Image_1_Heritable priming by Trichoderma: A sustainable approach for wheat protection against Bipolaris sorokiniana.tif

Crop plants encounter a variety of biotic challenges in the field and faces significant reduction in crop yield. In the current scenario of an ever increasing global population, there is an urgent need to protect plant health by using sustainable approach to maximize the crop productivity and to mitigate the food demands. Nowadays, we mostly rely on chemical crop protection techniques, which are causing a number of environmental and health difficulties. Defence priming is a chemical-free, eco-friendly, and sustainable strategy of crop protection, which is also called “green vaccination. In the present study, for the first time, we used Trichoderma as a priming agent to protect wheat crop from spot blotch disease. We have established Trichoderma-mediated defence priming in wheat against Bipolaris sorokiniana for sustainable crop improvement. We have characterised the morphological, disease phenotype, biochemical and yield parameters of Trichoderma-primed and non-primed wheat under disease pressure. Trichoderma-primed plants were found to be more protected against B. sorokiniana as compared to non-primed plants. Biochemical studies indicated that there is no direct defence response after priming stimulus but the defence response was activated only after triggering stimulus in terms of enhanced defence metabolites in primed plants as compared to non-primed plants. In the present study, since defence was activated only when required, that is under disease pressure, there was no unnecessary allocation of resources towards defence. Hence, no yield penalty was shown in primed plants as compared to control. We further evaluated the inheritance of primed state to the next generation and found that progeny of primed parents also performed better than progeny of non-primed parents under disease pressure in terms of protection from B. sorokiniana as well as yield performance. This strategy has the potential to protect crop without any yield penalty and causing environmental degradation. Our research findings indicate that Trichoderma-mediated defence priming could be an alternative approach for improving wheat productivity under biotic stress. To be our best knowledge, this is the first documented report for the Trichoderma-mediated defence priming and induced inheritance in wheat plant. This study will open new arenas in sustainable crop protection strategies for the exploitation of defence priming in crop plants.</p

DataSheet_1_Heritable priming by Trichoderma: A sustainable approach for wheat protection against Bipolaris sorokiniana.pdf

Crop plants encounter a variety of biotic challenges in the field and faces significant reduction in crop yield. In the current scenario of an ever increasing global population, there is an urgent need to protect plant health by using sustainable approach to maximize the crop productivity and to mitigate the food demands. Nowadays, we mostly rely on chemical crop protection techniques, which are causing a number of environmental and health difficulties. Defence priming is a chemical-free, eco-friendly, and sustainable strategy of crop protection, which is also called “green vaccination. In the present study, for the first time, we used Trichoderma as a priming agent to protect wheat crop from spot blotch disease. We have established Trichoderma-mediated defence priming in wheat against Bipolaris sorokiniana for sustainable crop improvement. We have characterised the morphological, disease phenotype, biochemical and yield parameters of Trichoderma-primed and non-primed wheat under disease pressure. Trichoderma-primed plants were found to be more protected against B. sorokiniana as compared to non-primed plants. Biochemical studies indicated that there is no direct defence response after priming stimulus but the defence response was activated only after triggering stimulus in terms of enhanced defence metabolites in primed plants as compared to non-primed plants. In the present study, since defence was activated only when required, that is under disease pressure, there was no unnecessary allocation of resources towards defence. Hence, no yield penalty was shown in primed plants as compared to control. We further evaluated the inheritance of primed state to the next generation and found that progeny of primed parents also performed better than progeny of non-primed parents under disease pressure in terms of protection from B. sorokiniana as well as yield performance. This strategy has the potential to protect crop without any yield penalty and causing environmental degradation. Our research findings indicate that Trichoderma-mediated defence priming could be an alternative approach for improving wheat productivity under biotic stress. To be our best knowledge, this is the first documented report for the Trichoderma-mediated defence priming and induced inheritance in wheat plant. This study will open new arenas in sustainable crop protection strategies for the exploitation of defence priming in crop plants.</p

Dysregulation of TFEB contributes to manganese-induced autophagic failure and mitochondrial dysfunction in astrocytes

Epidemiological and clinical studies have long shown that exposure to high levels of heavy metals are associated with increased risks of neurodegenerative diseases. It is widely accepted that autophagic dysfunction is involved in pathogenesis of various neurodegenerative disorders; however, the role of heavy metals in regulation of macroautophagy/autophagy is unclear. Here, we show that manganese (Mn) induces a decline in nuclear localization of TFEB (transcription factor EB), a master regulator of the autophagy-lysosome pathway, leading to autophagic dysfunction in astrocytes of mouse striatum. We further show that Mn exposure suppresses autophagic-lysosomal degradation of mitochondria and induces accumulation of unhealthy mitochondria. Activation of autophagy by rapamycin or TFEB overexpression ameliorates Mn-induced mitochondrial respiratory dysfunction and reactive oxygen species (ROS) generation in astrocytes, suggesting a causal relation between autophagic failure and mitochondrial dysfunction in Mn toxicity. Taken together, our data demonstrate that Mn inhibits TFEB activity, leading to impaired autophagy that is causally related to mitochondrial dysfunction in astrocytes. These findings reveal a previously unappreciated role for Mn in dysregulation of autophagy and identify TFEB as a potential therapeutic target to mitigate Mn toxicity. Abbreviations: BECN1: beclin 1; CTSD: cathepsin D; DMEM: Dulbecco’s Modified Eagle Medium; GFAP: glial fibrillary acid protein; GFP: green fluorescent protein; HBSS: hanks balanced salt solution; LAMP: lysosomal-associated membrane protein; LDH: lactate dehydrogenase; Lys Inh: lysosomal inhibitors; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; MAPK: mitogen-activated protein kinase; Mn: manganese; MTOR: mechanistic target of rapamycin kinase; OCR: oxygen consumption rate; PBS: phosphate-buffered saline; PFA: paraformaldehyde; PI: propidium iodide; ROS: reactive oxygen species; s.c.: subcutaneous; SQSTM1/p62: sequestosome 1; TEM: transmission electron microscopy; TFEB: transcription factor EB</p

Global Burden of Cardiovascular Diseases and Risks, 1990-2022

No description supplied</p