Effects of Scion Variety on the Phosphorus Efficiency of Grafted Camellia oleifera Seedlings

Grafting provides a way to improve tolerance to low phosphorus (P) stress for plants, and has been extensively applied in commercial cultivars grafted onto appropriate rootstocks. However, little literature is available concerning the scion-mediated effect on P efficiency in grafted plants. In this study, three different Camellia oleifera Abel. scion cultivars (G8, G83-1, and W2) were grafted onto the same rootstock (W2) under controls (0.5 mM) and low-P (0 mM) availability for eight months. The results showed that the scions significantly affected root-to-shoot weight ratios, the root morphology with a diameter larger than 1 mm, P accumulation, and the P utilization efficiency (PUE) of the root. A higher increase in the root-to-shoot weight ratio under the low-P supply was observed in the G83-1/W2 (26.15%) than in the G8/W2 (0%) and the W2/W2 (5.32%). Root PUE of the scion G8, G83-1, and W2 was improved by up to 113.73%, 45.46%, and 20.97% under the low-P supply. Moreover, G8/W2 exhibited higher shoot P accumulation and the highest root PUE under the low-P supply, indicating a high capability to tolerate P deficiency by maximizing the cost-effectiveness of P remobilization to photosynthetic organs. This suggested the vigorous variety of G8 could be a promising scion to improve grafted C. oleifera tolerance to low-P stress. Our results would have important implications for exploration and identification of a superior scion variety to enhance the ability of resistance concerning P deficiency stress in C. oleifera

Genetic variants in HFE are associated with non-alcoholic fatty liver disease in lean individuals

Background &amp; Aims: Around 20% of patients with non-alcoholic fatty liver disease (NAFLD) are lean. Increasing evidence suggests that lean NAFLD is a unique subtype of the disease. We aimed to explore the metabolic profile, genetic basis, causal risk factors, and clinical sequelae underlying lean NAFLD. Methods: NAFLD was diagnosed by whole liver proton density fat fraction ≥5%. Whole liver proton density fat fraction and hepatic iron were quantified using magnetic resonance imaging in the UK Biobank. Individuals in this study were stratified according to the World Health Organization criteria of obesity, into lean, overweight, and obese. Mediation analysis, Mendelian randomisation analysis, and Bayesian networks were used to identify a risk factor or a clinical sequela of lean/obese NAFLD. Results: Lean NAFLD manifested a distinct metabolic profile, featured by elevated hepatic iron and fasting glucose. Four loci, namely, HFE rs1800562, SLC17A3-SLC17A2-TRIM38 rs9348697, PNPLA3 rs738409, and TM6SF2 rs58542926, were associated with lean NAFLD (p <5 × 10-8). HFE rs1800562 was specifically associated with lean NAFLD and demonstrated a significant mediation effect through elevating hepatic iron. Type 2 diabetes was the most pronounced clinical sequela of lean NAFLD, followed by liver cirrhosis. Conclusions: Our study suggested that HFE plays a potential steatogenic role rather than regulating iron homoeostasis in patients with lean NAFLD. The increased liver iron deposition is associated with lean NAFLD, whereas obese NAFLD is not related to hepatic iron. The clinical management of patients with lean NAFLD shall be concerned with the prevention and treatment of type 2 diabetes and liver cirrhosis. Impact and implications: Lean NAFLD has a distinct natural history from obese NAFLD. This study underscored liver iron content and the genetic variant of the iron homoeostasis gene HFE as major risks of lean NAFLD, in addition to the unique metabolic profile. The development of type 2 diabetes or liver cirrhosis shall be closely monitored and prevented in patients with lean NAFLD

Image_4_Pan-cancer analysis of ASB3 and the potential clinical implications for immune microenvironment of glioblastoma multiforme.tif

BackgroundAnkyrin repeat and SOCS Box containing 3 (ASB3) is an E3 ubiquitin ligase. It has been reported to regulate the progression of some cancers, but no systematic pan-cancer analysis has been conducted to explore its function in prognosis and immune microenvironment.MethodIn this study, mRNA expression data were downloaded from TCGA and GTEx database. Next generation sequencing data from 14 glioblastoma multiforme (GBM) samples by neurosurgical resection were used as validation dataset. Multiple bioinformatics methods (ssGSEA, Kaplan-Meier, Cox regression analysis, GSEA and online tools) were applied to explore ASB3 expression, gene activity, prognosis of patients in various cancers, and its correlation with clinical information, immune microenvironment and pertinent signal pathways in GBM. The biological function of ASB3 in tumor-infiltrating lymphocytes (TILs) was verified using an animal model.ResultsWe found that ASB3 was aberrant expressed in a variety of tumors, especially in GBM, and significantly correlated with the prognosis of cancer patients. The level of ASB3 was related to the TMB, MSI and immune cell infiltration in some cancer types. ASB3 had a negative association with immune infiltration and TME, including regulatory T cells (Tregs), cancer-associated fibroblasts, immunosuppressors and related signaling pathways in GBM. ASB3 overexpression reduced the proportion of Tregs in TILs. GSEA and PPI analysis also showed negative correlation between ASB3 expression and oncogenetic signaling pathways in GBM.ConclusionA comprehensive pan-cancer analysis of ASB3 showed its potential function as a biomarker of cancer prognosis and effective prediction of immunotherapy response. This study not only enriches the understanding of the biological function of ASB3 in pan-cancer, especially in GBM immunity, but also provides a new reference for the personalized immunotherapy of GBM.</p