Nitric Oxide Mediates Nitrite-Sensing and Acclimation and Triggers a Remodeling of Lipids. Issue 3 (18th September 2017)

• Record Type: Journal Article
• Authors: Dolch, Lina-Juana; Lupette, Josselin; Tourcier, Guillaume; Bedhomme, Mariette; Collin, Séverine; Magneschi, Leonardo; Conte, Melissa; Seddiki, Khawla; Richard, Christelle; Corre, Erwan; Fourage, Laurent; Laeuffer, Frédéric; Richards, Robert; Reith, Michael; Rébeillé, Fabrice; Jouhet, Juliette; McGinn, Patrick; Maréchal, Eric
• Is Part Of: Plant physiology. Volume 175:Issue 3(2017)
• Page Start: 1407
• Page End: 1423
• Publication Date: 2017-09-18
• Subjects: Plant physiology -- Periodicals; Botany -- Periodicals; Periodicals; Electronic journals; 571.2
• DOI: 10.1104/pp.17.01042
• Languages: English
• ISSNs: 0032-0889

Abstract

Abstract : In Phaedactylum, NO produced from nitrite by the nitrate reductase up-regulates the expression of genes involved in nitrite assimilation into amino acids and triggers a remodeling of lipids. Abstract: Nitric oxide (NO) is an intermediate of the nitrogen cycle, an industrial pollutant, and a marker of climate change. NO also acts as a gaseous transmitter in a variety of biological processes. The impact of environmental NO needs to be addressed. In diatoms, a dominant phylum in phytoplankton, NO was reported to mediate programmed cell death in response to diatom-derived polyunsaturated aldehydes. Here, using the Phaeodactylum Pt1 strain, 2E, 4E-decadienal supplied in the micromolar concentration range led to a nonspecific cell toxicity. We reexamined NO biosynthesis and response in Phaeodactylum . NO inhibits cell growth and triggers triacylglycerol (TAG) accumulation. Feeding experiments indicate that NO is not produced from Arg but via conversion of nitrite by the nitrate reductase. Genome-wide transcriptional analysis shows that NO up-regulates the expression of the plastid nitrite reductase and genes involved in the subsequent incorporation of ammonium into amino acids, via both Gln synthesis and Orn-urea pathway. The phospho enol pyruvate dehydrogenase complex is also up-regulated, leading to the production of acetyl-CoA, which can feed TAG accumulation upon exposure to NO. Transcriptional reprogramming leading to higher TAG content is balanced with a decrease of monogalactosyldiacylglycerol (MGDG) in the plastid via posttranslational inhibition of MGDG synthase enzymatic activity by NO. Intracellular and transient NO emission acts therefore at the basis of a nitrite-sensing and acclimating system, whereas a long exposure to NO can additionally induce a redirection of carbon to neutral lipids and a stress response.