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 − ABAleon2.1 − treated with NAD+ showed increases in ABA content suggesting that NAD+ impacts on stomatal development through ABA synthesis and signaling. Our results demonstrate that intracellular NAD+ homeostasis as set by synthesis, breakdown and transport is essential for normal stomatal development, and provide a link between central metabolism, hormone signaling and developmental plasticity.
As sessile organisms, plants must adapt their physiology and developmental processes to cope with challenging environmental circumstances, such as the ongoing elevation in atmospheric carbon dioxide (CO 2 ) levels. Nicotinamide adenine dinucleotide (NAD + ) is a cornerstone of plant metabolism and plays an essential role in redox homeostasis. Given that plants impaired in NAD metabolism and transport often display growth defects, low seed production and disturbed stomatal development/movement, we hypothesized that subcellular NAD distribution could be a candidate for plants to exploit the effects of CO 2 fertilization. We report that an efficient subcellular NAD + distribution is required for the fecundity-promoting effects of elevated CO 2 levels. Plants with reduced expression of either mitochondrial (NDT1 or NDT2) or peroxisomal (PXN) NAD + transporter genes grown under elevated CO 2 exhibited reduced total leaf area compared with the wild-type while PXN mutants also displayed reduced leaf number. NDT2 and PXN lines grown under elevated CO 2 conditions displayed reduced rosette dry weight and lower photosynthetic rates coupled with reduced stomatal conductance. Interestingly, high CO 2 doubled seed production and seed weight in the wild-type, whereas the mutants were less responsive to increases in CO 2 levels during reproduction, producing far fewer seeds than the wild-type under both CO 2 conditions. These data highlight the importance of mitochondrial and peroxisomal NAD + uptake mediated by distinct NAD transporter proteins to modulate photosynthesis and seed production under high CO 2 levels.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.