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The effects of putrescine on improving rice growth under aluminum (Al) toxicity conditions have been previously demonstrated, however, the underlying mechanism remains unclear. In this study, treatment with 50 μmol/L Al significantly decreased rice root growth and whole rice dry weight, inhibited Ca2+ uptake, decreased ATP synthesis, and increased Al, H2O2 and malondialdehyde (MDA) contents, whereas the application of putrescine mitigated these negative effects. Putrescine increased root growth and total dry weight of rice, reduced total Al content, decreased H2O2 and MDA contents by increasing antioxidant enzyme (superoxide dismutase, peroxidase, catalase and glutathione S-transferase) activities, increased Ca2+ uptake and energy production. Proteomic analyses using data-independent acquisition successfully identified 7 934 proteins, and 59 representative proteins exhibiting fold-change values higher than 1.5 were randomly selected. From the results of the proteomic and biochemical analyses, we found that putrescine significantly inhibited ethylene biosynthesis and phosphorus uptake in rice roots, increased pectin methylation, decreased pectin content and apoplastic Al deposition in rice roots. Putrescine also alleviated Al toxicity by repairing damaged DNA and increasing the proteins involved in maintaining plasma membrane integrity and normal cell proliferation. These findings improve our understanding of how putrescine affects the rice response to Al toxicity, which will facilitate further studies on environmental protection, crop safety, innovations in rice performance and real-world production.

The oil derived from Psidium guajava seeds (TKSO) exhibits an abundance of diverse unsaturated fatty acids, notably oleic, linoleic, and α-linolenic acids, conferring substantial health advantages in addressing metabolic irregularities and human diseases. This research endeavor focused on elucidating the impacts of TKSO on colonic inflammatory responses and intestinal microbiota alterations in a murine model of colitis induced by dextran sulfate sodium (DSS), demonstrated that substantial supplementation with TKSO reduces the severity of colitis induced by DSS. Furthermore, TKSO effectively attenuated the abundance and expression of proinflammatory mediators while augmenting the expression of tight junction proteins in DSS-challenged mice. Beyond this, TKSO intervention modulated the intestinal microbial composition in DSS-induced colitis mice, specifically by enhancing the relative presence of Lactobacillus, Norank_f_Muribaculaceae, and Lachnospiraceae_NK4A136_group, while concurrently diminishing the abundance of Turicibacter. Additionally, an analysis of short-chain fatty acids (SCFAs) revealed noteworthy elevations in acetic, propionic, isobutyric, and butyric acids, and total SCFAs levels in TKSO-treated mice. In summary, these findings underscore the potential of TKSO to reduce the severity of colitis induced by DSS in mice through intricate modulation of the intestinal microbiota, metabolite profiles, and intestinal barrier repair, thereby presenting a promising avenue for the development of therapeutic strategies against intestinal inflammatory conditions. [ABSTRACT FROM AUTHOR]

Obesity has become one of the most serious chronic diseases threatening human health. Its onset and progression are closely related to the intestinal microbiota, as disruption of the intestinal flora promotes the production of endotoxins and induces an inflammatory response. This study aimed to investigate the variations in the physicochemical properties of various refined tea seed oils and their impact on intestinal microbiota disorders induced by a high-fat diet (HFD) through dietary intervention. In the present study, C57BL/6J mice on a HFD were randomly divided into three groups: HFD, T-TSO, and N-TSO. T-TSO and N-TSO mice were given traditionally refined and optimized tea seed oil for 12 weeks. The data revealed that tea seed oil obtained through degumming at 70 °C, deacidification at 50 °C, decolorization at 90 °C, and deodorization at 180 °C (at 0.06 MPa for 1 h) effectively removed impurities while minimizing the loss of active ingredients. Additionally, the optimized tea seed oil mitigated fat accumulation and inflammatory responses resulting from HFD, and reduced liver tissue damage in comparison to traditional refining methods. More importantly, N-TSO can serve as a dietary supplement to enhance the diversity and abundance of intestinal microbiota, increasing the presence of beneficial bacteria (norank_f__Muribaculaceae, Lactobacillus, and Bacteroides) while reducing pathogenic bacteria (Alistipes and Mucispirillum). Therefore, in HFD-induced obese C57BL/6J mice, N-TSO can better ameliorate obesity compared with a T-TSO diet, which is promising in alleviating HFD-induced intestinal microbiota disorders. [ABSTRACT FROM AUTHOR]

