The rice OsERF101 transcription factor regulates the NLR Xa1-mediated immunity induced by perception of TAL effectors

イネが病原菌の感染力の源を検出して免疫を誘導する仕組みを解明 --病気に強い植物の開発に期待--. 京都大学プレスリリース. 2022-09-07.Plant nucleotide-binding leucine-rich repeat receptors (NLRs) initiate immune responses by recognizing pathogen effectors. The rice gene Xa1 encodes an NLR with an N-terminal BED domain, and recognizes transcription activator-like (TAL) effectors of Xanthomonas oryzae pv. oryzae (Xoo). Our goal is to elucidate the molecular mechanisms controlling the induction of immunity by Xa1. We used yeast two-hybrid assays to screen for host factors that interact with Xa1 and identified the AP2/ERF-type transcription factor OsERF101/OsRAP2.6. Molecular complementation assays were used to confirm the interactions among Xa1, OsERF101, and two TAL effectors. We created OsERF101-overexpressing and knockout mutant lines in rice and identified genes differentially regulated in these lines, many of which are predicted to be involved in regulation of response to stimulus. Xa1 interacts in the nucleus with the TAL effectors and OsERF101 via the BED domain. Unexpectedly, both the overexpression and knockout lines of OsERF101 displayed Xa1-dependent, enhanced resistance to an incompatible Xoo strain. Different sets of genes were up- or down-regulated in the overexpression and knockout lines. Our results indicate that OsERF101 regulates the recognition of TAL effectors by Xa1, and functions as a positive regulator of Xa1-mediated immunity. Further, an additional Xa1-mediated immune pathway is negatively regulated by OsERF101

Competences in Project Management: A Case Study in Osaka Institute of Technology

This chapter briefly explains the distributed project management of four joint departments for first-grade joint project-based learning (PBL). That is, conventional studies and purpose, capital, competence and ability of four kinds of distributed project management were presented, and relations among them are shown after describing background (included prehistory of PBL in Osaka Institute of Technology (O.I.T.)). Then, consideration and analysis about communication, interaction, cooperation, merit, week-point, effect and inference were discussed. Some case studies were described about open innovation and competences in stakeholder management. They were distinctive and superior in first-grade PBL of O.I.T. Finally, some future themes were presented

One-year morbidity and mortality in patients treated with standard-dose and low-dose apixaban after acute large vessel occlusion stroke

The version of record of this article, first published in Journal of Thrombosis and Thrombolysis, is available online at Publisher’s website: https://doi.org/10.1007/s11239-024-02954-7.Although low-dose direct oral anticoagulants (DOACs) are recommended for patients at high risk of bleeding complications, it remains unclear whether the dose reduction in real-world setting is also appropriate in patients after large-vessel occlusion (LVO) stroke. This study hypothesized that patients with atrial fibrillation (AF) and LVO receiving low-dose DOACs have an increased risk of ischemic and hemorrhagic events. The study aimed to assess 1 year morbidity and mortality in patients treated with standard-dose and low-dose apixaban after LVO stroke. A post hoc analysis was performed using the acute LVO registry data, which enrolled patients with AF and LVO who received apixaban within 14 days of stroke onset. The incidences of ischemic events (ischemic stroke, acute coronary syndrome, acute myocardial infarction, and systemic embolism), major bleeding events, and death from any cause were compared between patients receiving standard- and low-dose apixaban. Of 643 patients diagnosed with LVO, 307 (47.7%) received low-dose apixaban. After adjustment for clinically relevant variables, no significant differences were observed in the incidence of ischemic events (adjusted hazard ratio [aHR]: 2.12, 95% confidence interval [CI] 0.75–6.02), major bleeding events (aHR: 1.17, 95% CI 0.50–2.73), and death from any cause (aHR: 1.95, 95% CI 0.78–4.89) between patients receiving standard- and low-dose apixaban. No significant differences were observed in the incidence of ischemic events, major bleeding events, or death from any cause between patients with AF and LVO receiving standard- and low-dose apixaban

