OsNLP3 enhances grain weight and reduces grain chalkiness in rice.

Grain weight, a key determinant of yield in rice (Oryza sativa L.), is governed primarily by genetic factors, whereas grain chalkiness, a detriment to grain quality, is intertwined with environmental factors such as mineral nutrients. Nitrogen (N) is recognized for its impact on grain chalkiness, yet the underlying molecular mechanisms remain elusive. This study revealed the pivotal role of rice NODULE INCEPTION-LIKE PROTEIN 3 (OsNLP3) in simultaneously regulating grain weight and grain chalkiness. Our investigation showed that the loss of OsNLP3 leads to a reduction in both grain weight and dimension, in contrast to the enhancement observed with OsNLP3 overexpression. OsNLP3 directly suppresses the expression of OsCEP6.1 and OsNF-YA8, which were identified as negative regulators associated with grain weight. Consequently, two novel regulatory modules, OsNLP3-OsCEP6.1 and OsNLP3-OsNF-YA8, were identified as key players in grain weight regulation. Notably, the OsNLP3-OsNF-YA8 module not only augments grain weight but also mitigates grain chalkiness in response to N. This research clarifies the molecular mechanisms orchestrating grain weight through the OsNLP3-OsCEP6.1 and OsNLP3-OsNF-YA8 modules, underscoring the pivotal role of the OsNLP3-OsNF-YA8 module in alleviating grain chalkiness. These findings offer potential targets for concurrently enhancing rice yield and quality.

Effectiveness and mechanism study of glutamine on alleviating hypermetabolism in burned rats.

OBJECTIVES: This study aimed to explore the effects of glutamine on hypermetabolic reactions in burned rats and its underlying mechanism. METHODS: Fifty-five Sprague-Dawley rats were randomly divided into three groups, namely, the control (C), burned (B), and burned + glutamine (B + G) groups. Rats in the glutamine treatment group were supplemented with 1 g glutamine per kg body weight. Changes in body weight and resting energy expenditure in all groups were observed daily. Blood glucose and glucose tolerance level were measured on days 1, 3, 7, 10 and 14 after burn injury. On days 7 and 14 after injury, the rats were sacrificed, and the weight and protein content of the skeletal muscle were measured. Moreover, the level of glutamine, inflammatory mediator, nicotinamide adenine dinucleotide phosphate (NADPH), glutathione, and the activity of glutamine metabolic enzymes were measured. RESULTS: The hypermetabolic reaction after burn injury was significantly inhibited by glutamine administration, and the range of variations in the resting energy expenditure and body weight indicators was narrowed remarkably (P < 0.05 or 0.01), whereas the weight and protein content of the skeletal muscle returned to normal (P < 0.05 or 0.01). Glutamine could increase glutaminase activity in various tissues, promote the utilization of glutamine, and appropriately reduce the degree of organ damage and inflammatory response (P < 0.05 or 0.01). Furthermore, glutamine could promote the synthesis of the reducing substances NADPH and glutathione (P < 0.05 or 0.01). CONCLUSIONS: Glutamine administration effectively reduces hypermetabolic reactions by promoting NADPH synthesis, inhibiting oxidative stress, and improving glutamine utilization after burn injury.

1H-NMR metabolomics identifies significant changes in hypermetabolism after glutamine administration in burned rats.

