161 research outputs found

    High temperature perception in leaves promotes vascular regeneration and graft formation in distant tissues

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    Cellular regeneration in response to wounding is fundamental to maintain tissue integrity. Various internal factors including hormones and transcription factors mediate healing, but little is known about the role of external factors. To understand how the environment affects regeneration, we investigated the effects of temperature upon the horticulturally relevant process of plant grafting. We found that elevated temperatures accelerated vascular regeneration in Arabidopsis thaliana and tomato grafts. Leaves were crucial for this effect, as blocking auxin transport or mutating PHYTOCHROME INTERACTING FACTOR 4 (PIF4) or YUCCA2/5/8/9 in the cotyledons abolished the temperature enhancement. However, these perturbations did not affect grafting at ambient temperatures, and temperature enhancement of callus formation and tissue adhesion did not require PIF4, suggesting leaf-derived auxin specifically enhanced vascular regeneration in response to elevated temperatures. We also found that elevated temperatures accelerated the formation of inter-plant vascular connections between the parasitic plant Phtheirospennum japonicum and host Arabidopsis, and this effect required shoot-derived auxin from the parasite. Taken together, our results identify a pathway whereby local temperature perception mediates long distance auxin signaling to modify regeneration, grafting and parasitism.This article has an associated 'The people behind the papers' interview

    High hydrostatic pressure induces slow contraction in mouse cardiomyocytes

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    Cardiomyocytes are contractile cells that regulate heart contraction. Ca2+ flux via Ca2+ channels activates actomyosin interactions, leading to cardiomyocyte contraction, which is modulated by physical factors (e.g., stretch, shear stress, and hydrostatic pressure). We evaluated the mechanism triggering slow contractions using a high-pressure microscope to characterize changes in cell morphology and intracellular Ca2+ concentration ([Ca2+]i) in mouse cardiomyocytes exposed to high hydrostatic pressures. We found that cardiomyocytes contracted slowly without an acute transient increase in [Ca2+]i, while a myosin ATPase inhibitor interrupted pressure-induced slow contractions. Furthermore, transmission electron microscopy showed that, although the sarcomere length was shortened upon the application of 20 MPa, this pressure did not collapse cellular structures such as the sarcolemma and sarcomeres. Our results suggest that pressure-induced slow contractions in cardiomyocytes are driven by the activation of actomyosin interactions without an acute transient increase in [Ca2+]i

    Brd4 binds to active enhancers to control cell identity gene induction in adipogenesis and myogenesis

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    The epigenomic reader Brd4 is an important drug target for cancers. However, its role in cell differentiation and animal development remains largely unclear. Using two conditional knockout mouse strains and derived cells, we demonstrate that Brd4 controls cell identity gene induction and is essential for adipogenesis and myogenesis. Brd4 co-localizes with lineage-determining transcription factors (LDTFs) on active enhancers during differentiation. LDTFs coordinate with H3K4 mono-methyltransferases MLL3/MLL4 (KMT2C/KMT2D) and H3K27 acetyltransferases CBP/p300 to recruit Brd4 to enhancers activated during differentiation. Brd4 deletion prevents the enrichment of Mediator and RNA polymerase II transcription machinery, but not that of LDTFs, MLL3/MLL4-mediated H3K4me1, and CBP/p300-mediated H3K27ac, on enhancers. Consequently, Brd4 deletion prevents enhancer RNA production, cell identity gene induction and cell differentiation. Interestingly, Brd4 is dispensable for maintaining cell identity genes in differentiated cells. These findings identify Brd4 as an enhancer epigenomic reader that links active enhancers with cell identity gene induction in differentiation

    The relation between subjective symptom and circulation during orthostatic stress using a tilt table

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    起立負荷時における気分不良の有無と体循環,脳循環との関係について検討することを目的とし,電動チルト台を用いて起立負荷を行った.対象者は20代の自律神経疾患を有さない健常女性12名とし,起立負荷によって気分不良を示さなかった群を正常群とし,示した群を気分不良群とした.電動tilt tableを0°→ 30°→ 45°→ 60°→ 0°と変化させ,各段階を約3分ずつ保持した.その際,平均動脈血圧(MBP),心拍出量,心拍数,1回拍出量,総末梢血管抵抗,腓腹筋内側頭部のTotal Hb,中大脳動脈の平均血流速度(FV)と末梢血管抵抗(PI)を測定し,気分不良尺度を10段階評価でもって記録した.その結果,正常群は起立負荷に伴いFVは低下を示したが,MBP,PIに著変はなく,気分不良群はMBPの上昇に対してPIは減少し,FVはほぼ変化はみられなかった.一般的にめまいなどの気分不良症状は脳血流量の減少により生じるとされていたが,今回の結果では気分不良には脳血流量の増加による脳細動脈へのストレスなどが考えられた.This study aimed at considering the relation between subjective symptoms and the circulation of healthy women during orthostatic stress using a tilt table. From 12 healthy women in there twenties who don't have autonomic nervous disorders, two groups were formed: 1) a normal group which didn't feel ill during orthostatic stress, and 2) a FI group which feel ill during orthostatic stress. An electric tilt table was changed from 0°→30°→45°→60°→0°, and each stage was held for about 3 minutes. Mean artery blood pressure (MBP), cardiac output, heart rate, stroke volume, total peripheral resistance and total hemoglobin at the part of interior gastrocnemius (Total Hb), flow velocity (FV) and peripheral resistance (PI) of the middle cerebral artery (MCA) were measured. The scale of poor feeling was also recorded by10 stage evaluations. Consequently, although the normal group showed an FV fall with orthostatic stress,there were no significant changes in MBP and PI. In the FI group, PI decreased but FV didn't show muchchange with the rise of MBP. According to this result, the stress to the arteriola caused not by a fall but anincrease in the cerebral blood flows etc. seems thus to have been the source of the feeling

