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Aarabi, F.

Publications and source records attributed to Aarabi, F..

4 recordsLinked to original sources

Chloroplastic ascorbate acts as a regulatory hub in plant metabolism regardless of oxidative stress

Ascorbate is a major plant metabolite that plays crucial roles in various processes, from reactive oxygen scavenging to epigenetic regulation. However, to what extent and how ascorbate modulates metabolism is largely unknown. To address this, we investigated the consequences of chloroplastic and total cellular ascorbate-deficiencies by studying chloroplastic ascorbate-transporter pht4;4 mutant lines, and the ascorbate-deficient vtc2-4 mutant of Arabidopsis thaliana. Under regular growth conditions, both ascorbate-deficiencies caused minor alterations in photosynthesis, with no apparent signs of oxidative damage. In contrast, metabolomics analysis revealed a global and largely overlapping metabolome rewiring in both ascorbate-deficiencies, suggesting that chloroplastic ascorbate modulates plant metabolism. We observed significant alterations in amino acid metabolism, particularly in arginine metabolism, activation of nucleotide salvage pathways, and changes in secondary metabolism. In addition, proteome-wide analysis of thermostability revealed that ascorbate may interact with enzymes involved in arginine metabolism, the Calvin-Benson cycle, and several photosynthetic electron transport components. Overall, our results suggest that, independently of oxidative stress, chloroplastic ascorbate interconnects and coordinates diverse metabolic pathways in vascular plants and thus acts as a regulatory hub.

plant biology↗

Degradation of Fatty Acid Export Protein1 by Rhomboid-Like Protease11 Contributes to Cold Tolerance in Arabidopsis

Plants need to adapt to different stresses to optimize growth under unfavorable conditions. The abundance of the chloroplast envelope located Fatty Acid Export Protein1 (FAX1) decreases after the onset of low temperatures. However, it was unclear how FAX1 degradation occurs and whether altered FAX1 abundance contributes to cold tolerance in plants. The rapid cold-induced increase in rhomboid-like protease11 (RBL11) transcript, the physical interaction of RBL11 with FAX1, the specific FAX1 degradation after RBL11 expression, and the absence of cold-induced FAX1 degradation in rbl11 loss-of-function mutants suggest that this enzyme is responsible for FAX1 degradation. Proteomic analyses showed that rbl11 mutants have higher levels of FAX1 and other proteins involved in membrane lipid homeostasis, suggesting that RBL11 is a key element in the remodeling of membrane properties during cold. Consequently, in the cold, rbl11 mutants show a shift in lipid biosynthesis towards the eukaryotic pathway, which coincides with impaired cold tolerance. To demonstrate that cold sensitivity is due to increased FAX1 levels, FAX1 overexpressors were analyzed. rbl11 and FAX1 overexpressor mutants show superimposable phenotypic defects upon exposure to cold temperatures. Our results show that the cold-induced degradation of FAX1 by RBL11 is critical for Arabidopsis to survive cold and freezing periods. One sentence summaryDegradation of the inner envelope protein Fatty Acid Export1 via Rhomboid Like Protease11 represents a critical process to achieve cold and frost tolerance in Arabidopsis

plant biology↗

Increased expression of mitochondrial dysfunction stimulon genes affects chloroplast redox status and photosynthetic electron transfer in Arabidopsis

Mitochondrial retrograde signals control expression of nuclear mitochondrial dysfunction stimulon (MDS) genes. Although MDS gene products mostly affect mitochondrial functions, they also influence production of reactive oxygen species (ROS) and redox status of chloroplasts. To study this inter-organellar interaction, we analysed the response of the Arabidopsis MDS-overexpressor mutant rcd1 to methyl viologen (MV), which catalyses electron transfer from Photosystem I (PSI) to molecular oxygen, generating ROS in Mehlers reaction. The response of plants to MV was investigated by imaging chlorophyll fluorescence in aerobic and hypoxic environments, and by membrane inlet mass spectrometry. Hypoxic treatment abolished the effect of MV on photosynthetic electron transfer in rcd1, but not in wild type. A similar reaction to hypoxia was observed in other MDS-activating lines and treatments. This suggests that MDS gene products contribute to oxygen depletion at the PSI electron-acceptor side. In unstressed growth conditions this MDS-related effect is likely masked by endogenous oxygen evolution and gas exchange with the atmosphere. In rcd1, altered Mehlers reaction coincided with more reduced state of the chloroplast NADPH-thioredoxin oxidoreductase C (NTRC) and its targets, suggesting that NTRC performs feedback control of photosynthesis. This regulation may represent a novel mechanism whereby mitochondrial retrograde signalling affects chloroplast functions.

plant biology↗

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↗