Cell wall integrity modulates RHO1 activity via the exchange factor ROM2

Bickle, Marc; Delley, Pierre-Alain; Schmidt, Anja; Hall, Michael N.

doi:10.1093/emboj/17.8.2235

Cited by 180 publications

(211 citation statements)

References 74 publications

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“…Accumulation of chitin in the cell wall is often concomitant with activation of the cell wall integrity pathway (CWIP) (Dallies et al, 1998;Bickle et al, 1998). This process is governed by protein kinase C and results in the upregulation of a cascade of MAP kinases and in turn in the activation of transcription factors regulating genes involved in the synthesis of the cell wall polymers (Lewin et al, 1990).…”

Section: Resultsmentioning

confidence: 99%

Defect in dolichol‐dependent glycosylation increases sensitivity of Saccharomyces cerevisiae towards anti‐fungal drugs

Juchimiuk

Pasikowska

Zatorska

et al. 2010

Yeast

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Two temperature-sensitive Saccharomyces cerevisiae mutants, sec59-1 and dpm1-6, impaired, respectively, in dolichol kinase (Sec59p) and dolichyl phosphate mannose (DolPMan) synthase (Dpm1p), have an aberrant cell wall structure and composition. We tested their sensitivity to four classes of antifungal drugs used in clinical practice: 5-fluorocytosine, amphotericin B, caspofungin and itraconasole. The strains were resistant to itraconazole and sensitive to the other drugs used. The minimal inhibitory concentration (MIC) of caspofungin and amphotericin B was two-fold lower for sec59-1 and dpm1-6 than for the respective wild-type strains. The sensitivity of both mutants could be brought back to the wild-type level by a multicopy suppressor of the thermosensitive phenotype, the RER2 gene, encoding cis-prenyltransferase involved in dolichol biosynthesis. Biochemical analysis revealed slight changes of the cell wall composition, different in the mutants as compared to the wild-type in response to the drugs. Our data strongly support a relationship between dolichol phosphate level, protein glycosylation and antifungal sensitivity.

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Section: Resultsmentioning

confidence: 99%

Defect in dolichol‐dependent glycosylation increases sensitivity of Saccharomyces cerevisiae towards anti‐fungal drugs

Juchimiuk

Pasikowska

Zatorska

et al. 2010

Yeast

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“…In the search for multicopy suppressors of the sec59-1 phenotype, clones carrying the ROT1 gene were also found. ROT1 encodes a protein involved in the biosynthesis of β1,6-glucan and suppression of the tor2∆ mutation, but also in the ER quality control of misfolded proteins (Bicle et al, 1998;Misuno et al, 2004;Takeuchi et al, 2006). Subsequently, we determined the cell wall composition of the mutants and strains bearing the multicopy suppressors.…”

Section: Mutation Of the Sec59 Protein Affects The Yeast Cell Wallmentioning

confidence: 99%

Dissecting the role of dolichol in cell wall assembly in the yeast mutants impaired in early glycosylation reactions

Orłowski

Machula

Janik

et al. 2007

Yeast

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Evidence is presented that temperature-sensitive Saccharomyces cerevisiae mutants, impaired in dolichol kinase (Sec59p) or dolichyl phosphate mannose synthase (Dpm1p) activity have an aberrant cell wall composition and ultrastructure. The mutants were oversensitive to Calcofluor white, an agent interacting with the cell wall chitin. In accordance with this, chemical analysis of the cell wall alkali-insoluble fraction indicated an increased amount of chitin and changes in the quantity of β1,6-and β1,3-glucan in sec59-1 and dpm1-6 mutants. In order to unravel the link between the formation of dolichyl phosphate and dolichyl phosphate mannose and the cell wall assembly, we screened a yeast genomic library for a multicopy suppressors of the thermosensitive phenotype. The RER2 and SRT1 genes, encoding cis-prenyltransferases, were isolated. In addition, the ROT1 gene, encoding protein involved in β1,6-glucan synthesis (Machi et al., 2004) and protein folding (Takeuchi et al., 2006) acted as a multicopy suppressor of the temperature-sensitive phenotype of the sec59-1 mutant. The cell wall of the mutants and of mutants bearing the multicopy suppressors was analysed for carbohydrate and mannoprotein content. We also examined the glycosylation status of the plasma membrane protein Gas1p, a β1,3-glucan elongase, and the degree of phosphorylation of the Mpk1/Slt2 protein, involved in the cell wall integrity pathway.

