Biology subjects

Rintamäki, E.

Publications and source records attributed to Rintamäki, E..

4 recordsLinked to original sources

bioRxiv2024

PGR5 is needed for redox-dependent regulation of ATP synthase both in chloroplasts and in cyanobacteria

The regulation of proton motive force (pmf) via ATP synthase activity is a critical mechanism by which photosynthetic organisms maintain redox homeostasis and activate photoprotective responses under fluctuating light conditions. Here, we used time-resolved electrochromic shift (ECS) measurements to investigate pmf dynamics across a range of photosynthetic organisms. Our results reveal that ATP synthase is dynamically regulated during light fluctuations, but in Arabidopsis thaliana could this regulation could not be explained by the known light-induced reduction of the CF{square}{gamma} subunit, suggesting alternative control mechanisms. The PROTON GRADIENT REGULATION 5 (PGR5) protein, previously proposed to facilitate cyclic electron transport (CET), also has a potential role in ATP synthase regulation. The physiological role of cyanobacterial Pgr5 has remained elusive. We characterised a {Delta}pgr5 mutant of Synechocystis sp. PCC 6803 and investigated pmf dynamics in pgr5 mutants of Chlamydomonas reinhardtii, Arabidopsis, and the C4 grass Setaria viridis. While PGR5 was not required for CET in Synechocystis, it was needed for downregulating ATP synthase under high irradiance in all tested organisms via a thiol redox state dependent mechanism. Furthermore, interaction between AtPGR5 and AtCF{square}{gamma} suggests that PGR5 functions as a conserved inhibitor of ATP synthase under high light, contributing to pmf retention and photoprotection. HighlightPGR5 is involved in regulation of ATP synthase in fluctuating light conditions across photosynthetic organisms in a manner that depends on the thiol redox state of the chloroplast or cell.

plant biology↗

bioRxiv2024

Jasmonic acid signaling and glutathione coordinate plant recovery from high light stress

High light-induced chloroplast retrograde signaling originates from the photosynthetic apparatus and regulates nuclear gene expression to enhance photoprotection and coordination of cell metabolism. Here, we analyzed the transcript profiles and accumulation of ROS, stress hormones and small molecule antioxidants to investigate the signaling mechanisms operating under HL stress, and in particular during plant recovery under growth conditions. Exposure to high light for 15 min induced a number of 1O2- and H2O2-responsive genes and accumulation of an oxidative form of glutathione and ascorbate, the hallmarks of oxidative stress in cells. Prolonged exposure to high light resulted in accumulation of transcripts encoding oxylipin biosynthesis enzymes, leading to accumulation of 12-oxo-phytodienoic acid and jasmonic acid. However, the expression of several jasmonic acid -responsive genes, already induced by HL, peaked during the recovery together with accumulation of jasmonic acid, reduced glutathione and ascorbate, highlighting the critical role of jasmonic acid signaling in restoring chloroplast redox balance following high light stress. The involvement of jasmonic acid signaling in recovery-sustained gene expression was further confirmed by conducting experiments with jasmonic acid receptor mutants. High light exposure of only two min was sufficient to induce some recovery-sustained genes, indicating rapid response of plants to changing light conditions. We propose that ROS production at high light induces the signaling cascade for early oxylipin biosynthesis and 12-oxo-phytodienoic acid accumulation, while increased accumulation of jasmonic acid in recovery-phase activates the genes that fully restore the glutathione metabolism, and ultimately allow recovery from short-term high light stress.

plant biology↗

bioRxiv2023

A complex and dynamic redox network regulating oxygen reduction at photosystem I

Thiol-dependent redox regulations of enzyme activities play a central role in regulating photosynthesis. Beside the regulation of metabolic pathways, alternative electron transport has been shown to be subjected to thiol-dependent regulation. We investigated the regulation of O2 reduction at photosystem I. The level of O2 reduction in leaves and isolated thylakoid membranes depends on the photoperiod in which plants are grown. We used a set of Arabidopsis mutant plants affected in the stromal, membrane and lumenal thiol network to study the redox protein partners involved in regulating O2 reduction. Light-dependent O2 reduction was determined in leaves and in thylakoids of plants grown in short day and long day conditions using a spin-trapping EPR assay. In wild type samples from short day, ROS generation was twice the amount of that in samples from long day, while this difference was abolished in several redoxin mutants. An in vitro reconstitution assays showed that thioredoxin m, NADPH-dependent reductase C (NTRC) and NADPH are required for high O2 reduction levels in long day thylakoids. Using isolated photosystem I, we also show that reduction of a PSI protein is responsible for the increase in O2 reduction. Furthermore, differences in the membrane localization of thioredoxins m and 2-Cys peroxiredoxin were demonstrated between thylakoids of short day and long day plants. Finally, we propose a model of redox regulation of O2 reduction according to the reduction power of the stroma and the capabilities of the different thiol-containing proteins to form a network of redox interactions.

biochemistry↗

bioRxiv2018

RCD1 Coordinates Chloroplastic and Mitochondrial Electron Transfer through Interaction with ANAC Transcription Factors

Signaling from chloroplasts and mitochondria, both dependent on reactive oxygen species (ROS), merge at the nuclear protein RADICAL-INDUCED CELL DEATH1 (RCD1). ROS produced in the chloroplasts affect the abundance, thiol redox state and oligomerization of RCD1. RCD1 directly interacts in vivo with ANAC013 and ANAC017 transcription factors, which are the mediators of the ROS-related mitochondrial complex III retrograde signa and suppresses activity of ANAC013 and ANAC017. Inactivation of RCD1 leads to increased expression of ANAC013 and ANAC017-regulated genes belonging to the mitochondrial dysfunction stimulon (MDS), including genes for mitochondrial alternative oxidases (AOXs). Accumulating AOXs and other MDS gene products alter electron transfer pathways in the chloroplasts, leading to diminished production of chloroplastic ROS and increased protection of photosynthetic apparatus from ROS damage. RCD1-dependent regulation affects chloroplastic and mitochondrial retrograde signaling including chloroplast signaling by 3-phosphoadenosine 5-phosphate (PAP). Sensitivity of RCD1 to organellar ROS provides feedback control of nuclear gene expression.

plant biology↗