Notes

Any multimode metamaterial for the stream-lined and powerful dualband wi-fi power shift system.
Abiotic and biotic factors cause plant wounding and trigger complex short- and long-term responses at the local and systemic levels. These responses are under the control of complex signaling pathways, which are still poorly understood. Here, we show that the rapid activation of clade-A Mitogen Activated Protein Kinases (MAPKs) MPK3 and MPK6 by wounding depends on the upstream MAPK Kinases (MAP2Ks) MKK4 and MKK5 but is independent of jasmonic acid (JA) signaling. In addition, this fast module does not control wound-triggered JA accumulation in Arabidopsis, unlike its orthologues in tobacco. We also demonstrate that a second MAPK module, composed of MKK3 and the clade-C MAPKs MPK½/7, is activated by wounding in a MKK4/5-independent manner. We provide evidence that the activation of this MKK3-MPK½/7 module occurs mainly through wound-induced JA production via the transcriptional regulation of upstream clade-III MAP3Ks, particularly MAP3K14. We show that mkk3 mutant plants are more susceptible to herbivory from larvae of the generalist lepidopteran herbivore Spodoptera littoralis, indicating that the MKK3-MPK½/7 module is involved in counteracting insect feeding. © 2020 American Society of Plant Biologists. All rights reserved.Spatiotemporal regulation of gene expression is critical for proper developmental timing in plants and animals. The transcription factor FUSCA3 (FUS3) regulates developmental phase transitions by acting as a link between hormonal pathways in Arabidopsis thaliana. However, the mechanisms governing its spatiotemporal expression pattern are poorly understood. Here, we show that FUS3 is repressed in the ovule integuments and seed endosperm. FUS3 repression requires class I BASIC PENTACYSTEINE (BPC) proteins, which directly bind GA/CT cis-elements in FUS3 and restrict its expression pattern. During vegetative and reproductive development, FUS3 derepression in bpc1-1 bpc2 (bpc½) double mutant or misexpression in ProML1FUS3 lines causes dwarf plants carrying defective flowers and aborted ovules. Postfertilization, ectopic FUS3 expression in bpc½ endosperm or ProML1FUS3 endosperm and endothelium increases endosperm nuclei proliferation and seed size, causing delayed or arrested embryo development. These phenotypes are rescued in bpc½ fus3-3. Lastly, class I BPCs interact with FIS-PRC2 (FERTILIZATION-INDEPENDENT SEED-Polycomb Repressive Complex2), which represses FUS3 in the endosperm during early seed development. We propose that BPC1 and 2 promote the transition from reproductive to seed development by repressing FUS3 in ovule integuments. After fertilization, BPC1 and 2 and FIS-PRC2 repress FUS3 in the endosperm to coordinate early endosperm and embryo growth. © 2020 American Society of Plant Biologists. All rights reserved.The antagonistic regulation of seed germination by the phytohormone ABA and GA has been well-established. However, how these phytohormones antagonistically regulate root growth and branching (tillering in rice) remains obscure. Rice Tiller Enhancer (TE) encodes an activator of the APC/CTE E3 ubiquitin ligase complex that represses tillering but promotes seed germination. In this study, we found a dual role of GA and APC/CTE in regulating root growth. High GA levels can activate APC/CTE to promote the degradation of OsSHR1 (a key promoting factor of root growth) in the root meristem (RM) or MOC1 (a key promoting factor of tillering) in the axillary meristem (AM), leading to restricted root growth and tillering; while low GA levels can activate the role of APC/CTE in stimulating RM cell division to promote root growth. In addition, we found that moderate enhancement of ABA signaling helps to maintain the RM or AM size to sustain root growth or tillering by antagonizing GA-promoted degradation of OsSHR1 and MOC1 through the SnRK2-APC/CTE regulatory module. selleck kinase inhibitor We conclude that APC/CTE plays a key role in regulating plant architecture by mediating the signaling cross talks between ABA and GA. © 2020 American Society of Plant Biologists. All rights reserved.Copy number variations (CNVs) greatly contribute to intraspecies genetic polymorphism and phenotypic diversity. Recent analyses of sequencing data for >1000 accessions of Arabidopsis thaliana were focused on small variations and did not include CNVs. Here, we performed a genome-wide analysis and identified large indels (50-499 bp) and CNVs (500 bp and larger) present in these accessions. The CNVs fully overlap with 18.3% of protein-coding genes, with enrichment for evolutionarily young genes and genes involved in stress and defense. By combined analysis of both genes and transposable elements affected by CNVs, we revealed that the variation statuses of genes and TEs are tightly linked and jointly contribute to the unequal distribution of these elements in the genome. We also determined the gene copy numbers in a set of 1,060 accessions, and we experimentally validated the accuracy of our predictions by multiplex ligation-dependent probe amplification assays. We then successfully used the CNVs as markers in an analysis of population structure and migration patterns. Additionally, we examined the impact of gene dosage variation triggered by a CNV spanning the SEC10 gene on SEC10 expression, both at the transcript and protein levels. The provided catalog of CNVs, CNV-overlapping genes and their genotypes in a top model dicot will stimulate the exploration of the genetic bases of phenotypic variation. © 2020 American Society of Plant Biologists. All rights reserved.The septo-hippocampal cholinergic system is critical for hippocampal learning and memory. However, a quantitative description of the in vivo firing patterns and physiological function of medial septal (MS) cholinergic neurons is still