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Plant Mol Biol. 2004 Jul;55(5):663-77.

The homeobox genes ATHB12 and ATHB7 encode potential regulators of growth in response to water deficit in Arabidopsis.

Author information

1
Department of Physiological Botany, Evolutionary Biology Centre, University of Uppsala, Villavägen 6, SE-752 36 Uppsala, Sweden.

Abstract

The Arabidopsis thaliana homeodomain leucine-zipper gene ATHB7 , which is active specifically under water deficit conditions, is proposed to act as a negative regulator of growth (Soderman et al ., 1996, Plant J. 10: 375 381; Hjellstrom et al ., 2003, Plant Cell Environ 26: 1127 1136). In this report we demonstrate that the paralogous gene, ATHB12 , has a similar expression pattern and function. ATHB12 ,like ATHB7 ,was up-regulated during water deficit conditions, the up-regulation being dependent on abscisic acid (ABA) and on the activity of the Ser/Thr phosphatases ABI1 and ABI2. Plants that are mutant for ATHB12 , as a result of T-DNA insertions in the ATHB12 gene, showed a reduced sensitivity to ABA in root elongation assays, whereas transgenic Arabidopsis plants expressing ATHB12 and/or ATHB7 as driven by the CaMV 35S promoter were hypersensitive in this response compared to wild-type. High-level expression of either gene also resulted in a delay in inflorescence stem elongation growth and caused plants to develop rosette leaves with a more rounded shape, shorter petioles, and increased branching of the inflorescence stem. Transgenic Arabidopsis plants expressing the reporter gene uidA under the control of the ATHB12 promoter showed marker gene activity in axillary shoot primordia, lateral root primordia, inflorescence stems and in flower organs. Treatment of plants with ABA or water deficit conditions caused the activity of ATHB12 to increase in the inflorescence stem, the flower organs and the leaves, and to expand into the vasculature of roots and the differentiation/elongation zone of root tips. Taken together, these results indicate that ATHB12 and ATHB7 act to mediate a growth response to water deficit by similar mechanisms.

PMID:
15604708
DOI:
10.1007/s11103-004-1581-4
[Indexed for MEDLINE]

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