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β-Amino-butyric acid protects Arabidopsis against low potassium stress
Potassium (K + ) is an essential element for plant growth and development. Under low-K + stress, Arabidopsis ( Arabidopsis thaliana ) plants show K + -deficient symptoms, typically leaf chlorosis and subsequent inhibition of plant growth and development. The non-protein amino acid β-amino-butyric ac...
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Published in: | Acta physiologiae plantarum 2008-05, Vol.30 (3), p.309-314 |
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Main Authors: | , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Potassium (K
+
) is an essential element for plant growth and development. Under low-K
+
stress,
Arabidopsis
(
Arabidopsis thaliana
) plants show K
+
-deficient symptoms, typically leaf chlorosis and subsequent inhibition of plant growth and development. The non-protein amino acid β-amino-butyric acid (BABA) has been shown to have roles in protecting
Arabidopsis
against various pathogens as well as drought, high salinity, and cadmium stresses; However, little is known about the role of BABA in protecting
Arabidopsis
against low-K
+
stress. Here, we showed that BABA protects
Arabidopsis
against low-K
+
stress by increasing K
+
uptake under low-K
+
condition. Leaf chlorosis of plants subjected to low-K
+
stress was abolished by BABA pretreatment, as indicated by a lower reduction in chlorophyll content in BABA-treated plants than water-treated plants. Low-K
+
stress-induced decreases in both lateral root length and the numbers of lateral roots were improved by BABA pretreatment. In addition, under low-K
+
stress, a significantly higher K
+
concentration was detected in BABA-pretreated plants than in water-treated plants, and the transcript levels of
AtHAK5
and
LKS1
genes involved in K
+
uptake in BABA-treated plants were higher than those of water-treated plants. Taken together, our results suggest that BABA plays a role in enhancing low-K
+
stress tolerance by increasing K
+
uptake, at least in part, via modulation of
AtHAK5
and
LKS1
under low-K
+
condition. |
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ISSN: | 0137-5881 1861-1664 |
DOI: | 10.1007/s11738-007-0122-6 |