation and this connectivity may have evolved to enhance competitiveness of C. albicans in niches where there is intense competition with other microbes for space and nutrients. gtr null/wildtype with four biological replicates. Dye swap included.
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2021-07-25
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