April 17, 2015

Strand et al. "Activation of cyclic electron flow by hydrogen peroxide in vivo"

Deserah D. Strand, Aaron K. Livingston, Mio Satoh-Cruz, John E. Froehlich, Veronica G. Maurino, and David M. Kramer

From the article:

Cyclic electron flow (CEF) around photosystem I is thought to balance the ATP/NADPH energy budget of photosynthesis, requiring that its rate be finely regulated. The mechanisms of this regulation are not well understood. We observed that mutants that exhibited constitutively high rates of CEF also showed elevated production of H2O2. We thus tested the hypothesis that CEF can be activated by H2O2 in vivo. CEF was strongly increased by H2O2 both by infiltration or in situ production by chloroplast-localized glycolate oxidase, implying that H2O2 can activate CEF either directly by redox modulation of key enzymes, or indirectly by affecting other photosynthetic processes. CEF appeared with a half time of about 20 min after exposure to H2O2, suggesting activation of previously expressed CEF-related machinery. H2O2-dependent CEF was not sensitive to antimycin A or loss of PGR5, indicating that increased CEF probably does not involve the PGR5-PGRL1 associated pathway. In contrast, the rise in CEF was not observed in a mutant deficient in the chloroplast NADPH:PQ reductase (NDH), supporting the involvement of this complex in CEF activated by H2O2. We propose that H2O2 is a missing link between environmental stress, metabolism, and redox regulation of CEF in higher plants. 

April 9, 2015

González-Cabanelas et al. "The diversion of 2-C-methyl-D-erythritol-2,4-cyclodiphosphate from the 2-C-methyl-D-erythritol 4-phosphate pathway to hemiterpene glycosides mediates stress responses in Arabidopsis thaliana"

Diego González-Cabanelas, Louwrance P. Wright, Christian Paetz, Nawaporn Onkokesung, Jonathan Gershenzon, Manuel Rodríguez-Concepción and Michael A. Phillips*
The Plant Journal, Volume 82, Issue 1, pages 122–137, April 2015 DOI:10.1111/tpj.12798

Today I would like to highlight a publication of my own, as self-serving as that might be. This is the product of a Master's project carried out by my former student Diego González-Cabanelas, who has since gone to a PhD program at the Max Planck Institute of  Chemical Ecology (Jena, Germany). In this report, we describe a metabolic "shunt" funneling carbon flux away from the main isoprenoid precursor pathway in the chloroplast when flux is elevated. That's pretty important information if you are trying to metabolically engineer this pathway and don't understand why so much of the expected flux seems to be disappearing when we use the standard 'upregulation of structural genes' approach. An unusual cyclic diphosphate intermediate in the pathway has been recently alleged to have signaling properties, activating defense gene expression in the nucleus. Naturally, this would require this metabolite to physically leave the confines of the plastid and interact with other factors in the cytosol, nucleus, or elsewhere to control gene expression. It is also quite strange that a metabolic intermediate in a pathway would be selected to play such a different parallel role in defense signaling, so the actual story may be much more complex. Due to our limited knowledge of how isoprenoid biosynthesis is regulated at the molecular level, we are still making early discoveries into how this biosynthetic network is controlled. I like to think this is one of them.