Molecular mechanisms of regulation of sulfate assimilation: first steps on a long road

Abstract

The pathway of sulfate assimilation, which provides plants with the essential nutrient sulfur, is tightly regulated and coordinated with the demand for reduced sulfur. The responses of metabolite concentrations, enzyme activities and mRNA levels to various signals and environmental conditions have been well described for the pathway. However, only little is known about the molecular mechanisms of this regulation. To date, nine transcription factors have been described to control transcription of genes of sulfate uptake and assimilation. In addition, other levels of regulation contribute to the control of sulfur metabolism. Post-transcriptional regulation has been shown for sulfate transporters, adenosine 5′phosphosulfate reductase, and cysteine synthase. Several genes of the pathway are targets of microRNA miR395. In addition, protein–protein interaction is increasingly found in the center of various regulatory circuits. On top of the mechanisms of regulation of single genes, we are starting to learn more about mechanisms of adaptation, due to analyses of natural variation. In this article, the summary of different mechanisms of regulation will be accompanied by identification of the major gaps in knowledge and proposition of possible ways of filling them.

A Post-Genomic View of the Ecophysiology, Catabolism and Biotechnological Relevance of Sulphate-Reducing Prokaryotes

“…1), a reaction that is catalysed by sulphate adenylyl transferase (Sat). Sat is a widespread enzyme present not only in SRP but also in SOB and in all organisms that reduce sulphate for assimilation, including plants, algae, yeasts, fungi and many bacteria (Koprivova & Kopriva, 2014;Leustek, Martin, Bick, & Davies, 2000). Sat from these different organisms is remarkably similar, with virtually identical substrate-binding sites, indicating that this is an ancient enzyme that arose prior to the divergence of the three domains of life (Parey, Demmer, et al, 2013;Parey, Fritz, et al, 2013).…”

A Program for Iron Economy during Deficiency Targets Specific Fe Proteins

“…Together a lack of APR and SIR should result in lower levels of reduced S compounds including glutathione. Lack of reduced S compounds should cause up-regulation of plant sulfate uptake, which explains the higher S content after Fe deficiency (Koprivova and Kopriva, 2014); indeed, Fe deficiency was shown to increase S uptake capacity in tomato and wheat (Ciaffi et al, 2013;Zuchi et al, 2015) In plant shoots, micronutrient economy, the idea that certain proteins under deficiency are preferred targets for down-regulation to benefit cofactor delivery to other essential functions, is documented for Cu (Burkhead et al, 2009) and Zn . The down-regulation at the transcript level of abundant Fe proteins, coordinated with the SUFB key factor of the Fe-S assembly system, should help to safely economize and perhaps prioritize Fe during Fe deficiency.…”

Phloem-Specific Methionine Recycling Fuels Polyamine Biosynthesis in a Sulfur-Dependent Manner and Promotes Flower and Seed Development

“…In particular, Brassica species have high S demands, presumably because of the large amounts of Cys-rich storage proteins in their cotyledons (Shewry and Casey, 1999) and the production of glucosinolates, which mostly derive from Met (Windsor et al, 2005). Both sulfate transport and assimilation pathways are highly regulated by S availability, and the expression and activity levels of the corresponding proteins are efficiently adjusted under low S availability (Saito, 2004;Koprivova and Kopriva, 2014). S deficiency promotes the synthesis of transport proteins of the SULFATE TRANSPORTER (SULTR) family to increase root sulfate uptake (Shinmachi et al, 2010;Maruyama-Nakashita et al, 2015) or sulfate efflux from storage vacuoles (Kataoka et al, 2004), which supports the remobilization of sulfate from source to sink tissues.…”