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Whole-cell response to nitrogen deprivation in the diatom Phaeodactylum tricornutum
Whole-cell response to nitrogen deprivation in the diatom Phaeodactylum tricornutum
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Whole-cell response to nitrogen deprivation in the diatom Phaeodactylum tricornutum
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Whole-cell response to nitrogen deprivation in the diatom Phaeodactylum tricornutum
Whole-cell response to nitrogen deprivation in the diatom Phaeodactylum tricornutum

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Whole-cell response to nitrogen deprivation in the diatom Phaeodactylum tricornutum
Whole-cell response to nitrogen deprivation in the diatom Phaeodactylum tricornutum
Journal Article

Whole-cell response to nitrogen deprivation in the diatom Phaeodactylum tricornutum

2015
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Overview
Algal growth is strongly affected by nitrogen (N) availability. Diatoms, an ecologically important group of unicellular algae, have evolved several acclimation mechanisms to cope with N deprivation. In this study, we integrated physiological data with transcriptional and metabolite data to reveal molecular and metabolic modifications in N-deprived conditions in the marine diatom Phaeodactylum tricornutum. Physiological and metabolite measurements indicated that the photosynthetic capacity and chlorophyll content of the cells decreased, while neutral lipids increased in N-deprived cultures. Global gene expression analysis showed that P. tricornutum responded to N deprivation through an increase in N transport, assimilation, and utilization of organic N resources. Following N deprivation, reduced biosynthesis and increased recycling of N compounds like amino acids, proteins, and nucleic acids was observed at the transcript level. The majority of the genes associated with photosynthesis and chlorophyll biosynthesis were also repressed. Carbon metabolism was restructured through downregulation of the Calvin cycle and chrysolaminarin biosynthesis, and co-ordinated upregulation of glycolysis, the tricarboxylic acid cycle, and pyruvate metabolism, leading to funnelling of carbon sources to lipid metabolism. Finally, reallocation of membrane lipids and induction of de novo triacylglycerol biosynthesis directed cells to accumulation of neutral lipids.

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