TY  - JOUR
A1  - Graus, Dorothea
A1  - Li, Kunkun
A1  - Rathje, Jan M.
A1  - Ding, Meiqi
A1  - Krischke, Markus
A1  - Müller, Martin J.
A1  - Cuin, Tracey Ann
A1  - Al‐Rasheid, Khaled A. S.
A1  - Scherzer, Sönke
A1  - Marten, Irene
A1  - Konrad, Kai R.
A1  - Hedrich, Rainer
T1  - Tobacco leaf tissue rapidly detoxifies direct salt loads without activation of calcium and SOS signaling
JF  - New Phytologist
N2  - Salt stress is a major abiotic stress, responsible for declining agricultural productivity. Roots are regarded as hubs for salt detoxification, however, leaf salt concentrations may exceed those of roots. How mature leaves manage acute sodium chloride (NaCl) stress is mostly unknown.

To analyze the mechanisms for NaCl redistribution in leaves, salt was infiltrated into intact tobacco leaves. It initiated pronounced osmotically‐driven leaf movements. Leaf downward movement caused by hydro‐passive turgor loss reached a maximum within 2 h.

Salt‐driven cellular water release was accompanied by a transient change in membrane depolarization but not an increase in cytosolic calcium ion (Ca\(^{2+}\)) level. Nonetheless, only half an hour later, the leaves had completely regained turgor. This recovery phase was characterized by an increase in mesophyll cell plasma membrane hydrogen ion (H\(^{+}\)) pumping, a salt uptake‐dependent cytosolic alkalization, and a return of the apoplast osmolality to pre‐stress levels. Although, transcript numbers of abscisic acid‐ and Salt Overly Sensitive pathway elements remained unchanged, salt adaptation depended on the vacuolar H\(^{+}\)/Na\(^{+}\)‐exchanger NHX1.

Altogether, tobacco leaves can detoxify sodium ions (Na\(^{+}\)) rapidly even under massive salt loads, based on pre‐established posttranslational settings and NHX1 cation/H+ antiport activity. Unlike roots, signaling and processing of salt stress in tobacco leaves does not depend on Ca\(^{2+}\) signaling.
KW  - calcium signaling
KW  - cytosolic pH
KW  - leaf response
KW  - NaCl transport
KW  - NHX1
KW  - osmotic effects
KW  - Salt Overly Sensitive pathway
KW  - salt stress
Y1  - 2023
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-312152
VL  - 237
IS  - 1
SP  - 217
EP  - 231
ER  - 
TY  - JOUR
A1  - Planes, Maria D.
A1  - Niñoles, Regina
A1  - Rubio, Lourdes
A1  - Bissoli, Gaetano
A1  - Bueso, Eduardo
A1  - García-Sánchez, María J.
A1  - Alejandro, Santiago
A1  - Gonzalez-Guzmán, Miguel
A1  - Hedrich, Rainer
A1  - Rodriguez, Pedro L.
A1  - Fernández, José A.
A1  - Serrano, Ramón
T1  - A mechanism of growth inhibition by abscisic acid in germinating seeds of Arabidopsis thaliana based on inhibition of plasma membrane \(H^+\)-ATPase and decreased cytosolic pH, \(K^+\), and anions
JF  - Journal of Experimental Botany
N2  - The stress hormone abscisic acid (ABA) induces expression of defence genes in many organs, modulates ion homeostasis and metabolism in guard cells, and inhibits germination and seedling growth. Concerning the latter effect, several mutants of Arabidopsis thaliana with improved capability for \(H^+\) efflux (wat1-1D, overexpression of AKT1 and ost2-1D) are less sensitive to inhibition by ABA than the wild type. This suggested that ABA could inhibit \(H^+\) efflux (\(H^+\)-ATPase) and induce cytosolic acidification as a mechanism of growth inhibition. Measurements to test this hypothesis could not be done in germinating seeds and we used roots as the most convenient system. ABA inhibited the root plasma-membrane H+-ATPase measured in vitro (ATP hydrolysis by isolated vesicles) and in vivo (\(H^+\) efflux from seedling roots). This inhibition involved the core ABA signalling elements: PYR/PYL/RCAR ABA receptors, ABA-inhibited protein phosphatases (HAB1), and ABA-activated protein kinases (SnRK2.2 and SnRK2.3). Electrophysiological measurements in root epidermal cells indicated that ABA, acting through the PYR/PYL/RCAR receptors, induced membrane hyperpolarization (due to \(K^+\) efflux through the GORK channel) and cytosolic acidification. This acidification was not observed in the wat1-1D mutant. The mechanism of inhibition of the \(H^+\)-ATPase by ABA and its effects on cytosolic pH and membrane potential in roots were different from those in guard cells. ABA did not affect the in vivo phosphorylation level of the known activating site (penultimate threonine) of (\(H^+\)-ATPase in roots, and SnRK2.2 phosphorylated in vitro the C-terminal regulatory domain of (\(H^+\)-ATPase while the guard-cell kinase SnRK2.6/OST1 did not.
KW  - ABA receptors
KW  - cytosolic pH
KW  - ion channels
KW  - microelectrodes
KW  - protein kinase
KW  - proton efflux
Y1  - 2015
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-121221
VL  - 66
IS  - 3
ER  -