Glutamine is an important amino acid that plays a crucial role in nutritional therapy for patients with burns, but its effects on post-burn metabolism and the underlying mechanisms are unclear. In this study, 1H nuclear magnetic resonance spectroscopy (1H-NMR) was used to examine the effects of glutamine on plasma metabolites in burned rats and to explore the underlying mechanisms. After burn injury, the rats exhibited significant increases in resting energy expenditure (REE) and hypercatabolism, and anabolism was inhibited. The levels of metabolites that reflect the proteolysis of skeletal muscle, such as alanine, histidine, leucine, valine, 3-methylhistidine and creatine, were significantly increased. In addition, the burned rats exhibited energy synthesis dysfunction, as evidenced by a decrease in the ATP concentration and increased levels of lactic acid. Notably, the concentration of α-ketoisovalerate, which reflects the function of the mitochondrial membrane, was significantly increased, suggesting an impairment in mitochondrial function and inhibition of oxidative phosphorylation. Glutamine administration significantly alleviated post-burn hypermetabolism and inhibited proteolysis in skeletal muscle. Consequently, the levels of glutamine metabolites, such as glutamic acid and α-ketoglutarate, along with ATP synthesis were significantly increased, whereas alanine, leucine, 3-methylhistidine and lactic acid were significantly depleted. Furthermore, after glutamine administration, the synthesis of reductive compounds was increased, leading to significantly increased levels of reduced glutathione and NADPH. This process may be an important mechanism by which glutamine alleviates oxidative stress, promotes ATP synthesis, and reduces hypermetabolism after burn.

Loss of Hippocampal Oligodendrocytes Contributes to the Deficit of Contextual Fear Learning in Adult Rats Experiencing Early Bisphenol A Exposure.

During early development, continuous exposure to environmental contaminants such as bisphenol A (BPA) is known to alter neuronal development, resulting in aberrant brain structure and predisposing individuals to developing neuropsychiatric disorders later in life. While the altered oligodendrocyte (OL) structure and function have been casually linked to the occurrence of numerous psychiatric diseases, it remains open whether early BPA exposure (EBE) also recruits OLs to mediate its toxicity in the brain. Here, we observed that EBE from birth to postnatal day 21 caused a substantial loss of hippocampal OLs in rat pups. The OL loss was enduring and manifested even when the affected pups spanned into their adulthood. In parallel, the expression of two key proteins in mature OLs, myelin basic protein (MBP), and monocarboxylate transporter 1 (MCT1) was markedly downregulated in adult hippocampus with a considerable reduction in the number of myelinated axons. By contrast, the myelination of individual axons remained intact. The altered hippocampal OLs were related to EBE-mediated disruption of estrogen receptor (ER) signaling in developing OLs and could be readily prevented by treatment with low level of ICI 182780, an ER antagonist. Importantly, the adult rats subject to EBE exhibited clear deficit in contextual fear memory, which highly correlated with OL loss and decreased MBP and MCT1 expression in hippocampus. The OL loss may thus represent an alternative route through which EBE has its adversity on the brain and contributes to the development of neuropsychiatric illness.

Bisphenol A regulates the estrogen receptor alpha signaling in developing hippocampus of male rats through estrogen receptor.

Bisphenol A (BPA), one of the most common environmental endocrine disruptors, has been recognized to have wide adverse effects on the brain development and behavior. These adversities are related to its ability to bind estrogen receptor (ER) with subsequent alteration of its expression in the target areas. However, very little is known about whether BPA exposure also affects ER phosphorylation and its translocation to nucleus during postnatal development, two critical steps for its function. Here, we found that during development from postnatal day 7 (P7) to P21, the alpha subtype of ER (ERα) in the hippocampus of male rats experienced remarkable alterations in terms of its expression, phosphorylation and translocation to nucleus. Exposure to low level of BPA had bidirectional, development-dependent effects on the expression of ERα mRNA and protein, but decreased ERα phosphorylation and impaired its translocation to nucleus throughout the period investigated. Treatment with low dose of ICI 182,780 (ICI), an ER antagonist to block the binding of ER with BPA, reversed the altered ERα following BPA exposure, highlighting critical involvement of ER. Moreover, ICI treatment rescued the hippocampus-dependent behavioral deficits in the adult rats experiencing early-life BPA exposure. Overall, our results indicate that BPA interferes with the ERα signaling in the developing hippocampus in an ER-dependent manner, which may underlie its adverse behavioral and cognitive outcomes in adult animals.