The desert plant Phoenix dactylifera closes stomata via nitrate‐regulated SLAC1 anion channel. Issue 1 (3rd July 2017)

• Record Type: Journal Article
• Authors: Müller, Heike M.; Schäfer, Nadine; Bauer, Hubert; Geiger, Dietmar; Lautner, Silke; Fromm, Jörg; Riederer, Markus; Bueno, Amauri; Nussbaumer, Thomas; Mayer, Klaus; Alquraishi, Saleh A.; Alfarhan, Ahmed H.; Neher, Erwin; Al‐Rasheid, Khaled A. S.; Ache, Peter; Hedrich, Rainer
• Is Part Of: New phytologist. Volume 216:Issue 1(2017)
• Page Start: 150
• Page End: 162
• Publication Date: 2017-07-03
• Subjects: abscisic acid (ABA) signalling -- cuticle -- cuticular waxes -- date palm Phoenix dactylifera -- guard cells -- SLAC1 -- S‐type anion channel -- stomata; Botany -- Periodicals; 580
• DOI: 10.1111/nph.14672
• Languages: English
• ISSNs: 0028-646X

Abstract

Summary: Date palm Phoenix dactylifera is a desert crop well adapted to survive and produce fruits under extreme drought and heat. How are palms under such harsh environmental conditions able to limit transpirational water loss? Here, we analysed the cuticular waxes, stomata structure and function, and molecular biology of guard cells from P. dactylifera . To understand the stomatal response to the water stress phytohormone of the desert plant, we cloned the major elements necessary for guard cell fast abscisic acid (ABA) signalling and reconstituted this ABA signalosome in Xenopus oocytes. The Phoenix SLAC1‐type anion channel is regulated by ABA kinase PdOST1. Energy‐dispersive X‐ray analysis (EDXA) demonstrated that date palm guard cells release chloride during stomatal closure. However, in Cl − medium, PdOST1 did not activate the desert plant anion channel PdSLAC1 per se . Only when nitrate was present at the extracellular face of the anion channel did the OST1‐gated PdSLAC1 open, thus enabling chloride release. In the presence of nitrate, ABA enhanced and accelerated stomatal closure. Our findings indicate that, in date palm, the guard cell osmotic motor driving stomatal closure uses nitrate as the signal to open the major anion channel SLAC1. This initiates guard cell depolarization and the release of anions together with potassium. Abstract : See also the Commentary on this article by Hõrak, 216 : 5–7 .