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Changes in intracellular NAD status affect stomatal development in an abscisic acid-dependent manner

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Medeiros,  D.B.
Central Metabolism, Department Willmitzer, Max Planck Institute of Molecular Plant Physiology, Max Planck Society;

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de Souza,  L. P.
Central Metabolism, Department Willmitzer, Max Planck Institute of Molecular Plant Physiology, Max Planck Society;

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Yoshida,  T.
Central Metabolism, Department Willmitzer, 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

Feitosa-Araujo, E., da Fonseca Pereira, P., Miranda Pena, M., Medeiros, D., de Souza, L. P., Yoshida, T., et al. (2020). Changes in intracellular NAD status affect stomatal development in an abscisic acid-dependent manner. The Plant Journal. Retrieved from https://doi.org/10.1111/tpj.15000.


Cite as: http://hdl.handle.net/21.11116/0000-0007-85DE-9
Abstract
SUMMARY Nicotinamide adenine dinucleotide (NAD) plays a central role in redox metabolism in all domains of life. Additional roles in regulating posttranslational protein modifications and cell signaling implicate NAD as a potential integrator of central metabolism and programs regulating stress responses and development. Here we found that NAD negatively impacts stomatal development in cotyledons of Arabidopsis thaliana. Plants with reduced capacity for NAD+ transport from the cytosol into the mitochondria or the peroxisomes exhibited reduced numbers of stomatal lineage cells and reduced stomatal density. Cotyledons of plants with reduced NAD+ breakdown capacity and NAD+-treated cotyledons also presented reduced stomatal number. Expression of stomatal lineage-related genes was repressed in plants with reduced expression of NAD+ transporters as well as in plants treated with NAD+. Impaired NAD+ transport was further associated with an induction of abscisic acid (ABA)-responsive genes. Inhibition of ABA synthesis rescued the stomatal phenotype in mutants deficient in intracellular NAD+ transport, whereas exogenous NAD+ feeding of aba-2 and ost1 seedlings, impaired in ABA synthesis and ABA signaling respectively, did not impact stomatal number, placing NAD upstream of ABA. Additionally, in vivo measurement of ABA dynamics in seedlings of an ABA-specific optogenetic reporter