The NAD Kinase Slr0400 Functions as a Growth Repressor in Synechocystis sp. PCC 6803
The NAD Kinase Slr0400 Functions as a Growth Repressor in Synechocystis sp. PCC 6803
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NAD 激酶 Slr0400 在集胞藻中发挥生长抑制因子的作用。
DOI：
10.1093/pcp/pcab023
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发表时间：
2021
影响因子：
4.9
通讯作者：
Kawai-Yamada Maki
中科院分区：
文献类型：
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作者：
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
NADP+是烟酰胺腺嘌呤二核苷酸（NAD）的磷酸化形式，在许多细胞过程中起着重要作用。NAD激酶（NADK）在所有生物体中是保守的，催化NAD+磷酸化为NADP+。然而，磷酸化的NAD+ NADP+在蓝藻Synechocystis的生理作用仍然不清楚。在这项研究中，我们报告了集胞藻中的NADK编码基因slr 0400在光激活的异养生长条件和葡萄糖存在的光暗循环条件下作为生长抑制因子发挥作用。我们通过NAD（P）（H）含量和酶活性的表征表明，slr 0400缺陷突变体中NAD+的积累导致糖酵解和三羧酸（TCA）循环酶的活性不受抑制。在确定slr 0400是否作为典型的NADK发挥功能时，我们发现slr 0400的组成型表达在一个突变体背景中补充了浅绿色表型。此外，为了确定slr 04000缺失突变体生长优势背后的生理背景，我们研究了slr 0400缺失突变体在强光条件下的光漂白表型。在theslr 0400缺陷型突变体中发现的光合作用分析是由于光系统II（PSII）光合机制的故障造成的。总体而言，我们的结果表明，yslr 0400维持NADP（H）/NAD（H）在调节糖酵解和三羧酸循环以抑制生长速率并维持光合能力方面发挥着重要作用。
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 cyanobacteriumSynechocystisremains unclear. In this study, we report thatslr0400, an NADK-encoding gene inSynechocystis, 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 activity, that NAD+accumulation inslr0400-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 ofslr0400in an Arabidopsisnadk2-mutant background complements the pale-green phenotype. Moreover, to determine the physiological background behind the growth advantage of mutants lackingslr04000, we investigated the photobleaching phenotype ofslr0400-deficient mutant under high-light conditions. Photosynthetic analysis found in theslr0400-deficient mutant resulted from malfunctions in the Photosystem II (PSII) photosynthetic machinery. Overall, our results suggest that NADP(H)/NAD(H) maintenance byslr0400plays a significant role in modulating glycolysis and the TCA cycle to repress the growth rate and maintain the photosynthetic capacity.