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Separate orexigenic hippocampal ensembles shape dietary choice by enhancing contextual memory and motivation
The hippocampus (HPC) has emerged as a critical player in the control of food intake, beyond its well-known role in memory. While previous studies have primarily associated the HPC with food intake inhibition, recent research suggests a role in appetitive processes. Here we identified spatially distinct neuronal populations within the dorsal HPC (dHPC) that respond to either fats or sugars, potent natural reinforcers that contribute to obesity development. Using activity-dependent genetic capture of nutrient-responsive dHPC neurons, we demonstrate a causal role of both populations in promoting nutrient-specific intake through different mechanisms. Sugar-responsive neurons encoded spatial memory for sugar location, whereas fat-responsive neurons selectively enhanced the preference and motivation for fat intake. Importantly, stimulation of either nutrient-responsive dHPC neurons increased food intake, while ablation differentially impacted obesogenic diet consumption and prevented diet-induced weight gain. Collectively, these findings uncover previously unknown orexigenic circuits underlying macronutrient-specific consumption and provide a foundation for developing potential obesity treatments.
Microbial controls over soil priming effects under chronic nitrogen and phosphorus additions in subtropical forests
The soil priming effect (PE), defined as the modification of soil organic matter decomposition by labile carbon (C) inputs, is known to influence C storage in terrestrial ecosystems. However, how chronic nutrient addition, particularly in leguminous and non-leguminous forests, will affect PE through interaction with nutrient (e.g., nitrogen and phosphorus) availability is still unclear. Therefore, we collected soils from leguminous and non-leguminous subtropical plantations across a suite of historical nutrient addition regimes. We added 13C-labeled glucose to investigate how background soil nutrient conditions and microbial communities affect priming and its potential microbial mechanisms. Glucose addition increased soil organic matter decomposition and prompted positive priming in all soils, regardless of dominant overstory tree species or fertilizer treatment. In non-leguminous soil, only combined nitrogen and phosphorus addition led to a higher positive priming than the control. Conversely, soils beneath N-fixing leguminous plants responded positively to P addition alone, as well as to joint NP addition compared to control. Using DNA stable-isotope probing, high-throughput quantitative PCR, enzyme assays and microbial C substrate utilization, we found that positive PE was associated with increased microbial C utilization, accompanied by an increase in microbial community activity, nutrient-related gene abundance, and enzyme activities. Our findings suggest that the balance between soil available N and P effects on the PE, was dependent on rhizosphere microbial community composition. Furthermore, these findings highlight the roles of the interaction between plants and their symbiotic microbial communities in affecting soil priming and improve our understanding of the potential microbial pathways underlying soil PEs.
Microbial phosphorus recycling in soil by intra- and extracellular mechanisms
Rising global stoichiometric imbalance between increasing nitrogen (N) availability and depleting phosphorus (P) resources increases the importance of soil microbial P recycling. The contribution of extra- versus intracellular P (re-)cycling depending on ecosystem nutrient status is vastly unclear, making soil microorganisms a blind spot in our understanding of ecosystem responses to increasing P deficiency. We quantified P incorporation into microbial DNA and phospholipids by 33P labeling under contrasting conditions: low/high P soil × low/high carbon (C)NP application. By combining 33P and 14C labeling with tracing of microbial community biomarkers and functional genes, we disengaged the role of DNA and phospholipids in soil P cycling. Microorganisms in low P soil preferentially allocated P to phospholipids with an acceleration of phospholipids metabolism driven by C addition, which was strongly related to high abundances of microbial community members (e.g. some G-) with a fast phospholipids turnover. In high P soil, however, more P was allocated to DNA with a microbial functional shift towards DNA synthesis to support a replicative growth when sufficient C was supplied, which was coupled with a strong enrichment of fungal copiotrophs and microbial genes coding DNA primase. Consequently, adaptation to low P availability accelerated microbial intracellular P recycling through reutilization of the P stored in phospholipids. However, microorganisms under high P availability commonly adopted extracellular P recycling with release and reuse of DNA P by microbial death-growth dynamics. These results advance our understanding on microbial adaptation to P deficiency in soil by regulating component-specific P pathways and reflect the specific functions of phospholipids and DNA for P recycling.
Frequency shift caused by nonuniform field and boundary relaxation in magnetic resonance and comagnetometers
In magnetic resonance experiments, it is widely recognized that a nonuniform magnetic field can lead to an increase in the resonance line width, as well as a reduction in sensitivity and spectral resolution. However, a nonuniform magnetic field can also cause shifts in resonance frequency, which has received far less attention. In this work, we investigate the frequency shift caused by boundary relaxation and nonuniform magnetic field with arbitrary spatial distribution. We find that this frequency shift is spin-species dependent, implying a systematic error in NMR gyroscopes and comagnetometers. The first order correction to this systematic error is proportional to the difference of boundary relaxation rate, and dominates for small cells. In contrast, the third and higher order corrections arise from the difference of gyromagnetic ratios of spin species, and dominates for large cells. This insight helps understanding the unexplained isotope shifts in recent NMR gyroscopes and new physics searching experiments that utilize comagnetometers. Finally, we propose a tool for wall interaction research based on the frequency shift’s dependency on boundary relaxation.
Regulation of mammalian cellular metabolism by endogenous cyanide production
Small, gaseous molecules such as nitric oxide, carbon monoxide and hydrogen sulfide are produced as signalling molecules in mammalian cells. Here, we show that low concentrations of cyanide are generated endogenously in various mammalian tissues and cells. We detect cyanide in several cellular compartments of human cells and in various tissues and the blood of mice. Cyanide production is stimulated by glycine, occurs at the low pH of lysosomes and requires peroxidase activity. When generated at a specific rate, cyanide exerts stimulatory effects on mitochondrial bioenergetics, cell metabolism and cell proliferation, but impairs cellular bioenergetics at high concentrations. Cyanide can modify cysteine residues via protein S-cyanylation, which is detectable basally in cells and mice, and increases in response to glycine. Low-dose cyanide supplementation exhibits cytoprotective effects in hypoxia and reoxygenation models in vitro and in vivo. Conversely, pathologically elevated cyanide production in nonketotic hyperglycinaemia is detrimental to cells. Our findings indicate that cyanide should be considered part of the same group of endogenous mammalian regulatory gasotransmitters as nitric oxide, carbon monoxide and hydrogen sulfide.
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