Phyto-pathogenic fungi can cause huge damage to crop production. During millions of years of coexistence, fungi have evolved diverse life-style to obtain nutrients from the host and to colonize upon ...them. They deploy various proteinaceous as well as non-proteinaceous secreted molecules commonly referred as effectors to sabotage host machinery during the infection process. The effectors are important virulence determinants of pathogenic fungi and play important role in successful pathogenesis, predominantly by avoiding host-surveillance system. However, besides being important for pathogenesis, the fungal effectors end-up being recognized by the resistant cultivars of the host, which mount a strong immune response to ward-off pathogens. Various recent studies involving different pathosystem have revealed the virulence/avirulence functions of fungal effectors and their involvement in governing the outcome of host–pathogen interactions. However, the effectors and their cognate resistance gene in the host remain elusive for several economically important fungal pathogens. In this review, using examples from some of the biotrophic, hemi-biotrophic and necrotrophic pathogens, we elaborate the double-edged functions of fungal effectors. We emphasize that knowledge of effector functions can be helpful in effective management of fungal diseases in crop plants.
Rhizoctonia solani is a highly destructive necrotrophic fungal pathogen having a diverse host range, including rice and tomato. Previously R. solani infection in rice has been found to cause ...large-scale readjustment in host primary metabolism and accumulation of various stress associated metabolites such as gamma aminobutyric acid (GABA). In this study, we report upregulation of GABA shunt genes during pathogenesis of R. solani in rice as well as tomato. The exogenous application of GABA provided partial resistance against R. solani infection in both the hosts. Further, using virus induced gene silencing (VIGS) approach, we knocked down the expression of some of the tomato genes involved in GABA biosynthesis (glutamate decarboxylase; GAD) and GABA catabolism (GABA-transaminase; GABA-T and succinic semialdehyde dehydrogenase; SSADH) to study their role in host defense against R. solani infection. The silencing of each of these genes was found to enhance disease susceptibility in tomato. Overall the results from gene expression analysis, exogenous chemical treatment and gene silencing studies suggest that GABA pathway plays a positive role in plant resistance against necrotrophic fungal pathogen R. solani.
Enzymes have replaced or decreased usage of toxic chemicals for industrial and medical applications leading toward sustainable chemistry. In this study, we report purification and characterization of ...a biofilm degrading protease secreted by
sp. SKS10. The protease was identified as a metalloprotease, Peptidase M16 using mass spectrometry. It showed optimum activity at 60°C, pH 12 and retained its activity in the presence of various salts and organic solvents. The enzyme was able to degrade biofilms efficiently at enzyme concentration lower than other known enzymes such as papain, trypsin and α-amylase. The presence of this protease increased the accessibility of antibiotics inside the biofilm, and was found to be non-cytotoxic toward human epidermoid carcinoma cells (A431) at the effective concentration for biofilm degradation. Thus, this protease may serve as an effective tool for management of biofilms.
Some bacteria can feed on fungi, a phenomenon known as mycophagy. Here we show that a prophage tail-like protein (Bg_9562) is essential for mycophagy in Burkholderia gladioli strain NGJ1. The ...purified protein causes hyphal disintegration and inhibits growth of several fungal species. Disruption of the Bg_9562 gene abolishes mycophagy. Bg_9562 is a potential effector secreted by a type III secretion system (T3SS) and is translocated into fungal mycelia during confrontation. Heterologous expression of Bg_9562 in another bacterial species, Ralstonia solanacearum, confers mycophagous ability in a T3SS-dependent manner. We propose that the ability to feed on fungi conferred by Bg_9562 may help the bacteria to survive in certain ecological niches. Furthermore, considering its broad-spectrum antifungal activity, the protein may be potentially useful in biotechnological applications to control fungal diseases.Some bacteria can feed on live fungi through unclear mechanisms. Here, the authors show that a T3SS-secreted protein, which is homologous to phage tail proteins, allows a Burkholderia gladioli strain to kill and feed on various fungal species.
A rice associated bacterium Burkholderia gladioli strain NGJ1 demonstrates mycophagy, a phenomenon wherein bacteria feed on fungi. Previously, we have reported that NGJ1 utilizes type III secretion ...system (T3SS) to deliver a prophage tail-like protein (Bg_9562) into fungal cells to establish mycophagy.
In this study, we report that calcium ion concentration influences the mycophagous ability of NGJ1 on Rhizoctonia solani, an important fungal pathogen. The calcium limiting condition promotes mycophagy while high calcium environment prevents it. The expression of various T3SS apparatus encoding genes of NGJ1 was induced and secretion of several potential T3SS effector proteins (including Bg_9562) into extracellular milieu was triggered under calcium limiting condition. Using LC-MS/MS proteome analysis, we identified several calcium regulated T3SS effector proteins of NGJ1. The expression of genes encoding some of these effector proteins was upregulated during mycophagous interaction of NGJ1 with R. solani. Further, mutation of one of these genes (endo-β-1, 3- glucanase) rendered the mutant NGJ1 bacterium defective in mycophagy while complementation with full length copy of the gene restored its mycophagous activity.