missing. In this study, we combined optogenetics with multi-channel in vivo recording and recorded MS cholinergic neurons' firings in freely behaving male mice for 5.5 - 72 hours. We found that their firing activities were highly correlated with hippocampal theta states. MS cholinergic neurons were highly active during theta-dominant epochs, such as active exploration (AE) and rapid eye movement (REM) sleep, but almost silent during non-theta epochs, such as slow wave sleep (SWS). Interestingly, optogenetic activation of these MS cholinergic neurons during SWS suppressed CA1 ripple oscillations. This suppression could be rescued by muscarinic M2 or M4 receptor antagonists. These results suggest an important physiological function of MS cholinergic neurons maintaining high hippocampal acetylcholine (ACh) level by persistent firing during theta epochs, consequently suppressing ripples and allowing theta oscillations to dominate.Significance StatementThe major source of acetylcholine in the hippocampus comes from the medial septum. Early experiments found that lesions to the MS result in the disappearance of hippocampal theta oscillation, which leads to the speculation of the septo-hippocampal cholinergic projection contributing to theta oscillation. In this paper, by long-term recording of MS cholinergic neurons, we found that they do show theta-state-related firing pattern. However, optogenetically activating these neurons shows little effect on theta rhythm in the hippocampus. Instead, we found that activating MS cholinergic neurons during SWS could suppress hippocampal ripple oscillations. This suppression is mediated by muscarinic M2 and M4 receptors. Copyright © 2020 Ma et al.The action potential (AP) waveform controls the opening of voltage-gated calcium channels and contributes to the driving force for calcium ion flux that triggers neurotransmission at presynaptic nerve terminals. Although the frog neuromuscular junction (NMJ) has long been a model synapse for the study of neurotransmission, its presynaptic AP waveform has never been directly studied, and thus the AP waveform shape and propagation through this long presynaptic nerve terminal are unknown. Using a fast voltage-sensitive dye, we have imaged the AP waveform from the presynaptic terminal of male and female frog NMJs and shown that the AP is very brief in duration and actively propagated down the entire length of the terminal. Furthermore, based on measured AP waveforms at different regions along the length of the nerve terminal, we show that the terminal is divided into three distinct electrical regions A beginning region immediately after the last node of Ranvier where the AP is broadest, a middle region with a relh et al.The Drosophila nervous system is ensheathed by a layer of outer glial cells, the perineurial glia, and a specialized extracellular matrix, the neural lamella. The function of perineurial glial cells and how they interact with the extracellular matrix is just beginning to be elucidated. Integrin-based focal adhesion complexes link the glial membrane to the extracellular matrix, but little is known about integrin's regulators in the glia. The transmembrane Ig domain protein Basigin/CD147/EMMPRIN is highly expressed in the perineurial glia surrounding the Drosophila larval nervous system. Here we show that Basigin associates with integrin at the focal adhesions in order to uphold the structure of the glia-extracellular matrix sheath. Knock down of Basigin in perineurial glia using RNAi results in significant shortening of the ventral nerve cord, compression of the glia and extracellular matrix in the peripheral nerves, and reduction in larval locomotion. We determined that Basigin is expressed in close proximityroper ensheathment of the central and peripheral nervous systems. Loss of Bsg in the glia results in an overall compression of the nervous system due to integrin dysregulation, which causes locomotor defects in the animals. This underlies the importance of glia-matrix communication for structural and functional support of the nervous system. Copyright © 2020 Hunter et al.Synaptic dysfunction provoking dysregulated cortical neural circuits is currently hypothesized as a key pathophysiological process underlying clinical manifestations in Alzheimer's disease and related neurodegenerative tauopathies. Here, we conducted positron emission tomography (PET) along with postmortem assays to investigate time-course changes of excitatory and inhibitory synaptic constituents in an rTg4510 mouse model of tauopathy, which develops tau pathologies leading to noticeable brain atrophy at 5-6 months of age. Both male and female mice were analyzed in this study. We observed that radiosignals derived from [11C]flumazenil, a tracer for benzodiazepine receptor, in rTg4510 mice were significantly lower than the levels in non-transgenic littermates at 2-3 months of age. In contrast, retentions of (E)-[11C]ABP688, a tracer for mGluR5, were unaltered relative to controls at 2 months of age but then gradually declined with aging in parallel with progressive brain atrophy. Biochemical and immunohistoch11C]ABP688 and [11C]flumazenil, respectively. We identified inhibitory synapse as being significantly dysregulated before brain atrophy at 2 months of age, while excitatory synapse stayed relatively intact at this stage. In line with this observation, postmortem assessment of brain tissues demonstrated selective attenuation of inhibitory synaptic constituents accompanied by the upregulation of cFos prior to the formation of tau pathology in the forebrain at young ages. Our findings indicate that selective degeneration of inhibitory synapse with hyperexcitability in the cortical circuit constitutes the critical early pathophysiology of tauopathy. Copyright © 2020 Shimojo et al.
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