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Ruschhaupt, M.* ; Mergner, J.* ; Mucha, S.* ; Papacek, M.* ; Doch, I.* ; Tischer, S.V.* ; Hemmler, D. ; Chiasson, D.* ; Edel, K.H.* ; Kudla, J.* ; Schmitt-Kopplin, P. ; Kuster, B.* ; Grill, E.*

Rebuilding core abscisic acid signaling pathways of Arabidopsis in yeast.

EMBO J. 38:e101859 (2019)
Publ. Version/Full Text Research data DOI PMC
Open Access Gold (Paid Option)
Creative Commons Lizenzvertrag
The phytohormone abscisic acid (ABA) regulates plant responses to abiotic stress, such as drought and high osmotic conditions. The multitude of functionally redundant components involved in ABA signaling poses a major challenge for elucidating individual contributions to the response selectivity and sensitivity of the pathway. Here, we reconstructed single ABA signaling pathways in yeast for combinatorial analysis of ABA receptors and coreceptors, downstream-acting SnRK2 protein kinases, and transcription factors. The analysis shows that some ABA receptors stimulate the pathway even in the absence of ABA and that SnRK2s are major determinants of ABA responsiveness by differing in the ligand-dependent control. Five SnRK2s, including SnRK2.4 known to be active under osmotic stress in plants, activated ABA-responsive transcription factors and were regulated by ABA receptor complexes in yeast. In the plant tissue, SnRK2.4 and ABA receptors competed for coreceptor interaction in an ABA-dependent manner consistent with a tight integration of SnRK2.4 into the ABA signaling pathway. The study establishes the suitability of the yeast system for the dissection of core signaling cascades and opens up future avenues of research on ligand-receptor regulation.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords Abscisic Acid ; Abf ; Abiotic Stress ; Clade A Pp2c ; Rcar ; Pyl ; Pyr1 ; Snrk2; Different Phosphorylation Mechanisms; Activated Protein-kinases; Osmotic-stress; Hyperosmotic Stress; Gene-expression; Snrk2 Kinases; Water-use; Aba; Identification; Receptors
ISSN (print) / ISBN 0261-4189
e-ISSN 1460-2075
Quellenangaben Volume: 38, Issue: 17, Pages: , Article Number: e101859 Supplement: ,
Publisher Wiley
Publishing Place Heidelberg, Germany
Non-patent literature Publications
Reviewing status Peer reviewed