    The DsbA-L gene is associated with respiratory function of the elderly via its adiponectin multimeric or antioxidant properties

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    Oxidative stress and inflammation play a key role in the age-related decline in the respiratory function. Adipokine in relation to the metabolic and inflammatory systems is attracting growing interest in the field of respiratory dysfunction. The present clinical and experimental studies investigated the role of the disulfide bond-forming oxidoreductase A-like protein (DsbA-L) gene, which has antioxidant and adiponectin multimeric (i.e. activation) properties, on the respiratory function of the elderly. We performed a retrospective longitudinal genotype-phenotype relationship analysis of 318 Japanese relatively elderly participants (mean age ± standard deviation: 67.0 ± 5.8 years) during a health screening program and an in vitro DsbA-L knock-down evaluation using 16HBE14o-cells, a commonly evaluated human airway epithelial cell line. The DsbA-L rs1917760 polymorphism was associated with a reduction in the ratio of forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC) and %FEV1 and with the elevation of the prevalence of FEV1/FVC < 70%. We also confirmed that the polymorphism was associated with a decreased respiratory function in relation to a decrease in the ratio of high-molecular-weight adiponectin/total adiponectin (as a marker of adiponectin multimerization) and an increase in the oxidized human serum albumin (as an oxidative stress marker). Furthermore, we clarified that DsbA-L knock-down induced oxidative stress and up-regulated the mucus production in human airway epithelial cells. These findings suggest that the DsbA-L gene may play a role in protecting the respiratory function of the elderly, possibly via increased systemic adiponectin functions secreted from adipocytes or through systemic and/or local pulmonary antioxidant properties

    Functional conservation in the SIAMESE-RELATED family of cyclin-dependent kinase inhibitors in land plants

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    © 2015 American Society of Plant Biologists. All rights reserved. The best-characterized members of the plant-specific SIAMESE-RELATED (SMR) family of cyclin-dependent kinase inhibitors regulate the transition from the mitotic cell cycle to endoreplication, also known as endoreduplication, an altered version of the cell cycle in which DNA is replicated without cell division. Some other family members are implicated in cell cycle responses to biotic and abiotic stresses. However, the functions of most SMRs remain unknown, and the specific cyclin- dependent kinase complexes inhibited by SMRs are unclear. Here, we demonstrate that a diverse group of SMRs, including an SMR from the bryophyte Physcomitrella patens, can complement an Arabidopsis thaliana siamese (sim) mutant and that both Arabidopsis SIM and P. patens SMR can inhibit CDK activity in vitro. Furthermore, we show that Arabidopsis SIM can bind to and inhibit both CDKA;1 and CDKB1;1. Finally, we show that SMR2 acts to restrict cell proliferation during leaf growth in Arabidopsis and that SIM, SMR1/LGO, and SMR2 play overlapping roles in controlling the transition from cell division to endoreplication during leaf development. These results indicate that differences in SMR function in plant growth and development are primarily due to differences in transcriptional and posttranscriptional regulation, rather than to differences in fundamental biochemical function

    Exotic Small Mammals as Potential Reservoirs of Zoonotic Bartonella spp.

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    To evaluate the risk for emerging human infections caused by zoonotic Bartonella spp. from exotic small mammals, we investigated the prevalence of Bartonella spp. in 546 small mammals (28 species) that had been imported into Japan as pets from Asia, North America, Europe, and the Middle and Near East. We obtained 407 Bartonella isolates and characterized them by molecular phylogenetic analysis of the citrate synthase gene, gltA. The animals examined carried 4 zoonotic Bartonella spp. that cause human endocarditis and neuroretinitis and 6 novel Bartonella spp. at a high prevalence (26.0%, 142/546). We conclude that exotic small mammals potentially serve as reservoirs of several zoonotic Bartonella spp
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