Objective: To investigate the potential beneficial effects of sciadonic acid (SA) on improving obesity induced by a high-fat diet in mice. Methods: Forty-eight male C57BL/6 mice were adaptively fed for one week and then randomly divided into the following groups: Control group (C), positive control group (S), model group (M), low-dose sciadonic acid group (LSA), medium-dose sciadonic acid group (MSA), and high-dose sciadonic acid group (HSA). The modeling process lasted for 16 weeks, and the low and high-dose groups were orally administered different doses of SA solution at a fixed time each day. After the modeling period, potential mechanisms of SA in regulating lipid metabolism in obese mice were explored, including aspects such as blood lipid metabolism, hepatic fat metabolism, hepatic oxidative stress, hepatic lipid synthesis, and expression of metabolism-related genes. Results: The high-dose SA intervention in obese mice significantly decreased the levels of total cholesterol (TC), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-C) in serum, while increasing high-density lipoprotein cholesterol (HDL-C) (P<0.05). It inhibited weight gain, reduced epididymal fat accumulation, and improved liver tissue damage. Additionally, SA significantly increased the activities of antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in mice (P<0.05), and significantly reduced the production of oxidative end products MDA (P<0.05), alleviated oxidative stress in vivo, and inhibited lipid synthesis by regulating the expression of genes related to lipid metabolism to improve lipid metabolism. Conclusion: SA could improve lipid metabolism disorders in obese mice by suppressing fat accumulation, alleviate oxidative stress, regulate lipid synthesis and metabolism. [ABSTRACT FROM AUTHOR]

Summary: Abiotic stresses such as extreme temperatures, water‐deficit and salinity negatively affect plant growth and development, and cause significant yield losses. It was previously shown that co‐overexpression of the Arabidopsis vacuolar pyrophosphatase gene AVP1 and the rice SUMO E3 ligase gene OsSIZ1 in Arabidopsis significantly increased tolerance to multiple abiotic stresses and led to increased seed yield for plants grown under single or multiple abiotic stress conditions. It was hypothesized that there might be synergistic effects between AVP1 overexpression and OsSIZ1 overexpression, which could lead to substantially increased yields if these two genes are co‐overexpressed in real crops. To test this hypothesis, AVP1 and OsSIZ1 were co‐overexpressed in cotton, and the impact of OsSIZ1/AVP1 co‐overexpression on cotton's performance under normal growth and multiple stress conditions were analysed. It was found that OsSIZ1/AVP1 co‐overexpressing plants performed significantly better than AVP1‐overexpressing, OsSIZ1‐overexpressing and wild‐type cotton plants under single, as well as under multiple stress conditions in laboratory and field conditions. Two field studies showed that OsSIZ1/AVP1 co‐overexpressing plants produced 133% and 81% more fibre than wild‐type cotton in the dryland conditions of West Texas. This research illustrates that co‐overexpression of AVP1 and OsSIZ1 is a viable strategy for engineering abiotic stress‐tolerant crops and could substantially improve crop yields in low input or marginal environments, providing a solution for food security for countries in arid and semiarid regions of the world. [ABSTRACT FROM AUTHOR]

Summary: The biosynthesis of very‐long‐chain fatty acids (VLCFAs) and their transport are required for fibre development. However, whether other regulatory factors are involved in this process is unknown. We report here that overexpression of an Arabidopsis gene ankyrin repeat‐containing protein 2A (AKR2A) in cotton promotes fibre elongation. RNA‐Seq analysis was employed to elucidate the mechanisms of AKR2A in regulating cotton fibre development. The VLCFA content and the ratio of VLCFAs to short‐chain fatty acids increased in AKR2A transgenic lines. In addition, AKR2A promotes fibre elongation by regulating ethylene and synergizing with the accumulation of auxin and hydrogen peroxide. Analysis of RNA‐Seq data indicates that AKR2A up‐regulates transcript levels of genes involved in VLCFAs' biosynthesis, ethylene biosynthesis, auxin and hydrogen peroxide signalling, cell wall and cytoskeletal organization. Furthermore, AKR2A interacted with KCS1 in Arabidopsis both in vitro and in vivo. Moreover, the VLCFA content and the ratio of VLCFAs to short‐chain fatty acids increased significantly in seeds of AKR2A‐overexpressing lines and AKR2A/KCS1 co‐overexpressing lines, while AKR2A mutants are the opposite trend. Our results uncover a novel cotton fibre growth mechanism by which the critical regulator AKR2A promotes fibre development via activating hormone signalling cascade by mediating VLCFA biosynthesis. This study provides a potential candidate gene for improving fibre yield and quality through genetic engineering. [ABSTRACT FROM AUTHOR]