1887

Abstract

There are six essential genes in the genome which encode proteins bearing the tetratricopeptide repeat (TPR) domain that mediates protein–protein interaction. Thus far, the function of one of them, , remains unknown. Our conditional mutants of display osmoremedial temperature sensitivity, hypersensitivity to both Calcofluor White and low concentrations of SDS, and osmoremedial caffeine sensitivity. These are hallmarks of mutants that display cell wall defects. Accordingly we rename the gene as (ssential for aintenance of the cell all). Loss of Emw1p function is not associated with abrogation of the cell wall integrity (CWI) MAP kinase cascade. Instead, mutants activate this cascade even at permissive temperature, indicating that loss of Emw1p function does not cause a defect in sensors and effectors of cell wall signalling, but leads to a cell wall defect directly. Constitutive activation of the CWI cascade is reflected by the overproduction of chitin by mutants, a compensatory response frequently displayed by cell wall mutants. Growth is restored to mutants incubated at otherwise non-permissive temperature when is overexpressed. encodes the hexosephosphate aminotransferase that catalyses the rate-limiting step in the pathway that synthesizes the chitin precursor UDP-GlcNAc. The possibility that Emw1p is required for function of Gfa1p was ruled out, because the phenotype persists when the requirement for Gfa1p is bypassed. Furthermore, if loss of Emw1p function leads to loss of function of Gfa1p, then chitin synthesis would be diminished. Instead, a stimulation of the synthesis of this polymer is detected. Consequently, the defect associated with mutants may be associated with compromise in one of the remaining processes that depend on UDP-GlcNAc, namely -glycosylation or glycosylphosphatidylinositol (GPI)-anchor synthesis.

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2011-04-01
2024-04-16
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