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Genome-wide association of the metabolic shifts underpinning dark-induced senescence in Arabidopsis

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Zhu,  F.
Central Metabolism, Department Willmitzer, Max Planck Institute of Molecular Plant Physiology, Max Planck Society;

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Alseekh,  S.
The Genetics of Crop Metabolism, Department Willmitzer, Max Planck Institute of Molecular Plant Physiology, Max Planck Society;

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Tong,  H.
Mathematical Modelling and Systems Biology - Nikoloski, Cooperative Research Groups, Max Planck Institute of Molecular Plant Physiology, Max Planck Society;

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Nikoloski,  Z.
Mathematical Modelling and Systems Biology - Nikoloski, Cooperative Research Groups, Max Planck Institute of Molecular Plant Physiology, Max Planck Society;

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Naake,  T.
Central Metabolism, Department Willmitzer, Max Planck Institute of Molecular Plant Physiology, Max Planck Society;

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Brotman,  Y.
Genetics of Metabolic Traits, Cooperative Research Groups, Max Planck Institute of Molecular Plant Physiology, Max Planck Society;

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Fernie,  A. R.
Central Metabolism, Department Willmitzer, Max Planck Institute of Molecular Plant Physiology, Max Planck Society;

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Citation

Zhu, F., Alseekh, S., Koper, K., Tong, H., Nikoloski, Z., Naake, T., et al. (2021). Genome-wide association of the metabolic shifts underpinning dark-induced senescence in Arabidopsis. The Plant Cell. doi:10.1093/plcell/koab251.


Cite as: http://hdl.handle.net/21.11116/0000-0009-68C2-7
Abstract
Dark-induced senescence provokes profound metabolic shifts to recycle nutrients and to guarantee plant survival. To date, research on these processes has largely focused on characterizing mutants deficient in individual pathways. Here, we adopted a time-resolved genome-wide association-based approach to characterize dark-induced senescence by evaluating the photochemical efficiency and content of primary and lipid metabolites at the beginning, or after 3 or 6 days in darkness. We discovered six patterns of metabolic shifts and identified 215 associations with 81 candidate genes being involved in this process. Among these associations, we validated the roles of four genes associated with glycine, galactinol, threonine, and ornithine levels. We also demonstrated the function of threonine and galactinol catabolism during dark-induced senescence. Intriguingly, we determined that the association between tyrosine contents and TYROSINE AMINOTRANSFERASE 1 influences enzyme activity of the encoded protein and transcriptional activity of the gene under normal and dark conditions, respectively. Moreover, the single-nucleotide polymorphisms affecting the expression of THREONINE ALDOLASE 1 and the amino acid transporter gene AVT1B, respectively, only underlie the variation in threonine and glycine levels in the dark. Taken together, these results allow us to present a very detailed model of the metabolic aspects of dark-induced senescence, as well as the process itself.