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Availability of nutrients in soil plays an important role in the productivity and quality of flowers in chrysanthemum. A set of novel biofilm inoculants- Anabaena-Azotobacter, Anabaena-Pseudomonas fluorescens (An-Psf) and Anabaena-Trichoderma (An-Tr) were applied as carrier based dry formulation or soil drench and their performance compared in two varieties of chrysanthemum (White Star and Zembla), in a climate-controlled greenhouse. Both the An-Psf and (An-Tr) inoculants enhanced glomalin related soil proteins in the rhizosphere of White Star, while in terms of polysaccharide content of soil, both these inoculants performed better in Zembla variety. Significant increases in the availability of selected macro and micronutrients in rhizosphere soil samples, in both chrysanthemum varieties were recorded, particularly when the inoculants were applied as soil drench. Principal Component analysis illustrated the significant interaction among soil and plant parameters, more specifically, the distinct effect of the inoculants, as compared to the application of carrier alone or control treatment. This investigation demonstrated the varietal effects on soil biological activities and significance of mode of application of microbial inoculants in influencing plant growth and rhizospheric metabolic activities.

Anti‐inflammatory and immune suppressive agents are required to moderate hyper‐activation of lymphocytes under disease conditions or organ transplantation. However, selective disruption of mitochondrial redox has not been evaluated as a therapeutic strategy for suppression of T‐cell‐mediated pathologies. Using mitochondrial targeted curcumin (MitoC), we studied the effect of mitochondrial redox modulation on T‐cell responses by flow cytometry, transmission electron microscopy, transcriptomics, and proteomics, and the role of Nrf2 was studied using Nrf2−/− mice. MitoC decreased mitochondrial TrxR activity, enhanced mitochondrial ROS (mROS) production, depleted mitochondrial glutathione, and suppressed activation‐induced increase in mitochondrial biomass. This led to suppression of T‐cell responses and metabolic reprogramming towards Treg differentiation. MitoC induced nuclear translocation and DNA binding of Nrf2, leading to upregulation of Nrf2‐dependent genes and proteins. MitoC‐mediated changes in mitochondrial redox and modulation of T‐cell responses are abolished in Nrf2−/− mice. Restoration of mitochondrial thiols abrogated inhibition of T‐cell responses. MitoC suppressed alloantigen‐induced lymphoblast formation, inflammatory cytokines, morbidity, and mortality in acute graft‐versus‐host disease mice. Disruption of mitochondrial thiols but not mROS increase inculcates an Nrf2‐dependent immune‐suppressive disposition in T cells for the propitious treatment of graft‐versus‐host disease. [ABSTRACT FROM AUTHOR]

Climate change inflicts several stresses on plants, of which dehydration stress severely affects growth and productivity. C4 plants possess better adaptability to dehydration stress; however, the role of epigenetic modifications underlying this trait is unclear. In particular, the molecular links between histone modifiers and their regulation remain elusive. In this study, genome-wide H3K9 acetylation (H3K9ac) enrichment using ChIP-sequencing was performed in two foxtail millet cultivars with contrasting dehydration tolerances (IC403579, cv. IC4—tolerant, and IC480117, cv. IC41—sensitive). It revealed that a histone deacetylase, SiHDA9 , was significantly up-regulated in the sensitive cultivar. Further characterization indicated that SiHDA9 interacts with SiHAT3.1 and SiHDA19 to form a repressor complex. SiHDA9 might be recruited through the SiHAT3.1 recognition sequence onto the upstream of dehydration-responsive genes to decrease H3K9 acetylation levels. The silencing of SiHDA9 resulted in the up-regulation of crucial genes, namely, SiRAB18 , SiRAP2.4, SiP5CS2 , SiRD22 , SiPIP1;4 , and SiLHCB2.3 , which imparted dehydration tolerance in the sensitive cultivar (IC41). Overall, the study provides mechanistic insights into SiHDA9-mediated regulation of dehydration stress response in foxtail millet. [ABSTRACT FROM AUTHOR]