<i>PMT</i> family of <i>Candida albicans</i>: five protein mannosyltransferase isoforms affect growth, morphogenesis and antifungal resistance

Prill, Stephan K.-H.; Klinkert, Birgit; Timpel, Claudia; Gale, Cheryl A.; Schröppel, Klaus; Ernst, Joachim F.

doi:10.1111/j.1365-2958.2004.04401.x

Cited by 152 publications

(248 citation statements)

References 49 publications

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“…The requirement of pmt2 was confirmed by spore analysis of the diploid strain FBD11 Dpmt2/pmt2 (see Supplemental Figure 3 online). Our results concur with those previously obtained for members of the PMT2 subfamily in S. cerevisiae, C. albicans, and S. pombe (Gentzsch and Tanner, 1996;Prill et al, 2005;Willer et al, 2005) and thus reaffirm the requirement of the PMT2 subfamily for fungal viability.…”

Section: Pmt4 Is Required For Virulence On Maizesupporting

confidence: 82%

“…The loss of PMTs from S. cerevisiae, S. pombe, and C. albicans causes several defects, such as abnormal morphology, cellular aggregation, alterations in polar growth, and hypersensitivity to antifungal drugs, among others (Proszynski et al, 2004;Prill et al, 2005;Willer et al, 2005). To determine the effects of the deletion of pmt4 on U. maydis biology, we performed an in-depth analysis of Dpmt4, looking at the different phases of the U. maydis life cycle.…”

Section: Pmt4 Is Required Only For the Pathogenic Phase Of The U Maymentioning

confidence: 99%

“…In order to determine other PMT targets, in silico studies based on the general characteristics of O-mannosylated proteins have been initiated (Hutzler et al, 2007). Mutations in PMT family proteins have been linked to defects in S. pombe morphogenesis (Willer et al, 2005), reduced pathogenicity of C. albicans (Timpel et al, 2000;Prill et al, 2005) and Cryptococcus neoformans (Olson et al, 2007;Willger et al, 2009), or, in the case of humans, to the WalterWarburg syndrome (Beltran-Valero de Bernabe et al, 2002;Lengeler et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

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TheO-Mannosyltransferase PMT4 Is Essential for Normal Appressorium Formation and Penetration inUstilago maydis

2009

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In Saccharomyces cerevisiae, the PMT, KRE2/MNT1, and MNN1 mannosyltransferase protein families catalyze the steps of the O-mannosylation pathway, sequentially adding mannoses to target proteins. We have identified members of all three families and analyzed their roles in pathogenesis of the maize smut fungus Ustilago maydis. Furthermore, we have shown that PMT4, one of the three PMT family members in U. maydis, is essential for tumor formation in Zea mays. Significantly, PMT4 seems to be required only for pathogenesis and is dispensable for other aspects of the U. maydis life cycle. We subsequently show that the deletion of pmt4 results in a strong reduction in the frequency of appressorium formation, with the few appressoria that do form lacking the capacity to penetrate the plant cuticle. Our findings suggest that the O-mannosylation pathway plays a key role in the posttranslational modification of proteins involved in the pathogenic development of U. maydis. The fact that PMT homologs are not found in plants may open new avenues for the development of fungal control strategies. Moreover, the discovery of a highly specific requirement for a single O-mannosyltransferase should aid in the identification of the proteins directly involved in fungal plant penetration, thus leading to a better understanding of plant-fungi interactions.

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Section: Pmt4 Is Required For Virulence On Maizesupporting

confidence: 82%

Section: Pmt4 Is Required Only For the Pathogenic Phase Of The U Maymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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TheO-Mannosyltransferase PMT4 Is Essential for Normal Appressorium Formation and Penetration inUstilago maydis

2009

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“…Those studied include members of the PMT and MNT gene families, all of which act in O-glycosylation, and the studies have demonstrated the importance of O-glycans in virulence (19,(21)(22)(23)(24). Also, Mnn9p is involved in extension of the N-linked glycan outer chain and hence is required for normal cell wall composition (25).…”

mentioning

confidence: 99%

Candida albicans Pmr1p, a Secretory Pathway P-type Ca2+/Mn2+-ATPase, Is Required for Glycosylation and Virulence

Bates

MacCallum

Bertram

et al. 2005

Journal of Biological Chemistry

175

213

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The cell surface of Candida albicans is the immediate point of contact with the host. The outer layer of the cell wall is enriched in highly glycosylated mannoproteins that are implicated in many aspects of the host-fungus interaction. Glycosylation of cell wall proteins is initiated in the endoplasmic reticulum and then elaborated in the Golgi as the protein passes through the secretory pathway. Golgi-bound mannosyltransferases require Mn 2؉ as an essential cofactor. In Saccharomyces cerevisiae, the P-type ATPase Pmr1p transports Ca 2؉ and Mn 2؉ ions into the Golgi. To determine the effect of a gross defect in glycosylation on host-fungus interactions of C. albicans, we disrupted the PMR1 homolog, CaPMR1. This mutation would simultaneously inhibit many Golgi-located, Mn 2؉ -dependent mannosyltransferases. The Capmr1⌬ null mutant was viable in vitro and had no growth defect even on media containing low Ca 2؉ /Mn 2؉ ion concentrations. However, cells grown in these media progressively lost viability upon entering stationary phase. Phosphomannan was almost completely absent, and O-mannan was severely truncated in the null mutant. A defect in N-linked outer chain glycosylation was also apparent, demonstrated by the underglycosylation of surface acid phosphatase. Consistent with the glycosylation defect, the null mutant had a weakened cell wall, exemplified by hypersensitivity to Calcofluor white, Congo red, and hygromycin B and constitutive activation of the cell integrity pathway. In a murine model of systemic infection, the null mutant was severely attenuated in virulence. These results demonstrate the importance of glycosylation for cell wall structure and virulence of C. albicans.

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“…The pmt1 mutant, defective in the first steps of the O-glycosylation and partially responsible for Hwp1 glycosylation, 75,76 shows also a decrease in b-M epitopes observed in fraction 1 (100 C), 3 (NaOH) and 4 (zymolyase) and a shift in mannansḿ olecular weight. Interestingly, cells defective in either OCH1 or PMT1 constitutively display an increased Cek1 activation, 49,77 supporting therefore the idea that the Cek1-mediated pathway is essential for cell wall remodeling in C. albicans.…”

Section: Discussionmentioning

confidence: 99%

The Cek1‑mediated MAP kinase pathway regulates exposure of α‑1,2 and β‑1,2‑mannosides in the cell wall ofCandida albicansmodulating immune recognition

et al. 2016

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PMT family of Candida albicans: five protein mannosyltransferase isoforms affect growth, morphogenesis and antifungal resistance

Cited by 152 publications

References 49 publications

TheO-Mannosyltransferase PMT4 Is Essential for Normal Appressorium Formation and Penetration inUstilago maydis

TheO-Mannosyltransferase PMT4 Is Essential for Normal Appressorium Formation and Penetration inUstilago maydis

Candida albicans Pmr1p, a Secretory Pathway P-type Ca2+/Mn2+-ATPase, Is Required for Glycosylation and Virulence

The Cek1‑mediated MAP kinase pathway regulates exposure of α‑1,2 and β‑1,2‑mannosides in the cell wall ofCandida albicansmodulating immune recognition

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