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Chandrasekar, B.

Publications and source records attributed to Chandrasekar, B..

7 recordsLinked to original sources

PINPOINT: Protease INhibitor PredictiOn at the plant-pathogen INTerface using protein language models and structural modeling

Cysteine and serine proteases act as an immune hub in the plant apoplast to provide robust extracellular immunity during microbial colonisation. Microbial pathogens counteract these immune proteases by inhibiting their activity using small secreted proteins (SSPs). Traditionally, SSPs with protease-inhibitory activity are predicted using sequence-dependent database searches. However, in recent years, fungal SSPs have been shown to exhibit protease-inhibitory functions despite lacking the inhibitor domain that is annotated through sequence similarity searches. Hence, a large number of these novel SSPs with putative protease inhibitor functions are missed during detection and filtered out during sequence similarity searches. This necessitates the development of newer approaches to predict SSPs lacking an annotated inhibitor domain. Machine learning approaches, such as protein language models, have emerged as powerful tools for predicting protein functions. To date, no machine learning models have been developed to predict the protease-inhibitory activities of SSPs lacking an annotated inhibitor domain. Here, we introduce a protease inhibitor prediction pipeline, PINPOINT (Protease INhibitor PredictiOn at plant-pathogen INTerface). The PINPOINT pipeline combines fine-tuned protein language model classifiers, a structure-aware autoencoder, and effector prediction into a multi-level framework for identifying SSPs with predicted protease inhibitor functions. PINPOINT predicts protease inhibitors using SSPs sequences and monomeric structures with pre-computed structures obtained from the AlphaFold Protein Structure Database or predicted using the ESMFold public API. We successfully validated the PINPOINT platform using SSPs from the plant fungal pathogen Macrophomina phaseolina. Notably, the PINPOINT platform robustly predicted several of these SSPs as protease inhibitors including Sequence-unrelated but structurally similar (SUSS) effectors. We further validated the inhibitory potential of these predicted M. phaseolina SSPs using AlphaFold Multimer (AFM) screening against candidate apoplastic soybean cysteine and serine proteases. Additionally, this platform can be used as a pre-filtering step in AFM screening approaches to reduce the number of candidates for discovering novel SSPs with protease inhibitor function for cross-kingdom plant-microbe interaction studies. The PINPOINT platform will accelerate the prediction of novel SSPs including SUSS effectors with protease inhibitor functions in proteomes of any organisms. We made the PINPOINT pipeline accessible to the research community as a web-based notebook environment for interactive computing in Google Colab, available at https://github.com/iitj-mpg-lab/PINPOINT

bioinformatics↗

Bacterial pathogen deploys iminosugar galactosyrin to manipulate plant glycobiology

The extracellular space (apoplast) of plants is an important molecular battleground during infection by many pathogens. We previously found that a plant-secreted {beta}-galactosidase BGAL1 acts in immunity by facilitating the release of immunogenic peptides from bacterial flagellin and that Pseudomonas syringae suppresses this enzyme by producing a small molecule inhibitor called galactosyrin. Here, we elucidated the structure and biosynthesis of galactosyrin and uncovered its multifunctional roles during infection. Structural elucidation by cryo-EM and chemical synthesis revealed that galactosyrin is an iminosugar featuring a unique geminal diol attached to the pyrrolidine moiety that mimics galactose binding to the {beta}-galactosidase active site. Galactosyrin biosynthesis branches off from purine biosynthesis and involves three enzymes of which the first is a reductase that is unique in iminosugar biosynthesis. Besides inhibiting BGAL1 to avoid detection, galactosyrin also changes the glycoproteome and metabolome of the apoplast. The manipulation of host glycobiology may be common to plant-associated bacteria that carry putative iminosugar biosynthesis clusters.

plant biology↗

Proteome Analysis of Soybean Root Apoplast Combined with AlphaFold Prediction Reveal Macrophomina phaseolina Infection Strategies and Potential Targets for Engineering Resistance

Macrophomina phaseolina (Tassi) Goid. is a hemibiotrophic pathogen that causes charcoal rot (CR) disease in various legumes, including soybean. To date, no reliable resistance gene sources have been identified in soybean or other legumes to combat M. phaseolina. Therefore, the identification of mechanistic targets is crucial for improving resistance against the pathogen. The apoplast is a critical region where intense molecular cross-talk occurs between plants and pathogens, and the outcome of their interactions is determined in this compartment. Here, we employed label-free quantitative (LFQ) proteomics to investigate the dynamics of soybean root apoplast during M. phaseolina infection. We have detected several secreted proteins of M. phaseolina and differential regulation of soybean-secreted proteins in root apoplast during infections. Glycome analysis and callose deposition assays have revealed changes in soybean root cell wall compositions and potential polysaccharide targets of M. phaseolina. AlphaFold 2 (AF2) analysis was instrumental in revealing several interesting sequence-unrelated structurally similar (SUSS) effectors and effectors with novel structural folds secreted by M. phaseolina. Structured-guided engineering of protease-inhibitor complexes is emerging as an important strategy to engineer resistance in plants against pathogens. AlphaFold Multimer (AFM) analysis of candidate-secreted proteins from soybean and M. phaseolina has predicted cysteine and serine protease-inhibitor complexes with high confidence. We have validated these interactions using molecular dynamics (MD) and competitive activity-based protein profiling (ABPP) approaches. Therefore, our work provides insights into Soybean-M. phaseolina interactions in the root apoplast and unveil potential candidates for engineering resistance.

