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Chief Editor | Wang Yi On October 30, 2021, the team of researcher Que Youxiong of the National Sugarcane Center of Fujian Agriculture and Forestry University and the team of Professor Haitao Cui of the Straits Joint Research Institute published online in New Phytologist entitled A sugarcane smut fungus effector simulates the host endogenous elicitor peptide to The suppress plant immunity research paper discovered for the first time that the secretory protein of S.
smutensis can compete with the endogenous polypeptide Pep1 of the host plant to bind to the kinase extramembrane domain in the apoplast space, thereby suppressing the plant-pathogen interaction of the host’s immune response.
Make a new mechanism
.
This research has laid a good foundation for in-depth analysis of the formation and mechanism of sugarcane smut resistance traits, and has important biological significance
.
Smut disease is the most important fungal disease in sugarcane planting.
It is caused by smut (Sporisorium scitamineum).
It is an airborne bacterial disease, which leads to a decrease in cane stalk yield and sucrose content, which seriously harms sugarcane production
.
Sugarcane smut can invade the top growth point of the host's apical and lateral buds, disturb the internal metabolic balance of the tissue, and make the host's apical growth point lose the ability to differentiate, the internode meristem cells divide and elongate rapidly, and finally protrude from the top of the sugarcane plant.
The black "whip"-like structure formed by the spores of Spike fungus encapsulating sugarcane tissue (Figure 1)
.
Cultivating smut-resistant sugarcane varieties is the most economical and effective measure to control the disease.
The analysis of the host disease resistance mechanism and the explanation of the pathogenic pathogenic mechanism are the premise and basis
.
Figure 1 Sugarcane smut Que Youxiong's research group used microscopic observation, genome, proteomic and transcriptome technologies, as well as molecular marker development and disease resistance gene cloning, to resist sugarcane at the morphological, physiological and molecular levels.
A series of studies have been carried out on the mechanism of smut disease and the pathogenic mechanism of smut fungus, and certain progress has been made
.
However, people still know little about the process and mechanism of how pathogens promote infection and promote reproduction by inhibiting host resistance
.
The study found that during the process of smut infecting sugarcane, with the extension of the infection time and the proliferation of the pathogen, the genes of the host sugarcane variety and the genes of the pathogenic smut have significant co-expression, especially the receptor Kinase and effector protein genes (Figure 2)
.
PEPR1 is an important receptor kinase in the molecular model related to plant damage.
Its extracellular domain can specifically recognize the endogenous plant elicitor polypeptide Peps, thereby activating a series of immune responses and increasing the level of self-resistance
.
Through protein interaction verification, the authors found that the effector protein of S.
smutella SsPele1 can specifically bind to the kinase receptor ScPEPR1 on the sugarcane membrane, and there is a sequence very similar to the plant endogenous polypeptide Pep1 at the C-terminus of the SsPele1 protein (Figure 3 )
.
Figure 2 Co-expression of genes from sugarcane and smutella
.
UmPele1 is a homolog of the effector protein SsPele1 of Smutella smut .
Previous studies revealed that UmPele1 is an important factor in the pathogenicity of corn smut, and its deletion will seriously affect the formation of tumors after being infected by smut
.
Surprisingly, like the effector protein SsPele1 of smut smut, UmPele1 can specifically bind to the kinase receptor ZmPEPR1 on the corn membrane.
At the same time, similar to SsPele1, the C-terminus of UmPele1 protein is also present.
A sequence that is highly homologous to Pep1 (Figure 3)
.
Figure 3 The effector protein SsPele1 of S.
smutensis can specifically recognize the kinase receptor ScPEPR1 on the host membrane.
Further, the authors used the protoplast system of sugarcane and Arabidopsis thaliana and found that the 25 amino acid peptide Pel25 at the C-terminal of SsPele1 inhibited Pep1-induced gene expression and MAPK Activate and inhibit the resistance response of host cells (Figure 4)
.
And through the competitive binding imprinting test, Pel25 and Pep1 competitively bind to the extracellular domain of ScPEPR1 (Figure 4)
.
Figure 4 The immune response of sugarcane infected by smut fungus is inhibited by the competitive combination of SsPele1 and ScPEPR1.
In summary, the study clarified a new mechanism of the interaction between pathogenic fungi and host plants in the apoplast space
.
During the infection of sugarcane by Smutella smut, the effector protein Pele1 is secreted into the apoplast space of the plant
.
Pele1 competes to bind to PEPR1 by mimicking the host plant Pep1 through the terminal peptide, inhibiting the immune response mediated by polypeptide-kinase (Pep1-PEPR1)-mediated damage associated molecular patterns (DAMPs) and weakening The resistance of the host plant is improved, and the infection and proliferation of pathogenic bacteria are promoted (Figure 5)
.
The new plant-pathogen interaction mechanism revealed by this study provides a new perspective for the analysis of the pathogenic mechanism of sugarcane smut and the directional improvement of sugarcane disease resistance breeding
.
Figure 5 The molecular model of SsPele1 mediating plant immune pathways by inhibiting the host PEPR1 signaling pathway.
The young teachers Ling Hui and Huang Ning of the School of Biology and Pharmaceuticals/Agriculture College, Yulin Normal University, and Fu Xueqin, a graduate student of Fujian Agriculture and Forestry University, are co-authors of this paper The first author, researcher Que Youxiong and Professor Cui Haitao are the co-corresponding authors
.
