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Misawa, N.

Publications and source records attributed to Misawa, N..

3 recordsLinked to original sources

Photosynthesis-derived carbohydrate supply sustains CuCl2-induced phytoalexin production in rice leaves

Phytoalexins are antimicrobial metabolites whose biosynthesis is triggered by signaling activated by both biotic and abiotic elicitors, but the physiological conditions that sustain their production remain poorly understood. Here, we examined how light and carbohydrate availability affect CuCl2-induced production of diterpenoid (phytocassanes and momilactones) and flavonoid (sakuranetin) phytoalexins in rice (Oryza sativa L.) leaf disks. Darkness strongly suppressed both the accumulation of all three phytoalexin groups and the induction of their biosynthetic genes. In darkness, endogenous sucrose, glucose, and fructose declined to 3%-8% of the levels in the light, whereas early accumulation of jasmonic acid and jasmonoyl-L-isoleucine (JA-Ile) was not detectably reduced. Exogenous sucrose restored phytoalexin accumulation in darkness in a dose-dependent manner, together with the expression of the suppressed biosynthetic genes, whereas equimolar mannitol had no effect. Glucose also restored sakuranetin accumulation in darkness but only partially restored diterpenoid accumulation, whereas the glucose analog 2-deoxy-D-glucose did not, and it suppressed CuCl2-induced accumulation in the light in a dose-dependent manner. In the light, 3-(3,4-dichlorophenyl)-1,1-dimethylurea (DCMU), an inhibitor of photosynthetic electron transport, depleted soluble sugars and suppressed phytoalexin accumulation, and sucrose reversed this suppression. Sugars alone induced little phytoalexin accumulation, indicating that carbohydrates act permissively rather than as elicitors. Diterpenoid phytoalexins depended more strongly on light than sakuranetin, yet both classes depended on carbohydrate availability. These results indicate that photosynthesis-derived carbohydrate supply sustains elicitor-induced phytoalexin production in rice leaves and largely accounts for its light dependence.

plant biology↗

Macrophage immunosenescence prolongs intraocular inflammation in aged mice via impaired induction of regulatory T cells

Immune-mediated intraocular inflammation, called uveitis, is a leading cause of global blindness, with the highest burden of visual impairment falling on older individuals. Immunosenescence, the functional changes in immune cells with aging, impacts the age-associated immune response, but how immunosenescence and the molecular regulators of the age-associated immune response affect the clinical course of uveitis remains unclear. In the murine model of experimental autoimmune uveitis (EAU), aged mice demonstrated a delayed onset and peak of intraocular inflammation compared to young mice. In contrast to the canonical monophasic inflammation that rapidly resolves in young mice, aged mice developed persistent, chronic inflammation. Transcriptomic and flow-cytometric analyses of immune cells and the receptor-ligand interactome revealed a dominant macrophage-CD4+ T cell signature. This signaling pathway was functionally altered on both ends: macrophages from aged mice had an impaired capacity to generate peripherally induced regulatory T cells (pTreg) through an IL-6 regulated pathway, while CD4+ T cells co-cultured with aged macrophages demonstrated increased proliferation. Our study establishes aging as a key regulator of the effector immune response in uveitis. Regulatory T cells, specifically pTreg, are essential for resolving inflammation in uveitis and an impaired ability to induce pTreg led to a sustained, chronic inflammatory uveitis phenotype in old mice, thereby linking immunosenescence to persistent neuroinflammation. These findings highlight potential therapeutic avenues for vision-threatening uveitis, especially in older patients.

immunology↗

Gorilla APOBEC3 restricts SIVcpz and influences lentiviral evolution in great ape cross-species transmissions

Restriction factors including APOBEC3 family proteins have the potential prevent cross-species lentivirus transmissions. Such events as well as ensuing pathogenesis require the viral Vif protein to overcome/neutralize/degrade the APOBEC3 enzymes of the new host species. Previous investigations have focused on the molecular interaction between human APOBEC3s and HIV-1 Vif. However, the evolutionary interplay between lentiviruses and great ape (including human, chimpanzee and gorilla) APOBEC3s has not been fully investigated. Here we demonstrate that gorilla APOBEC3G plays a pivotal role in restricting lentiviral transmission from chimpanzee to gorilla. We also reveal that a sole amino acid substitution in Vif is sufficient to overcome the gorilla APOBEC3G-mediated species barrier. Moreover, the antiviral effects of gorilla APOBEC3D and APOBEC3F are considerably weaker than those of human and chimpanzee counterparts, which can result in the skewed evolution of great ape lentiviruses leading to HIV-1.\n\nHighlightsO_LISIVcpz requires M16E mutation in Vif to counteract gorilla A3G\nC_LIO_LIAcidic residue at position 16 of Vif is crucial to counteract gorilla A3G\nC_LIO_LIGorilla A3D and A3F poorly suppress lentiviral infectivity\nC_LIO_LISIVgor and related HIV-1s counteract human A3D and A3F independently of DRMR motif\nC_LI

microbiology↗