Nitric oxide mediates nitrite-sensing and acclimation and triggers a remodeling of lipids

From National Research Council Canada

Download
  1. (PDF, 1 MB)
DOIResolve DOI: https://doi.org/10.1104/pp.17.01042
AuthorSearch for: ; Search for: ; Search for: ; Search for: ; Search for: ; Search for: ; Search for: ; Search for: ; Search for: ; Search for: ; Search for: ; Search for: ; Search for: 1; Search for: 1; Search for: ; Search for: ; Search for: 1; Search for:
Name affiliation
  1. National Research Council of Canada. Aquatic and Crop Resource Development
FormatText, Article
Journal titlePlant Physiology
ISSN0032-0889
1532-2548
Volume175
Issue3
Pages1407–1423
Subjectdiatoms; Phaeodactylum; nitric oxide; nitrogen cycle; NOA; triacylglycerol
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 phosphoenolpyruvate 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.
Publication date
PublisherAmerican Society of Plant Biologists
LanguageEnglish
Peer reviewedYes
NRC numberNRC-ACRD-56378
NPARC number23002593
Export citationExport as RIS
Report a correctionReport a correction
Record identifier5de6e632-ec22-4e7a-a6df-47eebc07f326
Record created2017-12-05
Record modified2020-06-04
Report a problem on this page
Date modified: