Parallels in Fungal Pathogenesis on Plant and Animal Hosts

Sexton, Adrienne; Howlett, Barbara J.

doi:10.1128/ec.00277-06

Cited by 140 publications

(107 citation statements)

References 96 publications

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“…Aromatic amino acid aminotransferases have been shown to play a role in IAA and phenylacetic acid (PAA) biosynthesis in fungi (Kishore et al 1976, Krings et al 1996. PAA is a virulence factor of R. solani (Orellana and Mandava 1983 Glycogen have been shown during appressorium turgor generation by Magnaporthe grisea (Sexton andHowlett 2006, Thines et al 2000).…”

Section: W3 Contigmentioning

confidence: 99%

Gene expression profiling of the plant pathogenic basidiomycetous fungus Rhizoctonia solani AG 4 reveals putative virulence factors

Lakshman¹,

Alkharouf²,

Roberts³

et al. 2012

Mycologia

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Section: W3 Contigmentioning

confidence: 99%

Gene expression profiling of the plant pathogenic basidiomycetous fungus Rhizoctonia solani AG 4 reveals putative virulence factors

Lakshman¹,

Alkharouf²,

Roberts³

et al. 2012

Mycologia

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“…30,31 These events identify an indirect mode of non-self recognition that has been recently described in the mechanics of the perception system of plants. 37,38 Indeed, a dual-sensor system to detect fungal infection seems to work throughout evolution, 39 because Drosophila senses fungi by sensing both the fungal cell wall and the activity of proteolytic virulence factors. 40 Several possible mechanisms have been described that may underlie the potential for receptor transactivation within the PAR or TLR family.…”

Section: Articlesmentioning

confidence: 99%

The contribution of PARs to inflammation and immunity to fungi

et al. 2008

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During inflammation, host-and microbial-derived proteases trigger the activation of protease-activated receptors (PARs), a family of G-protein-coupled receptors. We report here that activation of Toll-like receptors (TLRs) by fungi unmasks an essential and divergent role for PAR 1 and PAR 2 in downstream signaling and inflammation. TLRs activated PARs and triggered distinct signal transduction pathways involved in inflammation and immunity to Candida albicans and Aspergillus fumigatus. Inflammation was promoted by PAR 1 and PAR 2 activation in response to Candida and by PAR 2 inhibition in response to Aspergillus . This occurred by TLR regulation of PAR signaling, with TLR2 promoting PAR 1 activity, and TLR4 suppressing PAR 2 activity. Thus, tissue injury and pathogens induce signals that are integrated at the level of distinct TLR / PAR-dependent pathways, the exploitation or subversion of which contributes to divergence in microbial promotion of inflammatory response.

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“…Development of eukaryotic pathogens is accompanied by drastic changes in morphology, lifestyle, nutrient acquisition, and growth behavior (Heitman, 2006;Sexton and Howlett, 2006). Therefore, pathogens contain robust control systems to maintain cellular physiology and homeostasis and to adapt to changing host environments.…”

Section: Introductionmentioning

confidence: 99%

Crosstalk between the Unfolded Protein Response and Pathways That Regulate Pathogenic Development inUstilago maydis

et al. 2013

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The unfolded protein response (UPR) is a conserved eukaryotic signaling pathway regulating endoplasmic reticulum (ER) homeostasis during ER stress, which results, for example, from an increased demand for protein secretion. Here, we characterize the homologs of the central UPR regulatory proteins Hac1 (for Homologous to ATF/CREB1) and Inositol Requiring Enzyme1 in the plant pathogenic fungus Ustilago maydis and demonstrate that the UPR is tightly interlinked with the b mating-type-dependent signaling pathway that regulates pathogenic development. Exact timing of UPR is required for virulence, since premature activation interferes with the b-dependent switch from budding to filamentous growth. In addition, we found crosstalk between UPR and the b target Clampless1 (Clp1), which is essential for cell cycle release and proliferation in planta. The unusual C-terminal extension of the U. maydis Hac1 homolog, Cib1 (for Clp1 interacting bZIP1), mediates direct interaction with Clp1. The interaction between Clp1 and Cib1 promotes stabilization of Clp1, resulting in enhanced ER stress tolerance that prevents deleterious UPR hyperactivation. Thus, the interaction between Cib1 and Clp1 constitutes a checkpoint to time developmental progression and increased secretion of effector proteins at the onset of biotrophic development. Crosstalk between UPR and the b mating-type regulated developmental program adapts ER homeostasis to the changing demands during biotrophy.

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Parallels in Fungal Pathogenesis on Plant and Animal Hosts

Cited by 140 publications

References 96 publications

Gene expression profiling of the plant pathogenic basidiomycetous fungus Rhizoctonia solani AG 4 reveals putative virulence factors

Gene expression profiling of the plant pathogenic basidiomycetous fungus Rhizoctonia solani AG 4 reveals putative virulence factors

The contribution of PARs to inflammation and immunity to fungi

Crosstalk between the Unfolded Protein Response and Pathways That Regulate Pathogenic Development inUstilago maydis

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