plant biology↗

A GH81-type β-glucan-binding protein facilitates colonization by mutualistic fungi in barley

Cell walls are important interfaces of plant-fungal interactions. Host cell walls act as robust physical and chemical barriers against fungal invaders, making them an essential line of defense. Upon fungal colonization, plants deposit phenolics and callose at the sites of fungal penetration to reinforce their walls and prevent further fungal progression. Alterations in the composition of plant cell walls significantly impact host susceptibility. Furthermore, plants and fungi secrete glycan hydrolases acting on each others cell walls. These enzymes release a wide range of sugar oligomers into the apoplast, some of which trigger the activation of host immunity via host surface receptors. Recent characterization of cell walls from plant-colonizing fungi have emphasized the abundance of {beta}-glucans in different cell wall layers, which makes them suitable targets for recognition. To characterize host components involved in immunity against fungi, we performed a protein pull-down with the biotinylated {beta}-glucan laminarin. Thereby, we identified a glycoside hydrolase family 81-type glucan-binding protein (GBP) as the major {beta}-glucan interactor. Mutation of GBP1 and its only paralogue GBP2 in barley led to decreased colonization by the beneficial root endophytes Serendipita indica and S. vermifera, as well as the arbuscular mycorrhizal fungus Rhizophagus irregularis. The reduction of symbiotic colonization was accompanied by enhanced responses at the host cell wall. Moreover, GBP mutation in barley also increased resistance to fungal infections in roots and leaves by the hemibiotrophic pathogen Bipolaris sorokiniana and the obligate biotrophic pathogen Blumeria graminis f. sp. hordei, respectively. These results indicate that GBP1 is involved in the establishment of symbiotic associations with beneficial fungi, a role that has potentially been appropriated by barley-adapted pathogens. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=134 SRC="FIGDIR/small/536646v1_figu1.gif" ALT="Figure 1"> View larger version (39K): org.highwire.dtl.DTLVardef@c47957org.highwire.dtl.DTLVardef@fa6727org.highwire.dtl.DTLVardef@18a54d2org.highwire.dtl.DTLVardef@c6b103_HPS_FORMAT_FIGEXP M_FIG C_FIG In BriefGBP1, a family 81 glycoside hydrolase, is an important {beta}-glucan interactor in barley. Mutation of GBP1 and its sole paralogue GBP2 leads to reduced colonization by beneficial root endophytes, AM fungi and pathogens, accompanied by enhanced responses at the plant cell wall. This indicates that GBP1 and {beta}-glucans are compatibility factors involved in the establishment of symbiotic associations with beneficial fungi, a role possibly hijacked by pathogens.

plant biology↗

Angiotensin II Type 2 Receptor Potentiates Skeletal Muscle Satellite Cell Differentiation via the GSK3β/β-catenin Pathway

Patients with advanced congestive heart failure (CHF) or chronic kidney disease (CKD) often have increased systemic angiotensin II (Ang II) levels and cachexia. We previously demonstrated that Ang II infusion in rodents results in skeletal muscle wasting and reduced muscle regenerative potential via Ang II type 1 receptor (AT1R) signaling, potentially contributing to cachexia in CHF and CKD. Contrary to AT1R signaling, we found that signaling via Ang II type 2 receptor (AT2R) potentiates skeletal muscle satellite cell (SC) differentiation and muscle regenerative potential. However, mechanisms whereby AT2R regulates SC differentiation and cachexia development remain unknown. In this study, we found that GSK3{beta} activity was significantly suppressed during SC differentiation, whereas it was retained in SCs with AT2R knockdown. AT2R knockdown leads to higher GSK3{beta} and decreased {beta}-catenin activities both in vitro and in vivo. Treatment with GSK3{beta} inhibitor BIO restored {beta}-catenin activity and differentiation capacity of SCs with AT2R knockdown. Conversely, transgenic overexpression of AT2R in SCs inhibited GSK3{beta}, associated with increased {beta}-catenin activity and SC myogenic capacity both in vitro and in vivo. Interestingly, AT2R expression in undifferentiated SCs was regulated post-transcriptionally. An increase in systemic Ang II blunted AT2R induction during muscle regeneration. However, overexpression of AT2R restored AT2R levels and myogenesis in vivo. Together, these data suggest that the AT2R/GSK3{beta}/{beta}- catenin signaling pathway could serve as a potential therapeutic target to promote muscle regenerative capacity in chronic disease conditions characterized by heightened activation of the renin-angiotensin system, such as CHF and CKD.

