Major Intrinsic Proteins ( MIP ) are a family of channels facilitating the diffusion of water and/or small solutes across cellular membranes. X Intrinsic Proteins ( XIP ) form the least characterized MIP subfamily in vascular plants. XIP s are mostly impermeable to water but facilitate the diffusion of hydrogen peroxide, urea and boric acid when expressed in heterologous expression systems. However, their transport capabilities in planta and their impact on plant physiology are still unknown. Here, we demonstrated that overexpression of Nt XIP 1;1 in Nicotiana tabacum by the En2p PMA 4 or the 35S Ca MV promoter and in Arabidopsis, which does not contain any XIP gene, by the 35S Ca MV promoter, resulted in boron (B)‐deficiency symptoms such as death of the shoot apical meristem, infertile flowers, and puckered leaves. Leaf B concentrations in symptomatic tissues and B xylem sap concentrations were lower in the overexpressors than in control plants. Importantly, expression of Nt XIP 1;1 under the control of the At NIP 5;1 promoter complemented the B deficiency phenotype of the Atnip5;1 knockout mutant, defining its ability to act as a boric acid channel in planta . Protein quantification analysis revealed that Nt XIP 1;1 was predominantly expressed in young B‐demanding tissues and induced under B‐deficient conditions. Our results strongly suggest that Nt XIP 1;1 plays a role in B homeostasis and its tissue‐specific expression critically contributes to the distribution of B within tobacco.
Fish health personnel have limited tools in combatting viral diseases such as heart and skeletal muscle inflammation (HSMI) in open net-pen farmed Atlantic salmon. In this study, we aimed to predict HSMI by intensified health monitoring and apply clinical nutrition to mitigate the condition. We followed a commercial cohort (G1) of Atlantic salmon that was PRV-1 naïve when transferred to a sea cage at a location where HSMI outbreaks commonly occur. The fish in the other cages (G2-G6) at the location had a different origin than G1 and were PRV-1 positive prior to sea transfer. By continuous analysis of production data and sequentially (approximately every fourth week) performing autopsy, RT-qPCR (for PRV-1 and selected immune genes), blood and histological analysis of 10 fish from G1 and G2, we identified the time of PRV-1 infection in G1 and predicted the onset of HSMI prior to any clinical signs of disease. Identical sequences across partial genomes of PRV-1 isolates from G1 and G2 suggest the likely transfer from infected cages to G1. The isolates were grouped into a genogroup known to be of high virulence. A commercial health diet was applied during the HSMI outbreak, and the fish had low mortality and an unaffected appetite. In conclusion, we show that fish health and welfare can benefit from in-depth health monitoring. We also discuss the potential health value of clinical nutrition as a mean to mitigate HSMI.
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