Genomic characterization of plant cell wall degrading enzymes and in silico analysis of xylanses and polygalacturonases of Fusarium virguliforme

Abstract

BackgroundPlant cell wall degrading enzymes (PCWDEs) are a subset of carbohydrate-active enzymes (CAZy) produced by plant pathogens to degrade plant cell walls. To counteract PCWDEs, plants release PCWDEs inhibitor proteins (PIPs) to reduce their impact. Several transgenic plants expressing exogenous PIPs that interact with fungal glycoside hydrolase (GH)11-type xylanases or GH28-type polygalacturonase (PG) have been shown to enhance disease resistance. However, many plant pathogenic Fusarium species were reported to escape PIPs inhibition. Fusarium virguliforme is a soilborne pathogen that causes soybean sudden death syndrome (SDS). Although the genome of F. virguliforme was sequenced, there were limited studies focused on the PCWDEs of F. virguliforme. Our goal was to understand the genomic CAZy structure of F. viguliforme, and determine if exogenous PIPs could be theoretically used in soybean to enhance resistance against F. virguliforme.ResultsF. virguliforme produces diverse CAZy to degrade cellulose and pectin, similar to other necrotorphic and hemibiotrophic plant pathogenic fungi. However, some common CAZy of plant pathogenic fungi that catalyze hemicellulose, such as GH29, GH30, GH44, GH54, GH62, and GH67, were deficient in F. virguliforme. While the absence of these CAZy families might be complemented by other hemicellulases, F. virguliforme contained unique families including GH131, polysaccharide lyase (PL) 9, PL20, and PL22 that were not reported in other plant pathogenic fungi or oomycetes. Sequence analysis revealed two GH11 xylanases of F. virguliforme, FvXyn11A and FvXyn11B, have conserved residues that allow xylanase inhibitor protein I (XIP-I) binding. Structural modeling suggested that FvXyn11A and FvXyn11B could be blocked by XIP-I that serves as good candidate for developing transgenic soybeans. In contrast, one GH28 PG, FvPG2, contains an amino acid substitution that is potentially incompatible with the bean polygalacturonase-inhibitor protein II (PvPGIP2).ConclusionsIdentification and annotation of CAZy provided advanced understanding of genomic composition of PCWDEs in F. virguliforme. Sequence and structural analyses of FvXyn11A and FvXyn11B suggested both xylanases were conserved in residues that allow XIP-I inhibition, and expression of both xylanases were detected during soybean roots infection. We postulate that a transgenic soybean expressing wheat XIP-I may be useful for developing root rot resistance to F. virguliforme.Electronic supplementary materialThe online version of this article (doi:10.1186/s12866-016-0761-0) contains supplementary material, which is available to authorized users.

Dual Role of Humic Substances As Electron Donor and Shuttle for Dissimilatory Iron Reduction

“…The most abundant GHs in HA treatments were categorized as cellulases and endohemicellulases and debranching and oligosaccharide degrading enzymes. 33,42,57,62,67,68 Identical analysis of the HM treatments revealed cellulases, endohemicellulases, and debranching, and oligosaccharide degrading enzymes, but also included pectinases and fungal cell wall degrading enzymes. The higher abundance of these CAZyme families in the presence of HA compared to HM and/or glucose only treatments is another indication that chemically-extracted SOC contains polysaccharides that are bioavailable for microbial degradation into simpler organic acids utilized by DIRB.…”

Inhibitory effects of sodium silicate on the fungal growth and secretion of cell wall‐degrading enzymes by Trichothecium roseum

“…Similar results were reported in Fusarium oxysporum strain F3, Fusarium oxysporum f. sp. melonis , Fusarium virguliforme and Sclerotinia sclerotiorum (Alconada & Martinez, ; Chang, Yendrek, Caetanoanolles, & Hartman, ; Christakopoulos, Kekos, Macris, Claeyssens, & Bhat, ; Waksman, ). Sodium silicate treatment caused T. roseum cell wall to partly dissolve and show membrane shrinkage, which is part of hyphal cell nuclear fragmentation (Wang, Bi, Li, Yin, & Ge, ).…”

Transcriptome analysis of mycorrhizal and non-mycorrhizal soybean plantlets upon infection withFusarium virguliforme, one causal agent of sudden death syndrome

“…Using the same system, Marquez et al (2018), investigated transcriptional changes in mycorrhizal and non-mycorrhizal soybean plants upon infection with the fungal pathogen Macrophomina phaseolina revealing the complex underlying mechanisms involved in AMF-mediated biocontrol. Transcriptional changes during interaction between soybean plants and F. virguliforme have already been analysed and contributed to increasing our understanding of the virulence mechanisms of F. virguliforme to produce SDS (Chang et al , 2016; Sahu et al , 2017) and the molecular response of the plant to combat the pathogen (Radwan et al , 2011; Ngaki et al , 2016). Likewise, several studies have focused on the transcriptome profiles of AMF-colonized plants with the aim of analysing wide-scale gene reprogramming during the establishment and development of arbuscular mycorrhizal symbioses (Liu et al , 2007; Gallou et al , 2012) or during interaction of AMF-colonized plants with below-(e.g.…”