Mechanosensory trichome cells evoke a mechanical stimuli–induced immune response in Arabidopsis thaliana

Perception of pathogen-derived ligands by corresponding host receptors is a pivotal strategy in eukaryotic innate immunity. In plants, this is complemented by circadian anticipation of infection timing, promoting basal resistance even in the absence of pathogen threat. Here, we report that trichomes, hair-like structures on the epidermis, directly sense external mechanical forces, including raindrops, to anticipate pathogen infections in Arabidopsis thaliana. Exposure of leaf surfaces to mechanical stimuli initiates the concentric propagation of intercellular calcium waves away from trichomes to induce defence-related genes. Propagating calcium waves enable effective immunity against pathogenic microbes through the CALMODULIN-BINDING TRANSCRIPTION ACTIVATOR 3 (CAMTA3) and mitogen-activated protein kinases. We propose an early layer of plant immunity in which trichomes function as mechanosensory cells that detect potential risks

Introduction for Fisheries and Aquatic Biology

Chapter I. Aquatic Environment. Ken FURUYA and Ichiro YASUDA : chapter_1.pdfChapter II. Biology and Ecology of Aqua-Shere. Toyoji KANEKO, Katsumi TSUKAMOTO, Atsushi TSUDA, Yuzuru SUZUKI and Katsufumi SATOH : chapter_2.pdfChapter III. Aquatic Resource and Production. Ichiro AOKI, Kazuo OGAWA, Taku YAMAKAWA and Tomoyoshi YOSHINAGA : chapter_3.pdfChapter IV. Chemistry of Aquatic Organism and Their Utilization. Hiroki ABE, Shugo WATABE, Yoshihiro OCHIAI, Shigeru OKADA, Naoko YOSHIKAWA, Yoshiharu KINOSHITA, Gen KANEKO and Shigeki MATSUNAGA : chapter_4.pdfChapter V. Relation between Aqua-Shere and Human Life. Hisashi KUROKURA, Hirohide MATSUSHIMA, Shingo KUROHAGI, Haruko YAMASHITA, Akinori HINO, Kazumasa IKUTA, Satoquo SEINO, Masahiko ARIJI, Ken FURUYA, Junichiro OKAMOTO and Nobuyuki YAGI : chapter_5.pdfPart of "Introduction for Fisheries and Aquatic Biology

Up-regulation of activation-induced cytidine deaminase causes genetic aberrations at the CDKN2b-CDKN2a in gastric cancer.

The DNA/RNA editing enzyme activation-induced cytidine deaminase (AID) is mutagenic and has been implicated in human tumorigenesis. Helicobacter pylori infection of gastric epithelial cells leads to aberrant expression of AID and somatic gene mutations. We investigated whether AID induces genetic aberrations at specific chromosomal loci that encode tumor-related proteins in gastric epithelial cells

Mice Deficient in Proglucagon-Derived Peptides Exhibit Glucose Intolerance on a High-Fat Diet but Are Resistant to Obesity

<div><p>Homozygous glucagon-GFP knock-in mice (<i>Gcg</i>^{<i>gfp/gfp</i>}) lack proglucagon derived-peptides including glucagon and GLP-1, and are normoglycemic. We have previously shown that <i>Gcg</i>^{<i>gfp/gfp</i>} show improved glucose tolerance with enhanced insulin secretion. Here, we studied glucose and energy metabolism in <i>Gcg</i>^{<i>gfp/gfp</i>} mice fed a high-fat diet (HFD). Male <i>Gcg</i>^{<i>gfp/gfp</i>} and <i>Gcg</i>^<i>gfp/+</i> mice were fed either a normal chow diet (NCD) or an HFD for 15–20 weeks. Regardless of the genotype, mice on an HFD showed glucose intolerance, and <i>Gcg</i>^{<i>gfp/gfp</i>} mice on HFD exhibited impaired insulin secretion whereas <i>Gcg</i>^<i>gfp/+</i> mice on HFD exhibited increased insulin secretion. A compensatory increase in β-cell mass was observed in <i>Gcg</i>^<i>gfp/+</i>mice on HFD, but not in <i>Gcg</i>^{<i>gfp/gfp</i>} mice on the same diet. Weight gain was significantly lower in <i>Gcg</i>^{<i>gfp/gfp</i>} mice than in <i>Gcg</i>^<i>gfp/+</i>mice. Oxygen consumption was enhanced in <i>Gcg</i>^{<i>gfp/gfp</i>} mice compared to <i>Gcg</i>^<i>gfp/+</i> mice on an HFD. HFD feeding significantly increased uncoupling protein 1 mRNA expression in brown adipose and inguinal white adipose tissues of <i>Gcg</i>^{<i>gfp/gfp</i>} mice, but not of <i>Gcg</i>^<i>gfp/+</i>mice. Treatment with the glucagon-like peptide-1 receptor agonist liraglutide (200 mg/kg) improved glucose tolerance in <i>Gcg</i>^{<i>gfp/gfp</i>} mice and insulin content in <i>Gcg</i>^{<i>gfp/gfp</i>} and <i>Gcg</i>^<i>gfp/+</i> mice was similar after liraglutide treatment. Our findings demonstrate that <i>Gcg</i>^{<i>gfp/gfp</i>} mice develop diabetes upon HFD-feeding in the absence of proglucagon-derived peptides, although they are resistant to diet-induced obesity.</p></div

Analysis of adipose tissue with regard to energy metabolism.

<p>(A) Intrascapular BAT weights after NCD- or HFD-feeding (n = 6–8). (B) Representative H&E staining of BAT. (C) Triglyceride contents in BAT (n = 4). (D) mRNA expression of <i>Ucp1</i>, <i>Ppargc1a</i>, and <i>Dio2</i> in BAT (n = 5–8). (E) mRNA expression of <i>Ucp1</i>, <i>Ppargc1a</i>, <i>Dio2</i>, <i>F4/80</i>, <i>Mcp1</i>, <i>Tnfa</i>, <i>Tbx1</i>, <i>Cd137</i>, and <i>Cidea</i> in inguinal WAT. White bars, mice fed on a NCD; black bars, mice fed on an HF diet (n = 4–5). *p < 0.05; ***p < 0.001. Data are presented as means ± SEM.</p

Changes in body weight and quantification of energy expenditure. Indirect calorimetry was analyzed by using CLAMS.

<p>(A) Body weight changes during HFD feeding. (B) Body weight gain at 15 weeks of HFD-feeding. (C) Oxygen consumption (<i>VO</i>_<i>2</i>). (D) Carbon dioxide output (<i>VCO</i>_<i>2</i>). (E) Respiratory exchange rates (RER). (F) Energy intake. (G) Physical activity. White bars, mice fed NCD; black bars, mice fed HFD (n = 6–8). *p < 0.05; **p < 0.01; ***p < 0.001. Data are presented as means ± SEM.</p

Effect of liraglutide on glucose metabolism. Liraglutide (200 mg/kg) was subcutaneously administered once a day for last 4 weeks of HFD-feeding.

<p>(A) body weights during liraglutide treatment (n = 6–7). Open circles, liraglutide-treated <i>Gcg</i>^<i>gfp/+</i> mice on HFD; closed circles, liraglutide-treated <i>Gcg</i>^{<i>gfp/gfp</i>} mice on HFD. **p < 0.01 vs <i>Gcg</i>^<i>gfp/+</i> mice. ^#p < 0.05; ^##p < 0.01 vs. before liraglutide treatment. (B) Blood glucose levels during IPGTT (n = 6–7). Open circles, liraglutide-treated <i>Gcg</i>^<i>gfp/+</i> mice on HFD; closed circles, liraglutide-treated <i>Gcg</i>^{<i>gfp/gfp</i>} mice on HFD. *p < 0.05; ***p < 0.001 vs. <i>Gcg</i>^<i>gfp/+</i> mice. (C) Plasma insulin levels 0 min (white bars) and 15 min (black bars) after i.p. glucose loading (n = 6–7). (D) Insulin contents in pancreata. White bars, liraglutide-treated <i>Gcg</i>^<i>gfp/+</i> mice on HFD; black bars, liraglutide-treated <i>Gcg</i>^{<i>gfp/gfp</i>} mice on HFD (n = 5–7). Data are presented as means ± SEM.</p