The research was funded by the National Key Research and Development Program, the National Natural Science Foundation of China, the Fujian Outstanding Youth Science Foundation and the National Sugar Industry Technology System Project
.
Original link: https://nph.
onlinelibrary.
wiley.
com/doi/abs/10.
1111/nph.
17835
smutensis can compete with the endogenous polypeptide Pep1 of the host plant to bind to the kinase extramembrane domain in the apoplast space, thereby suppressing the plant-pathogen interaction of the host’s immune response.
Make a new mechanism
.
This research has laid a good foundation for in-depth analysis of the formation and mechanism of sugarcane smut resistance traits, and has important biological significance
.
Smut disease is the most important fungal disease in sugarcane planting.
It is caused by smut (Sporisorium scitamineum).
It is an airborne bacterial disease, which leads to a decrease in cane stalk yield and sucrose content, which seriously harms sugarcane production
.
Sugarcane smut can invade the top growth point of the host's apical and lateral buds, disturb the internal metabolic balance of the tissue, and make the host's apical growth point lose the ability to differentiate, the internode meristem cells divide and elongate rapidly, and finally protrude from the top of the sugarcane plant.
The black "whip"-like structure formed by the spores of Spike fungus encapsulating sugarcane tissue (Figure 1)
.
Cultivating smut-resistant sugarcane varieties is the most economical and effective measure to control the disease.
The analysis of the host disease resistance mechanism and the explanation of the pathogenic pathogenic mechanism are the premise and basis
.
Figure 1 Sugarcane smut Que Youxiong's research group used microscopic observation, genome, proteomic and transcriptome technologies, as well as molecular marker development and disease resistance gene cloning, to resist sugarcane at the morphological, physiological and molecular levels.
A series of studies have been carried out on the mechanism of smut disease and the pathogenic mechanism of smut fungus, and certain progress has been made
.
However, people still know little about the process and mechanism of how pathogens promote infection and promote reproduction by inhibiting host resistance
.
The study found that during the process of smut infecting sugarcane, with the extension of the infection time and the proliferation of the pathogen, the genes of the host sugarcane variety and the genes of the pathogenic smut have significant co-expression, especially the receptor Kinase and effector protein genes (Figure 2)
.
PEPR1 is an important receptor kinase in the molecular model related to plant damage.
Its extracellular domain can specifically recognize the endogenous plant elicitor polypeptide Peps, thereby activating a series of immune responses and increasing the level of self-resistance
.
Through protein interaction verification, the authors found that the effector protein of S.
smutella SsPele1 can specifically bind to the kinase receptor ScPEPR1 on the sugarcane membrane, and there is a sequence very similar to the plant endogenous polypeptide Pep1 at the C-terminus of the SsPele1 protein (Figure 3 )
.
Figure 2 Co-expression of genes from sugarcane and smutella
.
UmPele1 is a homolog of the effector protein SsPele1 of Smutella smut .
Previous studies revealed that UmPele1 is an important factor in the pathogenicity of corn smut, and its deletion will seriously affect the formation of tumors after being infected by smut
.
Surprisingly, like the effector protein SsPele1 of smut smut, UmPele1 can specifically bind to the kinase receptor ZmPEPR1 on the corn membrane.
At the same time, similar to SsPele1, the C-terminus of UmPele1 protein is also present.
A sequence that is highly homologous to Pep1 (Figure 3)
.
Figure 3 The effector protein SsPele1 of S.
smutensis can specifically recognize the kinase receptor ScPEPR1 on the host membrane.
Further, the authors used the protoplast system of sugarcane and Arabidopsis thaliana and found that the 25 amino acid peptide Pel25 at the C-terminal of SsPele1 inhibited Pep1-induced gene expression and MAPK Activate and inhibit the resistance response of host cells (Figure 4)
.
And through the competitive binding imprinting test, Pel25 and Pep1 competitively bind to the extracellular domain of ScPEPR1 (Figure 4)
.
Figure 4 The immune response of sugarcane infected by smut fungus is inhibited by the competitive combination of SsPele1 and ScPEPR1.
In summary, the study clarified a new mechanism of the interaction between pathogenic fungi and host plants in the apoplast space
.
During the infection of sugarcane by Smutella smut, the effector protein Pele1 is secreted into the apoplast space of the plant
.
Pele1 competes to bind to PEPR1 by mimicking the host plant Pep1 through the terminal peptide, inhibiting the immune response mediated by polypeptide-kinase (Pep1-PEPR1)-mediated damage associated molecular patterns (DAMPs) and weakening The resistance of the host plant is improved, and the infection and proliferation of pathogenic bacteria are promoted (Figure 5)
.
The new plant-pathogen interaction mechanism revealed by this study provides a new perspective for the analysis of the pathogenic mechanism of sugarcane smut and the directional improvement of sugarcane disease resistance breeding
.
Figure 5 The molecular model of SsPele1 mediating plant immune pathways by inhibiting the host PEPR1 signaling pathway.
The young teachers Ling Hui and Huang Ning of the School of Biology and Pharmaceuticals/Agriculture College, Yulin Normal University, and Fu Xueqin, a graduate student of Fujian Agriculture and Forestry University, are co-authors of this paper The first author, researcher Que Youxiong and Professor Cui Haitao are the co-corresponding authors
.
The research was funded by the National Key Research and Development Program, the National Natural Science Foundation of China, the Fujian Outstanding Youth Science Foundation and the National Sugar Industry Technology System Project
.
Original link: https://nph.
onlinelibrary.
wiley.
com/doi/abs/10.
1111/nph.
17835
