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  - Subramanian, Hariharan
A1  - Döring, Frank
A1  - Kollert, Sina
A1  - Rukoyatkina, Natalia
A1  - Sturm, Julia
A1  - Gambaryan, Stepan
A1  - Stellzig-Eisenhauer, Angelika
A1  - Meyer-Marcotty, Philipp
A1  - Eigenthaler, Martin
A1  - Wischmeyer, Erhard
T1  - PTH1R Mutants Found in Patients with Primary Failure of Tooth Eruption Disrupt G-Protein Signaling
JF  - PLoS One
N2  - Aim

Primary failure of tooth eruption (PFE) is causally linked to heterozygous mutations of the parathyroid hormone receptor (PTH1R) gene. The mutants described so far lead to exchange of amino acids or truncation of the protein that may result in structural changes of the expressed PTH1R. However, functional effects of these mutations have not been investigated yet.

Materials and Methods

In HEK293 cells, PTH1R wild type was co-transfected with selected PTH1R mutants identified in patients with PFE. The effects on activation of PTH-regulated intracellular signaling pathways were analyzed by ELISA and Western immunoblotting. Differential effects of wild type and mutated PTH1R on TRESK ion channel regulation were analyzed by electrophysiological recordings in Xenopus laevis oocytes.

Results

In HEK293 cells, activation of PTH1R wild type increases cAMP and in response activates cAMP-stimulated protein kinase as detected by phosphorylation of the vasodilator stimulated phosphoprotein (VASP). In contrast, the PTH1R mutants are functionally inactive and mutant PTH1R/Gly452Glu has a dominant negative effect on the signaling of PTH1R wild type. Confocal imaging revealed that wild type PTH1R is expressed on the cell surface, whereas PTH1R/Gly452Glu mutant is mostly retained inside the cell. Furthermore, in contrast to wild type PTH1R which substantially augmented K+ currents of TRESK channels, coupling of mutated PTH1R to TRESK channels was completely abolished.

Conclusions

PTH1R mutations affect intracellular PTH-regulated signaling in vitro. In patients with primary failure of tooth eruption defective signaling of PTH1R mutations is suggested to occur in dento-alveolar cells and thus may lead to impaired tooth movement.
KW  - phosphorylation
KW  - xenopus oocytes
KW  - calcium signaling
KW  - intracellular receptors
KW  - mutation
KW  - teeth
KW  - tooth eruption
KW  - transfection
Y1  - 2016
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-147967
VL  - 11
IS  - 11
ER  -