The role of Jasmonic Acid (JA) and Abscisic Acid (ABA) in salt resistance of maize (Zea mays L.)
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Salt stress is a major constraint to crop production. The expansion of young growing leaves isarrested by osmotic problems faced by roots in the first phase of salt stress. The leaf growth ofsalt-sensitive maize genotype Pioneer 3906 has been shown to be limited due to reducedplasmalemma H+-ATPase proton pumping into the leaf apoplast. This leads to a loweracidification of the cell wall, which according to the acid growth theory decreases the cellwallextensibility and cell elongation. However cell-wall acidification of a newly developedmaize hybrid SR 03 does not change and therefore accounts for its resistance during the firstphase of salt stress. It has been proposed in some studies that the events that limit leaf growthfollowing osmotic stress are controlled by root-sourced signals. Inhibition of leaf growth bysalt stress is a complex mechanism and may involve multiple signals. So it was assumed thatthe salt resistance of SR 03 may involve a signal distinct from that of salt-sensitive ones ordiffers in pathway of a common signal. The hormonal signal abscisic acid (ABA) accumulatesin plant tissues under salt stress and the maize genotypes differing in salt resistance haveshown variations in ABA synthesis. In addition there are also some indications that the stresshormone jasmonic acid (JA) also takes part in osmotic stress signaling.The aims of the current study were to test the hypotheses that I) salt stress stimulates thesynthesis of JA in the root and shoot tissues of maize genotypes II) leaf growth andacidification of the leaf apoplast in maize genotypes during the first phase of salt stress arecontrolled by long-distance signaling of JA and/or ABA; III) differential acidification of theleaf apoplast in maize genotypes in response to salt stress is caused by differential expressionof plasmalemma H+-ATPase isoforms; IV) variation of maize genotypes in salt resistanceduring the first phase of salt stress depends on the type of hormone signal and/or thesensitivity to these signals.The results obtained in this study support the following conclusions:1. Increased concentrations of JA in root tissues of only salt-sensitive Acoss 8023showed that JA signaling is different in maize genotypes of variable sensitivity duringthe first phase of salt stress. JA improved Na+ exclusion at the root surface.2. The expansion of young leaves was significantly reduced during the first phase of saltstress and the reduction was more pronounced in salt-sensitive Pioneer 3906 ascompared to the salt-resistant SR 03. A similar pattern of leaf growth inhibition byexogenous ABA in both maize genotypes supports the hypothesis that leaf growthduring the first phase of salt stress is controlled by ABA. In comparison to saltsensitivePioneer 3906, leaf expansion of salt-resistant SR 03 was less sensitive toABA-induced inhibition and is responsible for the resistance of SR 03 during the firstphase of salt stress.3. The decrease in cell-wall acidification due to lower plasmalemma H+-ATPase protonpumping during the first phase of salt stress is a major cause of reduction in leafexpansion of salt-sensitive Pioneer 3906. The results reported in this study provideevidence that the partial inhibition of plasmalemma H+-ATPase proton pumping inleaves of Pioneer 3906 under salt stress involves ABA signaling, which downregulatesthe transcription of MHA3. The data support the conclusion that MHA3 is anefficient isoform of H+-ATPase with higher H+/ATP coupling ratio. Unchanged levelsof enzyme concentration in the membranes of the ABA and salt-treated plants showthat the ABA-induced down regulation of MHA3 is compensated with the upregulationof an unknown inefficient isoform.4. In contrast, H+-ATPase proton pumping and cell-wall acidification remainedunaffected in leaves of salt-resistant SR 03 during the first phase of salt stress. Adifferential response of MHA3 transcription to ABA reduced the sensitivity of SR 03to ABA-induced inhibition of leaf growth and therefore contributed to the saltresistance of SR 03.Verknüpfung zu Publikationen oder weiteren Datensätzen
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Giessen : VVB Laufersweiler