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This study aimed to investigate the effects of adding Nano-Selenium (NSe) and Nano-clay (NC) as feed supplements on European Sea Bass (Dicentrarchus labrax). Two separate experiments were conducted, one with NC and the other with NSe. Each experiment consisted of four sub-groups with varying concentrations of NC or NSe. The expression levels of five immune-related genes (TNF-α, TNF-β, IL-2, IL-6 and IL-12) were measured using Real-time Quantitative PCR (Rt-PCR) Assay. The results showed an increase in the expression of interleukins (IL-2, IL-6 and IL-12) and pro-inflammatory cytokines (TNF-α and TNF-β) after exposure to NC and NSe. TNF-α gene expression was significantly higher with both 1 mg and 10 mg concentrations of NC and NSe. TNF-β gene expression was highest with the 5 mg concentration of NC. The concentrations of 1 mg and 10 mg for NC, and 1 mg, 5 mg, and 10 mg for NSe, led to the highest (p < 0.05) levels of IL-2 expression compared to the control. Similar trends were observed for IL-6 and IL-12 gene expression. Understanding the impact of these concentrations on gene expression, growth rate, biochemical indices, and antioxidant status can provide valuable insights into the potential applications of NC and NSe supplements on European Sea Bass., (© 2024. The Author(s).)

Tomato mosaic disease, caused by Tomato Mosaic Virus (ToMV), is one of the most destructive diseases which results in serious crop losses. Research investigations dealing with the biocontrol activity of arbuscular mycorrhizal fungi (AMF) against this viral disease are limited. In this study, the biocontrol activity of AMF on tomato plants infected with ToMV was evaluated in the greenhouse. In addition, their impacts on the transcriptional expression levels of thirteen genes controlling the phenylpropanoid, flavonoid and chlorogenic acid biosynthetic pathways were also investigated using quantitative real-time PCR. Transcriptional expressions of the majority of the studied genes were up-regulated by mycorrhizal colonization in the presence of ToMV, particularly PAL1 and HQT, suggesting their pathogen-dependent inducing effect. Under greenhouse conditions, a significant reduction in the disease severity and incidence, as well as the viral accumulation level was observed as a response to the mycorrhizal colonization of the infected plants. Moreover, the evaluated growth parameters, photosynthetic pigments, and flavonoid content were significantly enhanced by AMF colonization. The obtained results demonstrated the protective role of AMF in triggering the plant immunity against ToMV in a pathogen-dependent manner. Beside their protective and growth-promotion activities, AMF are characterized by low-cost and environment-friendly properties which support their possible use for control of tomato mosaic disease.

3-ketodihydrosphingosine reductase (KDSR) is the key enzyme in the de novo sphingolipid synthesis. We identified a novel missense kdsr I105R mutation in zebrafish that led to a loss of function, and resulted in progression of hepatomegaly to steatosis, then hepatic injury phenotype. Lipidomics analysis of the kdsr I105R mutant revealed compensatory activation of the sphingolipid salvage pathway, resulting in significant accumulation of sphingolipids including ceramides, sphingosine and sphingosine 1-phosphate (S1P). Ultrastructural analysis revealed swollen mitochondria with cristae damage in the kdsr I105R mutant hepatocytes, which can be a cause of hepatic injury in the mutant. We found elevated sphingosine kinase 2 (sphk2) expression in the kdsr I105R mutant. Genetic interaction analysis with the kdsr I105R and the sphk2 wc1 mutants showed that sphk2 depletion suppressed liver defects observed in the kdsr I105R mutant, suggesting that liver defects were mediated by S1P accumulation. Further, both oxidative stress and ER stress were completely suppressed by deletion of sphk2 in kdsr I105R mutants, linking these two processes mechanistically to hepatic injury in the kdsr I105R mutants. Importantly, we found that the heterozygous mutation in kdsr induced predisposed liver injury in adult zebrafish. These data point to kdsr as a novel genetic risk factor for hepatic injury.