Upregulation of casein kinase 1ε in dorsal root ganglia and spinal cord after mouse spinal nerve injury contributes to neuropathic pain

<p>Abstract</p> <p>Background</p> <p>Neuropathic pain is a complex chronic pain generated by damage to, or pathological changes in the somatosensory nervous system. Characteristic features of neuropathic pain are allodynia, hyperalgesia and spontaneous pain. Such abnormalities associated with neuropathic pain state remain to be a significant clinical problem. However, the neuronal mechanisms underlying the pathogenesis of neuropathic pain are complex and still poorly understood. Casein kinase 1 is a serine/threonine protein kinase and has been implicated in a wide range of signaling activities such as cell differentiation, proliferation, apoptosis, circadian rhythms and membrane transport. In mammals, the CK1 family consists of seven members (α, β, γ1, γ2, γ3, δ, and ε) with a highly conserved kinase domain and divergent amino- and carboxy-termini.</p> <p>Results</p> <p>Preliminary cDNA microarray analysis revealed that the expression of the <it>casein kinase 1 epsilon </it>(<it>CK1ε</it>) mRNA in the spinal cord of the neuropathic pain-resistant N- type Ca²⁺channel deficient (<it>Ca</it>_<it>v</it><it>2.2</it>^-/-) mice was decreased by the spinal nerve injury. The same injury exerted no effects on the expression of <it>CK1ε </it>mRNA in the wild-type mice. Western blot analysis of the spinal cord identified the downregulation of CK1ε protein in the injured <it>Ca</it>_<it>v</it><it>2.2</it>^-/-mice, which is consistent with the data of microarray analysis. However, the expression of CK1ε protein was found to be up-regulated in the spinal cord of injured wild-type mice. Immunocytochemical analysis revealed that the spinal nerve injury changed the expression profiles of CK1ε protein in the dorsal root ganglion (DRG) and the spinal cord neurons. Both the percentage of CK1ε-positive neurons and the expression level of CK1ε protein were increased in DRG and the spinal cord of the neuropathic mice. These changes were reversed in the spinal cord of the injured <it>Ca</it>_<it>v</it><it>2.2</it>^-/-mice. Furthermore, intrathecal administration of a CK1 inhibitor IC261 produced marked anti-allodynic and anti-hyperalgesic effects on the neuropathic mice. In addition, primary afferent fiber-evoked spinal excitatory responses in the neuropathic mice were reduced by IC261.</p> <p>Conclusions</p> <p>These results suggest that CK1ε plays important physiological roles in neuropathic pain signaling. Therefore CK1ε is a useful target for analgesic drug development.</p

Simultaneous enlargement of SRAM read/write noise margin by controlling virtual ground lines

金沢大学理工研究域電子情報学系The SRAM operating margin in 65nm technology is analyzed. The peak characteristic in the read margin versus the supply voltage was found to be caused by the channel length modulation effect. Controlling the memory cell virtual ground line proved to be effective in enlarging the operating margin simultaneously in the read and the write operations. A simple o ptimum circuit which does not require any dynamic voltage c ontrol is proposed, realizing an improvement in the operating m argin comparable to conventional circuits requiring dynamic voltage control. © 2010 IEEE

Accelerated evaluation method for the SRAM cell write margin using word line voltage shift

An accelerated evaluation method for the SRAM cell write margin is proposed based on the conventional Write Noise Margin (WNM) definition. The WNM is measured under a lower word line voltage than the power supply voltage VDD. A lower word line voltage is used because the access transistor operates in the saturation mode over a wide range of threshold voltage variation. The final WNM at the VDD word line voltage, the Accelerated Write Noise Margin (AWNM), is obtained by shifting the measured WNM at the lower word line voltage. The amount of WNM shift is determined from the WNM dependence on the word line voltage. As a result, the cumulative frequency of the AWNM displays a normal distribution. A normal distribution of the AWNM drastically improves development efficiency, because the write failure probability can be estimated by a small number of samples. Effectiveness of the proposed method is verified using the Monte Carlo simulation. © 2011 IEEE