Managing activity and Ca2+ dependence through mutation in the Junction of the AtCPK1 coordinates the salt tolerance in transgenic tobacco plants

Copyright © 2021 Elsevier Masson SAS. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Plant physiology and biochemistry : PPB. - 1991. - 165(2021) vom: 07. Aug., Seite 104-113
1. Verfasser: Veremeichik, G N (VerfasserIn)
Weitere Verfasser: Shkryl, Y N, Silantieva, S A, Gorpenchenko, T Y, Brodovskaya, E V, Yatsunskaya, M S, Bulgakov, V P
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2021
Zugriff auf das übergeordnete Werk:Plant physiology and biochemistry : PPB
Schlagworte:Journal Article Arabidopsis Calcium-dependent protein kinases Heat shock factors Nicotiana tabacum Reactive oxygen species Salt tolerance Plant Proteins
Beschreibung
Zusammenfassung:Copyright © 2021 Elsevier Masson SAS. All rights reserved.
Calcium-dependent protein kinases (CDPKs) are Ca2+ decoders in plants. AtCPK1 is a positive regulator in the plant response to biotic and abiotic stress. Inactivation of the autoinhibitory domain of AtCPK1 in the mutated form KJM23 provides constitutive activity of the kinase. In the present study, we investigated the effect of overexpressed native and mutant KJM23 forms on salinity tolerance in Nicotiana tabacum. Overexpression of native AtCPK1 provided tobacco resistance to 120 mM NaCl during germination and 180 mM NaCl during long-term growth, while the resistance of plants increased to 240 mM NaCl during both phases of plant development when transformed with KJM23. Mutation in the junction KJM4, which disrupted Ca2+ induced activation, completely nullified the acquired salt tolerance up to levels of normal plants. Analysis by confocal microscopy showed that under high salinity conditions, overexpression of AtCPK1 and KJM23 inhibited reactive oxygen species (ROS) accumulation to levels observed in untreated plants. Quantitative real-time PCR analysis showed that overexpression of AtCPK1 and KJM23 was associated with changes in expression of genes encoding heat shock factors. In all cases, the KJM23 mutation enhanced the effect of AtCPK1, while the KJM4 mutation reduced it to the control level. We suggest that the autoinhibitory domains in CDPKs could be promising targets for manipulation in engineering salt-tolerant plants
Beschreibung:Date Completed 15.06.2021
Date Revised 13.12.2023
published: Print-Electronic
Citation Status MEDLINE
ISSN:1873-2690
DOI:10.1016/j.plaphy.2021.05.026