Search

Your search keyword '"Nishiyama, Yoshitaka"' showing total 443 results
Start Over Author "Nishiyama, Yoshitaka"
443 results on '"Nishiyama, Yoshitaka"'

25. Improved capacity for the repair of photosystem II via reinforcement of the translational and antioxidation systems in Synechocystis sp. PCC 6803.

Author

Napaumpaiporn, Pornpan, Ogawa, Takako, Sonoike, Kintake, and Nishiyama, Yoshitaka

Abstract

SUMMARY: In the cyanobacterium Synechocystis sp. PCC 6803, translation factor EF‐Tu is inactivated by reactive oxygen species (ROS) via oxidation of Cys82 and the oxidation of EF‐Tu enhances the inhibition of the repair of photosystem II (PSII) by suppressing protein synthesis. In our present study, we generated transformants of Synechocystis that overexpressed a mutated form of EF‐Tu, designated EF‐Tu (C82S), in which Cys82 had been replaced by a Ser residue, and ROS‐scavenging enzymes individually or together. Expression of EF‐Tu (C82S) alone in Synechocystis enhanced the repair of PSII under strong light, with the resultant mitigation of PSII photoinhibition, but it stimulated the production of ROS. However, overexpression of superoxide dismutase and catalase, together with the expression of EF‐Tu (C82S), lowered intracellular levels of ROS and enhanced the repair of PSII more significantly under strong light, via facilitation of the synthesis de novo of the D1 protein. By contrast, the activity of photosystem I was hardly affected in wild‐type cells and in all the lines of transformed cells under the same strong‐light conditions. Furthermore, transformed cells that overexpressed EF‐Tu (C82S), superoxide dismutase, and catalase were able to survive longer under stronger light than wild‐type cells. Thus, the reinforced capacity for both protein synthesis and ROS scavenging allowed both photosynthesis and cell proliferation to tolerate strong light. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

47. The NAD Kinase Slr0400 Functions as a Growth Repressor in Synechocystis sp. PCC 6803

Author

Ishikawa, Yuuma, Cassan, Cedric, Kadeer, Aikeranmu, Yuasa, Koki, Sato, Nozomu, Sonoike, Kintake, Kaneko, Yasuko, Miyagi, Atsuko, Takahashi, Hiroko, Ishikawa, Toshiki, Yamaguchi, Masatoshi, Nishiyama, Yoshitaka, Hihara, Yukako, Gibon, Yves, Kawai-Yamada, Maki, Ishikawa, Yuuma, Cassan, Cedric, Kadeer, Aikeranmu, Yuasa, Koki, Sato, Nozomu, Sonoike, Kintake, Kaneko, Yasuko, Miyagi, Atsuko, Takahashi, Hiroko, Ishikawa, Toshiki, Yamaguchi, Masatoshi, Nishiyama, Yoshitaka, Hihara, Yukako, Gibon, Yves, and Kawai-Yamada, Maki

Abstract

NADP(+), the phosphorylated form of nicotinamide adenine dinucleotide (NAD), plays an essential role in many cellular processes. NAD kinase (NADK), which is conserved in all living organisms, catalyzes the phosphorylation of NAD(+) to NADP(+). However, the physiological role of phosphorylation of NAD(+ )to NADP(+) in the cyanobacterium Synechocystis remains unclear. In this study, we report that slr0400, an NADK-encoding gene in Synechocystis, functions as a growth repressor under light-activated heterotrophic growth conditions and light and dark cycle conditions in the presence of glucose. We show, via characterization of NAD(P)(H) content and enzyme that NAD(+) accumulation in slr0400-deficient mutant results in the unsuppressed activity of glycolysis and tricarboxylic acid (TCA) cycle enzymes. In determining whether Slr0400 functions as a typical NADK, we found that constitutive expression of slr0400 in an Arabidopsis nadk2-mutant background complements the pale-green phenotype. Moreover, to determine the physiological background behind the growth advantage of mutants lacking slr04000, we investigated the photobleaching phenotype of slr0400-deficient mutant under high-light conditions. Photosynthetic analysis found in the slr0400-deficient mutant resulted from malfunctions in the Photosystem II (PSII) photosynthetic machinery. Overall, our results suggest that NADP(H)/NAD(H) maintenance by slr0400 plays a significant role in modulating glycolysis and the TCA cycle to repress the growth rate and maintain the photosynthetic capacity.

Published
2021

Catalog

Books, media, physical & digital resources
See catalog results