The Tetraspanin Protein CD37 Regulates IgA Responses and Anti-Fungal Immunity

Understanding the host anti-fungal immunity induced by beta-glucan has been one of the most challenging conundrums in the field of biomedical research. During the last couple of decades, insights on the role of beta-glucan in fungal disease progression, susceptibility, and resistance have been greatly augmented through the utility of various beta-glucan cognate receptor-deficient mouse models. Analysis of dectin-1 knockout mice has clarified the downstream signaling pathways and adaptive effector responses triggered by beta-glucan in anti-fungal immunity. On the other hand, assessment of CR3-deficient mice has elucidated the compelling action of beta-glucans in neutrophil-mediated fungal clearance, and the investigation of EphA2-deficient mice has highlighted its novel involvement in host sensing and defense to oral mucosal fungal infection. Based on these accounts, this review focuses on the recent discoveries made by these gene-targeted mice in beta-glucan research with particular emphasis on the multifaceted aspects of fungal immunity.

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Isoform localization of Dectin-1 regulates the signaling quality of anti-fungal immunity

European Journal of Immunology ◽

10.1002/eji.201646849 ◽

2017 ◽

Vol 47 (5) ◽

pp. 848-859 ◽

Cited By ~ 10

Author(s):

Mike Fischer ◽

Jörg P. Müller ◽

Bärbel Spies-Weisshart ◽

Christine Gräfe ◽

Oliver Kurzai ◽

...

Keyword(s):

Signaling Quality ◽

Fungal Immunity ◽

Anti Fungal

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Insights into the susceptibility of rice to a floral disease

10.1101/2021.03.03.433744 ◽

2021 ◽

Author(s):

Guo-Bang Li ◽

Jing Fan ◽

Jie Liu ◽

Jin-Long Wu ◽

Xiao-Hong Hu ◽

...

Keyword(s):

Immune Responses ◽

Virulence Factor ◽

Rice Varieties ◽

Ustilaginoidea Virens ◽

Yield And Quality ◽

Causal Fungus ◽

False Smut ◽

Grain Yield And Quality ◽

Fungal Immunity ◽

Anti Fungal

Crop floral diseases are economically important as they reduce grain yield and quality and even introduce food toxins. Rice false smut has emerged as a serious floral disease producing mycotoxins. However, very little is known on the interaction mechanisms between rice flower and the causal fungus Ustilaginoidea virens. Here we show that a conserved anti-fungal immunity in rice flower is disarmed by U. virens via a secreted protein UvChi1. UvChi1 functioned as an essential virulence factor and directly interacted with the chitin receptor CEBiP and co-receptor CERK1 in rice to disrupt their oligomerizations and subsequent immune responses. Moreover, intraspecific-conserved UvChi1 could target OsCEBiP/OsCERK1 receptor complex in at least 98.5% of 5232 surveyed rice accessions. These results demonstrate that U. virens utilizes a crucial virulence factor to subvert chitin-triggered flower immunity in most rice varieties, providing new insights into the susceptibility of rice to false smut disease.

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Anion channel SLAH3 is a regulatory target of chitin receptor-associated kinase PBL27 in microbial stomatal closure

eLife ◽

10.7554/elife.44474 ◽

2019 ◽

Vol 8 ◽

Cited By ~ 12

Author(s):

Yi Liu ◽

Tobias Maierhofer ◽

Katarzyna Rybak ◽

Jan Sklenar ◽

Andy Breakspear ◽

...

Keyword(s):

Stomatal Closure ◽

Anion Channel ◽

Anion Channels ◽

Slow Type ◽

Leaf Level ◽

Short Signal ◽

Molecular Patterns ◽

Fungal Immunity ◽

Anti Fungal ◽

Full Activation

In plants, antimicrobial immune responses involve the cellular release of anions and are responsible for the closure of stomatal pores. Detection of microbe-associated molecular patterns (MAMPs) by pattern recognition receptors (PRRs) induces currents mediated via slow-type (S-type) anion channels by a yet not understood mechanism. Here, we show that stomatal closure to fungal chitin is conferred by the major PRRs for chitin recognition, LYK5 and CERK1, the receptor-like cytoplasmic kinase PBL27, and the SLAH3 anion channel. PBL27 has the capacity to phosphorylate SLAH3, of which S127 and S189 are required to activate SLAH3. Full activation of the channel entails CERK1, depending on PBL27. Importantly, both S127 and S189 residues of SLAH3 are required for chitin-induced stomatal closure and anti-fungal immunity at the whole leaf level. Our results demonstrate a short signal transduction module from MAMP recognition to anion channel activation, and independent of ABA-induced SLAH3 activation.

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