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排序方式: 共有148条查询结果,搜索用时 15 毫秒
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Imaizumi-Anraku H Takeda N Charpentier M Perry J Miwa H Umehara Y Kouchi H Murakami Y Mulder L Vickers K Pike J Downie JA Wang T Sato S Asamizu E Tabata S Yoshikawa M Murooka Y Wu GJ Kawaguchi M Kawasaki S Parniske M Hayashi M 《Nature》2005,433(7025):527-531
The roots of most higher plants form arbuscular mycorrhiza, an ancient, phosphate-acquiring symbiosis with fungi, whereas only four related plant orders are able to engage in the evolutionary younger nitrogen-fixing root-nodule symbiosis with bacteria. Plant symbioses with bacteria and fungi require a set of common signal transduction components that redirect root cell development. Here we present two highly homologous genes from Lotus japonicus, CASTOR and POLLUX, that are indispensable for microbial admission into plant cells and act upstream of intracellular calcium spiking, one of the earliest plant responses to symbiotic stimulation. Surprisingly, both twin proteins are localized in the plastids of root cells, indicating a previously unrecognized role of this ancient endosymbiont in controlling intracellular symbioses that evolved more recently. 相似文献
73.
Sleep is a widespread biological phenomenon, and its scientific study is proceeding at multiple levels at the same time. Marked progress is being made in answering three fundamental questions: what is sleep, what are its mechanisms and what are its functions? The most salient answers to these questions have resulted from applying new techniques from basic and applied neuroscience research. The study of sleep is also shedding light on our understanding of consciousness, which undergoes alteration in parallel with sleep-induced changes in the brain. 相似文献
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Soon after the crowd streamed on to London's Millennium Bridge on the day it opened, the bridge started to sway from side to side: many pedestrians fell spontaneously into step with the bridge's vibrations, inadvertently amplifying them. Here we model this unexpected and now notorious phenomenon--which was not due to the bridge's innovative design as was first thought--by adapting ideas originally developed to describe the collective synchronization of biological oscillators such as neurons and fireflies. Our approach should help engineers to estimate the damping needed to stabilize other exceptionally crowded footbridges against synchronous lateral excitation by pedestrians. 相似文献
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Bohlen CJ Chesler AT Sharif-Naeini R Medzihradszky KF Zhou S King D Sánchez EE Burlingame AL Basbaum AI Julius D 《Nature》2011,479(7373):410-414
Natural products that elicit discomfort or pain represent invaluable tools for probing molecular mechanisms underlying pain sensation. Plant-derived irritants have predominated in this regard, but animal venoms have also evolved to avert predators by targeting neurons and receptors whose activation produces noxious sensations. As such, venoms provide a rich and varied source of small molecule and protein pharmacophores that can be exploited to characterize and manipulate key components of the pain-signalling pathway. With this in mind, here we perform an unbiased in vitro screen to identify snake venoms capable of activating somatosensory neurons. Venom from the Texas coral snake (Micrurus tener tener), whose bite produces intense and unremitting pain, excites a large cohort of sensory neurons. The purified active species (MitTx) consists of a heteromeric complex between Kunitz- and phospholipase-A2-like proteins that together function as a potent, persistent and selective agonist for acid-sensing ion channels (ASICs), showing equal or greater efficacy compared with acidic pH. MitTx is highly selective for the ASIC1 subtype at neutral pH; under more acidic conditions (pH < 6.5), MitTx massively potentiates (>100-fold) proton-evoked activation of ASIC2a channels. These observations raise the possibility that ASIC channels function as coincidence detectors for extracellular protons and other, as yet unidentified, endogenous factors. Purified MitTx elicits robust pain-related behaviour in mice by activation of ASIC1 channels on capsaicin-sensitive nerve fibres. These findings reveal a mechanism whereby snake venoms produce pain, and highlight an unexpected contribution of ASIC1 channels to nociception. 相似文献
78.
Ishizuka K Kamiya A Oh EC Kanki H Seshadri S Robinson JF Murdoch H Dunlop AJ Kubo K Furukori K Huang B Zeledon M Hayashi-Takagi A Okano H Nakajima K Houslay MD Katsanis N Sawa A 《Nature》2011,473(7345):92-96
Regulatory mechanisms governing the sequence from progenitor cell proliferation to neuronal migration during corticogenesis are poorly understood. Here we report that phosphorylation of DISC1, a major susceptibility factor for several mental disorders, acts as a molecular switch from maintaining proliferation of mitotic progenitor cells to activating migration of postmitotic neurons in mice. Unphosphorylated DISC1 regulates canonical Wnt signalling via an interaction with GSK3β, whereas specific phosphorylation at serine 710 (S710) triggers the recruitment of Bardet-Biedl syndrome (BBS) proteins to the centrosome. In support of this model, loss of BBS1 leads to defects in migration, but not proliferation, whereas DISC1 knockdown leads to deficits in both. A phospho-dead mutant can only rescue proliferation, whereas a phospho-mimic mutant rescues exclusively migration defects. These data highlight a dual role for DISC1 in corticogenesis and indicate that phosphorylation of this protein at S710 activates a key developmental switch. 相似文献
79.
Yusa K Rashid ST Strick-Marchand H Varela I Liu PQ Paschon DE Miranda E Ordóñez A Hannan NR Rouhani FJ Darche S Alexander G Marciniak SJ Fusaki N Hasegawa M Holmes MC Di Santo JP Lomas DA Bradley A Vallier L 《Nature》2011,478(7369):391-394
Human induced pluripotent stem cells (iPSCs) represent a unique opportunity for regenerative medicine because they offer the prospect of generating unlimited quantities of cells for autologous transplantation, with potential application in treatments for a broad range of disorders. However, the use of human iPSCs in the context of genetically inherited human disease will require the correction of disease-causing mutations in a manner that is fully compatible with clinical applications. The methods currently available, such as homologous recombination, lack the necessary efficiency and also leave residual sequences in the targeted genome. Therefore, the development of new approaches to edit the mammalian genome is a prerequisite to delivering the clinical promise of human iPSCs. Here we show that a combination of zinc finger nucleases (ZFNs) and piggyBac technology in human iPSCs can achieve biallelic correction of a point mutation (Glu342Lys) in the α(1)-antitrypsin (A1AT, also known as SERPINA1) gene that is responsible for α(1)-antitrypsin deficiency. Genetic correction of human iPSCs restored the structure and function of A1AT in subsequently derived liver cells in vitro and in vivo. This approach is significantly more efficient than any other gene-targeting technology that is currently available and crucially prevents contamination of the host genome with residual non-human sequences. Our results provide the first proof of principle, to our knowledge, for the potential of combining human iPSCs with genetic correction to generate clinically relevant cells for autologous cell-based therapies. 相似文献
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