cell biology↗

Multi-omic analysis of the cardiac cellulome defines a vascular contribution to cardiac diastolic dysfunction in obese female mice

Coronary microvascular dysfunction (CMD) is associated with cardiac dysfunction and predictive of cardiac mortality in obesity, especially in females. Emerging evidence suggests development of heart failure with preserved ejection fraction in females with CMD and that mineralocorticoid receptor (MR) antagonism may be more efficacious in obese female, versus male, HFpEF patients. Accordingly, we examined the hypothesis that smooth muscle cell (SMC)-specific MR deletion prevents obesity-associated coronary and cardiac diastolic dysfunction in females. Obesity was induced in female mice via western diet (WD) feeding alongside littermates fed standard diet. Initial studies revealed that global MR blockade with spironolactone prevented impaired coronary vasodilation and diastolic dysfunction in obese females. Importantly, specific deletion of SMC-MR similarly prevented obesity-associated coronary and cardiac dysfunction. Cardiac gene expression profiling suggested reduced cardiac inflammation in WD-fed mice with SMC-MR deletion independent of blood pressure, aortic stiffening, and cardiac hypertrophy. Further mechanistic studies utilizing single-cell RNA sequencing of non-cardiomyocyte cell populations revealed novel impacts of SMC-MR deletion on the cardiac cellulome in obese mice. Specifically, WD feeding induced inflammatory gene signatures in multiple non-myocyte populations (B/T cells, macrophages, and endothelium), independent of cardiac fibrosis, that was prevented by SMC-MR deletion. Further, SMC-MR deletion induced a basal reduction in cardiac mast cells and prevented WD-induced cardiac pro-inflammatory chemokine expression and leukocyte recruitment. These data reveal a central role for SMC-MR signaling in obesity-associated coronary and cardiac dysfunction thus supporting the emerging paradigm of a vascular origin of cardiac dysfunction in obesity.

physiology↗

Fungi hijack a plant apoplastic endoglucanase to release a ROS scavenging β-glucan decasaccharide to subvert immune responses

Plant pathogenic and beneficial fungi have evolved several strategies to evade immunity and cope with host-derived hydrolytic enzymes and oxidative stress in the apoplast, the extracellular space of plant tissues. Fungal hyphae are surrounded by an inner, insoluble cell wall (CW) layer and an outer, soluble extracellular polysaccharide (EPS) matrix. Here we show by proteomics and glycomics that these two layers have distinct protein and carbohydrate signatures, implicating different biological functions. The barley (Hordeum vulgare) {beta}-1,3-endoglucanase HvBGLUII, which belongs to the widely distributed apoplastic glycoside hydrolase 17 family (GH17), releases a conserved {beta}-1,3;1,6-glucan decasaccharide ({beta}-GD) from the EPS matrices of fungi with different lifestyles and taxonomic positions. This low molecular weight {beta}-GD does not activate plant immunity, is resilient to further enzymatic hydrolysis by {beta}-1,3-endoglucanases due to the presence of three {beta}-1,6-linked glucose branches and can scavenge reactive oxygen species. Additionally, exogenous application of {beta}-GD leads to enhanced fungal colonization in barley. Our data highlights the hitherto undescribed capacity of this often overseen fungal EPS layer to act as an outer protective barrier important for fungal accommodation within the hostile environment at the apoplastic plant-microbe interface. SignificanceHere we identify and characterize a conserved {beta}-1,3;1,6-glucan decasaccharide with antioxidant activity released from the fungal extracellular polysaccharide (EPS) matrix by the activity of a plant apoplastic endoglucanase. In addition, we provide a quantitative proteomic analysis of the fungal EPS and cell wall (CW) layers. HIGHLIGHTSO_LIThe fungal extracellular polysaccharide (EPS) matrix and the cell wall (CW) are specific layers with distinct protein and carbohydrate signatures C_LIO_LIA conserved {beta}-1,3;1,6-glucan decasaccharide ({beta}-GD) is released from the EPS matrices of different fungi by the activity of the barley {beta}-1,3-endoglucanase BGLUII, a member of the widely distributed apoplastic GH17 family C_LIO_LIThe {beta}-GD efficiently scavenges reactive oxygen species (ROS) and enhances fungal colonization C_LIO_LIThe immunomodulatory potential as microbe-associated molecular pattern (MAMP) as well as the biochemical activity as ROS scavenger of soluble low molecular weight {beta}-glucans are defined by the presence of {beta}-1,6-glucose branches C_LI

microbiology↗