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Hexokinase is necessary for glucose-mediated photosynthesis repression and lipid accumulation in a green alga

Global primary production is driven largely by oxygenic photosynthesis, with algae as major contributors. The green alga Chromochloris zofingiensis reversibly switches off photosynthesis in the presence of glucose in the light and augments production of biofuel precursors (triacylglycerols) and the...

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Bibliographic Details
Published in:Communications biology 2019-09, Vol.2 (1), p.347-347, Article 347
Main Authors: Roth, Melissa S., Westcott, Daniel J., Iwai, Masakazu, Niyogi, Krishna K.
Format: Article
Language:English
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Summary:Global primary production is driven largely by oxygenic photosynthesis, with algae as major contributors. The green alga Chromochloris zofingiensis reversibly switches off photosynthesis in the presence of glucose in the light and augments production of biofuel precursors (triacylglycerols) and the high-value antioxidant astaxanthin. Here we used forward genetics to reveal that this photosynthetic and metabolic switch is mediated by the glycolytic enzyme hexokinase (CzHXK1). In contrast to wild-type, glucose-treated hxk1 mutants do not shut off photosynthesis or accumulate astaxanthin, triacylglycerols, or cytoplasmic lipid droplets. We show that CzHXK1 is critical for the regulation of genes related to photosynthesis, ketocarotenoid synthesis and fatty acid biosynthesis. Sugars play fundamental regulatory roles in gene expression, physiology, metabolism, and growth in plants and animals, and we introduce a relatively simple, emerging model system to investigate conserved eukaryotic sugar sensing and signaling at the base of the green lineage. In plants, exogenous glucose represses photosynthesis but this phenomenon has been little studied in green algae. Roth et. al. discover through a forward genetics screen in C. zofingiensis that hexokinase 1 is needed to turn off photosynthesis in the presence of glucose and for glucose-mediated upregulation of lipid metabolism.
ISSN:2399-3642
2399-3642
DOI:10.1038/s42003-019-0577-1