在日朝鮮族のアイデンティティ -マルチリンガリズムとトランスナショナリズムが自己認識に及ぼす影響-

BACKGROUND: Previous work showed that miRNAs play key roles in the regulation of metamorphosis in the hemimetabolan species Blattella germanica. To gain insight about which miRNAs might be important, we have constructed two miRNA libraries, one of the penultimate, pre-metamorphic nymphal instar (N5) and the other of the last, metamorphic nymphal instar (N6). RESULTS: High throughput sequencing gave 61 canonical miRNAs present in the N5 and N6 libraries, although at different proportions in each. Comparison of both libraries led to the identification of three and 37 miRNAs significantly more expressed in N5 and N6 respectively. Twelve of these 40 miRNAs were then investigated further by qRT-PCR and results indicated that miR-252-3p was well expressed in N5 but not in N6, whereas let-7-5p, miR-100-5p and miR-125-5p showed the reverse pattern. 20-Hydroxyecdysone (20E) tended to stimulate miRNA expression, whereas juvenile hormone (JH) inhibited the 20E stimulatory effect. Expression of let-7, miR-100 and miR-125 was increased by 20E, which has also been observed in D. melanogaster. The only miRNA that was inhibited by 20E was miR-252-3p. The involvement of let-7, miR-100 and miR-125 in metamorphosis has been demonstrated in other insects. Depletion of miR-252-3p caused growth and developmental delays, which suggests that this miRNA is involved in regulating these processes prior to metamorphosis. CONCLUSIONS: The comparative analysis of miRNA libraries from pre-metamorphic (N5) and metamorphic stages (N6) of B. germanica proved to be a useful tool to identify miRNAs with roles in hemimetabolan metamorphosis. Three miRNAs emerged as important factors in the metamorphic stage (N6): let-7-5p, miR-100-5p and miR-125-5p, whereas miR-252-3p appears to be important in the pre-metamorphic stage (N5)

Transcriptomic analysis of oocyte resorption after hydric stress in the German cockroach

Trabajo presentado en el XXIV International Congress of Entomology "New era in Entomology" (ICE 2012), celebrado en Daegu (Corea del Sur) del 19 al 25 de agosto de 2012.N

MicroRNAs in metamorphic and non-metamorphic transitions in hemimetabolan insect metamorphosis

Abstract Background Previous work showed that miRNAs play key roles in the regulation of metamorphosis in the hemimetabolan species Blattella germanica. To gain insight about which miRNAs might be important, we have constructed two miRNA libraries, one of the penultimate, pre-metamorphic nymphal instar (N5) and the other of the last, metamorphic nymphal instar (N6). Results High throughput sequencing gave 61 canonical miRNAs present in the N5 and N6 libraries, although at different proportions in each. Comparison of both libraries led to the identification of three and 37 miRNAs significantly more expressed in N5 and N6 respectively. Twelve of these 40 miRNAs were then investigated further by qRT-PCR and results indicated that miR-252-3p was well expressed in N5 but not in N6, whereas let-7-5p, miR-100-5p and miR-125-5p showed the reverse pattern. 20-Hydroxyecdysone (20E) tended to stimulate miRNA expression, whereas juvenile hormone (JH) inhibited the 20E stimulatory effect. Expression of let-7, miR-100 and miR-125 was increased by 20E, which has also been observed in D. melanogaster. The only miRNA that was inhibited by 20E was miR-252-3p. The involvement of let-7, miR-100 and miR-125 in metamorphosis has been demonstrated in other insects. Depletion of miR-252-3p caused growth and developmental delays, which suggests that this miRNA is involved in regulating these processes prior to metamorphosis. Conclusions The comparative analysis of miRNA libraries from pre-metamorphic (N5) and metamorphic stages (N6) of B. germanica proved to be a useful tool to identify miRNAs with roles in hemimetabolan metamorphosis. Three miRNAs emerged as important factors in the metamorphic stage (N6): let-7-5p, miR-100-5p and miR-125-5p, whereas miR-252-3p appears to be important in the pre-metamorphic stage (N5).</p

Molecular changes underlying oocyte resorption derived from water stress in the cockroach Blattella germanica

Trabajo presentado en el I Congrés Internacional de Biologia de Catalunya "Global Questions on Advanced Biology" (CIBICAT), celebrado en Barcelona del 9 al 12 de julio de 2012.N

F4/80hiCCR2hi macrophage infiltration into the intra-abdominal fat worsens the severity of experimental IBD in obese mice with DSS colitis

Background & aims: Intra-abdominal fat is pathogenically involved in both type 2 diabetes and inflammatory bowel disease (IBD). However, little is known about the interrelationships between these two widespread and devastating diseases. The goal of this study is to investigate the effect of obesity in the severity of colitis and, in turn, examine the impact of IBD on glucose tolerance during obesity. In this context, we have explored the role of infiltrating macrophages in the severity of diabetes and IBD. Methods: The infiltration of macrophages and T cells into intra-abdominal WAT, liver and the colonic lamina propria was examined in db/db and lean mice after a 7-day dextran sodium sulfate (DSS) challenge by tissue fractionation and flow cytometry. Disease activity indices (DAI), weight loss and colonic histology were examined during the course of the DSS challenge, and colonic pro-inflammatory cytokine expression was quantified by real-time RT-PCR. To determine the impact of obesity and intestinal inflammation on glucose tolerance, mice were administered an intraperitoneal glucose tolerance test. Results: We found that obesity increases the severity of experimental IBD. Following a DSS challenge, obese mice express greater concentrations of colonic TNF-a mRNA than lean mice. In addition, experimental IBD in combination with obesity worsens glucose tolerance beyond the effect caused by obesity alone. F4/80hiCCR2hi macrophages infiltrate the lamina propria of mice with DSS colitis and the WAT of obese mice. Conclusions: Infiltration of F4/80hiCCR2hi macrophages into intra-abdominal fat worsens the severity of experimental IBD during obesity. In turn, experimental IBD in obese mice repressed skeletal muscle PPAR g and GLUT4 mRNA expression, upregulated MCP-1 and worsened type 2 diabetes