Our study provides evidence that low calcium environment triggers secretion of various T3SS effectors proteins into the extracellular milieu and suggests the importance of cocktail of these proteins in promoting mycophagy.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Burkholderia gladioli strain NGJ1 exhibits mycophagous activity on a broad range of fungi, including Rhizoctonia solani, a devastating plant pathogen. Here, we demonstrate that the nicotinic acid ...(NA) catabolic pathway in NGJ1 is required for mycophagy. NGJ1 is auxotrophic to NA and it potentially senses R. solani as a NA source. Mutation in the
and
genes involved in NA catabolism renders defects in mycophagy and the mutant bacteria are unable to utilize R. solani extract as the sole nutrient source. As supplementation of NA, but not FA (fumaric acid, the end product of NA catabolism) restores the mycophagous ability of Δ
Δ
mutants, we anticipate that NA is not required as a carbon source for the bacterium during mycophagy. Notably,
, a MarR-type of transcriptional regulator that functions as a negative regulator of the NA catabolic pathway is upregulated in Δ
/Δ
mutant and upon NA supplementation the
expression is reduced to the basal level in both the mutants. The Δ
mutant produces excessive biofilm and is completely defective in swimming motility. On the other hand, Δ
/Δ
mutants are compromised in swimming motility as well as biofilm formation, potentially due to the upregulation of
. Our data suggest that a defect in NA catabolism alters the NA pool in the bacterium and upregulates
which in turn suppresses bacterial motility as well as biofilm formation, leading to mycophagy defects.
Mycophagy is an important trait through which certain bacteria forage over fungal mycelia and utilize fungal biomass as a nutrient source to thrive in hostile environments. The present study emphasizes that nicotinic acid (NA) is important for bacterial motility and biofilm formation during mycophagy by Burkholderia gladioli strain NGJ1. Defects in NA catabolism potentially alter the cellular NA pool, upregulate the expression of
, a negative regulator of biofilm, and therefore suppress bacterial motility as well as biofilm formation, leading to mycophagy defects.
Rhizoctonia solani is a polyphagous necrotrophic fungal pathogen that causes sheath blight disease in rice. It deploys effector molecules as well as carbohydrate‐active enzymes and enhances the ...production of reactive oxygen species for killing host tissues. Understanding R. solani ability to sustain growth under an oxidative‐stress‐enriched environment is important for developing disease control strategies. Here, we demonstrate that R. solani upregulates methionine biosynthetic genes, including Rs_MET13 during infection in rice, and double‐stranded RNA‐mediated silencing of these genes impairs the pathogen's ability to cause disease. Exogenous treatment with methionine restores the disease‐causing ability of Rs_MET13‐silenced R. solani and facilitates its growth on 10 mM H2O2‐containing minimal‐media. Notably, the Rs_MsrA gene that encodes methionine sulfoxide reductase A, an antioxidant enzyme involved in the repair of oxidative damage of methionine, is upregulated upon H2O2 treatment and also during infection in rice. Rs_MsrA‐silenced R. solani is unable to cause disease, suggesting that it is important for the repair of oxidative damage in methionine during host colonization. We propose that spray‐induced gene silencing of Rs_MsrA and designing of antagonistic molecules that block MsrA activity can be exploited as a drug target for effective control of sheath blight disease in rice.
Upregulation of methionine biosynthesis and methionine sulfoxide reductase A facilitates Rhizoctonia solani to establish sheath blight disease in rice: To sustain growth and establish disease, R. solani upregulates its methionine biosynthesis pathway to replenish the methionine pool, and methionine sulfoxide reductase A (Rs_MsrA) to repair the damaged methionine residues of various proteins, under oxidative stress‐enriched environment that is encountered during host colonization.
Intricate cellular and molecular events occur during plant–pathogen interactions. They cause major metabolic perturbations in the host and alterations in sugar metabolism play a pivotal role in ...governing the outcome of various kinds of plant–pathogen interactions. Sugar metabolizing enzymes and transporters of both host and pathogen origin get differentially regulated during the interactions. Both plant and pathogen compete for utilizing the host sugar metabolic machinery and in turn promote resistant or susceptible responses. However, the kind of sugar metabolism alteration that is beneficial for the host or pathogen is yet to be properly understood. Recently developed tools and methodologies are facilitating research to understand the intricate dynamics of sugar metabolism during the interactions. The present review elaborates current understanding, future challenges and ongoing quest on sugar metabolism, mobilization and regulation during various plant–pathogen interactions.
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