Effect of Soil Salinity on the Expression of Betaine Aldehyde Dehydrogenase in Leaves: Investigation of Hydraulic, Ionic and Biochemical Signals.

1992 ◽  
Vol 19 (5) ◽  
pp. 555 ◽  
Author(s):  
KF Mccue ◽  
AD Hanson

Betaine aldehyde dehydrogenase (BADH) catalyses the last step in glycine betaine synthesis. The levels of BADH enzyme and BADH mRNA have previously been shown to be increased several-fold by salt stress. To characterise this induction more thoroughly, BADH mRNA levels and enzyme activities were analysed in leaves of sugar beet plants (Beta vulgaris L.) subjected to different salinisation regimes. Following a salt shock (transfer from 0 to 400 mM NaCI) BADH enzyme activity rose slowly for several days. In contrast, BADH mRNA level first decreased for several hours, and then increased. When salt was leached from the rooting medium of salinised plants, BADH enzyme activity declined, with a half-life of more than 4 days. However, the level of BADH mRNA declined sharply with an apparent half-life of 2 h showing that transcription of the BADH gene or the stability of BADH mRNA in leaves can respond very dynamically to salinity changes around the root. In plants which had been gradually salinised and then held at various NaCl concentrations, the steady state level of enzyme rose continuously between 0 and 500 mM NaCl, whereas that of BADH mRNA reached a plateau at 100 mM NaCl. In general, the observed BADH mRNA fluctuations could not be satisfactorily explained by assuming them to be responses to hydraulic signals. This suggests the participation of a non-hydraulic signal or signals coming from the root. The non-hydraulic signal is unlikely to be NaCl, because leaf disks exposed to salt concentrations typical of the apoplast of salinised leaves did not accumulate BADH mRNA. A biochemical messenger is thus implied. Although abscisic acid application to leaf disks elicited significant increases in BADH mRNA level, these were several-fold smaller than those observed in leaves of intact salinised plants, suggesting the involvement of some other substance.

Author(s):  
Ramses Cruz-Valencia ◽  
Aldo A. Arvizu-Flores ◽  
Jesús A. Rosas-Rodríguez ◽  
Elisa M. Valenzuela-Soto

1996 ◽  
Vol 317 (3) ◽  
pp. 925-931 ◽  
Author(s):  
Volker DANGEL ◽  
Jeanette GIRAY ◽  
Dieter RATGE ◽  
Hermann WISSER

The regulation of the expression of β-adrenoceptors (β-ARs) is not thoroughly understood. We demonstrate that the rat heart cell-line H9c2 expresses both β1- and β2-ARs. In radioligand-binding experiments, the maximal binding capacity of (-)-[125I]-iodocyanopindolol was determined as 18±0.6 fmol/mg of protein with a KD of 35.4±4.1 pM. Competitive radioligand-binding experiments with subtype-specific β-antagonists reveal a subtype ratio of β1- to β2-ARs of 29%:71%. With competitive reverse-transcriptase PCR we found β2-mRNA to be up to 1600 times more frequent than β1-mRNA. Treatment of the H9c2 cell-line with the β-adrenergic agonist (-)-isoproterenol (10-6 M), the antagonist (-)-propranolol (10-6 M) and the glucocorticoid dexamethasone (500 nM) induces regulatory effects on both the β-AR protein and mRNA level. Isoproterenol treatment leads to down-regulation of the total receptor number by 56±4%, due to a decrease in β2-ARs, while maintaining the β1-AR number constant. On the transcription level, both β1-and β2-mRNAs are decreased by 30% and 42% respectively. mRNA stability measurements reveal a reduced half-life of β2-mRNA from 9.3 h to 6.5 h after isoproterenol treatment. Incubation of cells with (-)-propranolol does not affect the amounts of β-ARs and their mRNAs. Dexamethasone induces a 1.8±0.2-fold increase in β-AR number over the basal level as well as a 1.9±0.2-fold increase in the amount of β2-mRNA. Because the half-life of β2-mRNA was unaffected by dexamethasone, the increased β2-mRNA level must be due to an enhanced transcription rate. The β1-mRNA levels are unchanged during dexamethasone-incubation of the cells. Our data clearly demonstrate that treatment of H9c2 rat heart cells with isoproterenol and dexamethasone induces alterations in the level of RNA stability as well as gene transcription, leading to altered receptor numbers.


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