3,997 research outputs found

    Genome-Wide Analysis of WRKY Genes and Their Response to Hormone and Mechanic Stresses in Carrot

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    The WRKY gene family plays a vital role in plant development and environment response. Although previous studies suggested that the WRKY genes in carrot (Kuroda type) involved in biotic and abiotic stress responses, the information of WRKY genes in the latest version of the carrot genome (Daucus carota v2.0, Nantes type carrot) and their response to hormone and injury stresses have not been reported. In this study, we performed a genome-wide analysis of WRKYs using a chromosome-scale genome assembly of carrot (Daucus carota subsp. sativus L.). We identified a total of 67 WRKY genes, which were further classified into the three groups. These WRKY genes are unevenly distributed on carrot chromosomes. We found that more than half of them were derived from whole-genome duplication (WGD) events, suggesting that WGDs have played a major role during the evolution of the WRKY gene family. We experimentally ascertained the expression divergence existed between WGD-derived WRKY duplicated gene pairs, which is indicative of functional differentiation between duplicated genes. Our analysis of cis-acting elements indicated that WRKY genes were transcriptionally regulated upon hormone and mechanic injury stresses. Gene expression analyses by qRT-PCR further presented that WRKY genes were involved in hormone and mechanic injury stresses

    Effects of central activation of serotonin 5-HT2A/2C or dopamine D-2/3 receptors on the acute and repeated effects of clozapine in the conditioned avoidance response test

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    Acute administration of clozapine (a gold standard of atypical antipsychotics) disrupts avoidance response in rodents, while repeated administration often causes a tolerance effect

    Digital Twin-based 3D Map Management for Edge-assisted Device Pose Tracking in Mobile AR

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    Edge-device collaboration has the potential to facilitate compute-intensive device pose tracking for resource-constrained mobile augmented reality (MAR) devices. In this paper, we devise a 3D map management scheme for edge-assisted MAR, wherein an edge server constructs and updates a 3D map of the physical environment by using the camera frames uploaded from an MAR device, to support local device pose tracking. Our objective is to minimize the uncertainty of device pose tracking by periodically selecting a proper set of uploaded camera frames and updating the 3D map. To cope with the dynamics of the uplink data rate and the user's pose, we formulate a Bayes-adaptive Markov decision process problem and propose a digital twin (DT)-based approach to solve the problem. First, a DT is designed as a data model to capture the time-varying uplink data rate, thereby supporting 3D map management. Second, utilizing extensive generated data provided by the DT, a model-based reinforcement learning algorithm is developed to manage the 3D map while adapting to these dynamics. Numerical results demonstrate that the designed DT outperforms Markov models in accurately capturing the time-varying uplink data rate, and our devised DT-based 3D map management scheme surpasses benchmark schemes in reducing device pose tracking uncertainty.Comment: Accepted by IEEE Internet of Things Journa

    1,3-Bis[5-(2-pyrid­yl)-1H-tetra­zol-1-yl]propane

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    The title compound, C15H14N10, is a multidentate ligand obtained by the reaction of 5-(2-pyrid­yl)tetra­zole with 1,3-dibromo­propane. The mol­ecule consists of two 5-(2-pyrid­yl)-1H-tetra­zol-1-yl units connected by a propyl­ene bridge in a U-like conformation. A twofold rotation axis passes through the central C atom

    Epilepsy phenotype and response to KCNQ openers in mice harboring the Kcnq2 R207W voltage-sensor mutation

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    KCNQ2-encoded Kv7.2 subunits play a critical role in balancing neuronal excitability. Mutations in KCNQ2 are responsible for highly-heterogenous epileptic and neurodevelopmental phenotypes ranging from self-limited familial neonatal epilepsy (SeLFNE) to severe developmental and epileptic encephalopathy (DEE). Pathogenic KCNQ2 variants cluster at the voltage sensor domain (VSD), the pore domain, and the C-terminal tail. Although several knock-in mice harboring Kcnq2 pore variants have been developed, no mouse line carrying Kcnq2 voltage-sensor mutations has been described. KCNQ2-R207W is an epilepsy-causing mutation located in the VSD, mainly affecting voltage-dependent channel gating. To study the physiological consequence of Kcnq2 VSD dysfunction, we generated a Kcnq2-R207W mouse line and analyzed the pathological and pharmacological phenotypes of mutant mice. As a result, both homozygous (Kcnq2RW/RW) and heterozygous (Kcnq2RW/+) mice were viable. While Kcnq2RW/RW mice displayed a short lifespan, growth retardation, and spontaneous seizures, Kcnq2RW/+ mice survived and developed normally, although only a fraction (9/64; 14%) of them showed behavioral- and ECoG-confirmed spontaneous seizures. Kcnq2RW/+ mice displayed increased susceptibility to evoked seizures, which was dramatically ameliorated by treatment with the novel KCNQ opener pynegabine (HN37). Our results show that the Kcnq2-R207W mouse line, the first harboring a Kcnq2 voltage-sensor mutation, exhibits a unique epileptic phenotype with both spontaneous seizures and increased susceptibility to evoked seizures. In Kcnq2-R207W mice, the potent KCNQ opener HN37, currently in clinical phase I, shows strong anticonvulsant activity, suggesting it may represent a valuable option for the severe phenotypes of KCNQ2-related epilepsy
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