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“…In Saccharomyces cerevisiae, a complex surveillance system monitors cell wall integrity. This system includes (1!3)-b-D-glucan synthase FK506 sensitivity (FKS) genes, cell-surface proteins that act as mechanosensors of changes in wall shape and a signalling cascade [14,15]. If surveillance of cell wall integrity is conserved in plants, one would expect that biotrophic fungi will have evolved means to manipulate components of cell wall integrity in order to suppress SA-dependent resistance.…”

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confidence: 99%

Knocking on the heaven’s wall: pathogenesis of and resistance to biotrophic fungi at the cell wall

Schulze‐Lefert

2004

Current Opinion in Plant Biology

124

101

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New findings challenge the traditional view of the plant cell wall as passive structural barrier to invasion by fungal microorganisms. A surveillance system for cell wall integrity appears to sense perturbation of the cell wall structure upon fungal attack and is interconnected with known plant defence signalling pathways. Biotrophic fungi might manipulate this surveillance system for the establishment of biotrophy. The attempts of fungi to invade also induce a sub-cellular polarisation in attacked cells, which activates an ancient vesicle-associated resistance response that possibly enables the focal transport of regulatory cargo and the secretion of toxic cargo. The underlying resistance machinery might have been subverted by biotrophic fungi for pathogenesis. IntroductionPenetration through the plant cell wall represents an Achilles heel in the pathogenesis of most biotrophic fungi and marks a lifestyle transition from extra-cellular to invasive growth. Modification of the plant cell wall was recognised for the first time as potential resistance mechanism almost 80 years ago following work in which 78 plant species and varieties were challenged with Alternaria spp. and other leaf-spotting fungi [1]. The termination of fungal pathogenesis at the cell wall was commonly associated with wall 'thickenings' and the formation of local additions or 'callosities' in the paramural space (i.e. the space between the cell wall and the plasma membrane). Formation of these cell wall appositions (CWAs) or papillae is usually accompanied by a co-localised accumulation of phenolics and reactive oxygen species [2][3][4][5][6]. The complex process of sub-cellular cell wall remodelling is tightly linked to the rapid disassembly and subsequent focal reassembly of the plant cytoskeleton at fungal entry sites, which is indicative of a pathogen-triggered cell polarisation [6][7][8][9]. There has been a long-standing controversy, however, over whether CWAs function in disease resistance or facilitate the entry of fungal pathogens into host cells by providing a structural collar for the intruder. New molecular genetic data from Arabidopsis and barley have indeed revealed that molecular processes at and in CWAs have Janus-faced functions, that is, functions for fungal pathogenesis and in resistance responses. Focal vesicle transport and vesicle fusion events that are dependent on SNAP (soluble N-ethylmaleimide-sensitive-factor-association protein) receptor (SNARE) proteins at the plasma membrane emerge as potential common underlying mechanisms that might be interconnected with a poorly understood cell wall integrity surveillance system. In this review, I discuss the seemingly paradoxical functions of these processes in establishing the biotrophic lifestyle and in disease resistance at the cell periphery.Linking cell wall structure to biotic stress signalling Callose, a (1!3)-b-D-glucan, has long been known to be synthesised and deposited rapidly at CWAs upon microbial attack. This polymer was thought to contribute to a physical barrie...

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Cell wall integrity modulates RHO1 activity via the exchange factor ROM2

Cited by 180 publications

References 74 publications

Defect in dolichol‐dependent glycosylation increases sensitivity of Saccharomyces cerevisiae towards anti‐fungal drugs

Defect in dolichol‐dependent glycosylation increases sensitivity of Saccharomyces cerevisiae towards anti‐fungal drugs

Dissecting the role of dolichol in cell wall assembly in the yeast mutants impaired in early glycosylation reactions

Knocking on the heaven’s wall: pathogenesis of and resistance to biotrophic fungi at the cell wall

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