Biology subjects

Muthukumar, G.

Publications and source records attributed to Muthukumar, G..

4 recordsLinked to original sources

bioRxiv2025

A BIOPOLYMER LAMINARIN ELICITS ANTIOXIDANT DEFENSE IN DIFFERENT CULTIVARS OF SOLANUM LYCOPERSICUM AGAINST EARLY BLIGHT DISEASE CAUSED BY ALTERNARIA SOLANI

The study evaluates the potential of laminarin (LaM), a biopolymer, in inducing antioxidative defense in tomato against early blight disease caused by Alternaria solani. Histological analysis of A. solani infection in susceptible (PKM-1) and tolerant (Arka Rakshak) cultivars of tomato showed increased pathogen colonization in PKM-1 by day 8 compared to Arka Rakshak. Fluorescent microscopic analysis with a chitin-specific dye, Calcofluor white, demonstrated reduced A. solani colonization in PKM-1 pretreated with LaM (0.1%), followed by A. solani infection on par with Arka Rakshak. A significant increase in the accumulation of hydrogen peroxide was observed in LaM-pretreated leaves (0.050%, 0.075% and 0.1%) at 24- and 48-hours post-infection in both cultivars. A quantitative increase in guaiacol peroxidase (GPX) activity was recorded in LaM (0.025%), followed by A. solani infection leaves at 36 hrs in Arka Rakshak, whereas LaM (0.010%) followed by A. solani infection recorded maximum GPX activity at 24 hrs in PKM-1. Induction of new GPX isoform was evident in LaM (0.075% and 0.1%) pretreated, and LaM pretreated, followed by A. solani infected leaves of both cultivars at 24 hrs. There was a significant reduction in disease severity in tomato leaves pretreated with LaM (0.1%) and infected with A. solani. The results suggest that LaM could be a potential elicitor of antioxidant defense in tomato against A. solani infection, which can further be harnessed to develop sustainable strategies for managing early blight disease while reducing dependence on chemical fungicides.

plant biology↗

bioRxiv2025

Comparative transcriptome analysis of tomato cultivars pretreated with Laminarin reveals differential expression of defense-responsive genes against Early blight disease

Eco-friendly measures to control disease progression are the need of the hour since chemical fungicides have been harmful to the environment. This study observed that the algal polysaccharide Laminarin triggers a defense response against early blight disease in both tolerant and susceptible tomato cultivars. A dose-dependent reduction in cell death was observed in tomato leaves pre-treated with 0.1% Laminarin and then infected with Alternaria solani in a susceptible and tolerant cultivar. As a result, 0.1% Laminarin was chosen for transcriptome analysis. Transcriptome analysis revealed the upregulation of defense-related genes, such as EF-hand domain-containing protein, Heat shock protein 70, Heat shock factor (HSF) type DNA binding domain-containing protein, Non-specific serine/threonine protein kinase, AP2/ERF domain-containing protein, Leucine-rich repeat-containing N-terminal plant type domain-containing protein, and Subtilisin-like protease. The study also validated the differentially expressed genes using qRT-PCR for bZIP, nsLTP, SKP1, and V-type ATPase genes. Overall, the study demonstrated that the algal polysaccharide Laminarin could induce defense-related genes and provide resistance against early blight disease in tomato plants. KEY MESSAGETomatoes defense-responsive genes showed differential expression in tolerant and susceptible cultivars when treated with laminarin, followed by Alternaria solani infection.

plant biology↗

bioRxiv2023

Triaging of -helical proteins to the mitochondrial outer membrane by distinct chaperone machinery based on substrate topology

Mitochondrial outer membrane -helical proteins play critical roles in mitochondrial-cytoplasmic communication, but the rules governing the targeting and insertion of these biophysically diverse substrates remain unknown. Here, we first defined the complement of required mammalian biogenesis machinery through genome-wide CRISPRi screens using topologically distinct membrane proteins. Systematic analysis of nine identified factors across 21 diverse -helical substrates reveals that these components are organized into distinct targeting pathways which act on substrates based on their topology. NAC is required for efficient targeting of polytopic proteins whereas signal-anchored proteins require TTC1, a novel cytosolic chaperone which physically engages substrates. Biochemical and mutational studies reveal that TTC1 employs a conserved TPR domain and a hydrophobic groove in its C-terminal domain to support substrate solubilization and insertion into mitochondria. Thus, targeting of diverse mitochondrial membrane proteins is achieved through topological triaging in the cytosol using principles with similarities to ER membrane protein biogenesis systems.

cell biology↗

bioRxiv2022

MTCH2 is a mitochondrial outer membrane protein insertase

In the mitochondrial outer membrane, tail-anchored (TA) proteins play critical roles in cytoplasmic-mitochondrial communication. Using genome-wide CRISPRi screens, we identify factors involved in mitochondrial TA biogenesis in human cells. We show that MTCH2, and its paralog MTCH1, are required for insertion of biophysically diverse mitochondrial TAs, but not outer membrane {beta}-barrel proteins. In a reconstituted system, purified MTCH2 is sufficient to mediate insertion into proteoliposomes. Functional and mutational studies reveal that MTCH2 uses membrane-embedded hydrophilic residues to function as a gatekeeper for outer membrane protein biogenesis, controlling mislocalization of TAs into the endoplasmic reticulum and the sensitivity of leukemia cells to apoptosis. Our identification of MTCH2 as an insertase provides a mechanistic explanation for the diverse phenotypes and disease states associated with MTCH2 dysfunction. One-Sentence SummaryMTCH2 is both necessary and sufficient for insertion of diverse -helical proteins into the mitochondrial outer membrane, and is the defining member of a family of insertases that have co-opted the SLC25 transporter fold.

cell biology↗