Abstract
Aluminum (Al) stress is a major limiting factor for plant growth and crop production in acid soils. At present, only a few transcription factors involved in the regulation of Al resistance have been characterized. Here, we used reversed genetic approach through phenotype analysis of overexpressors and mutants to demonstrate that AtHB7 and AtHB12, two HD-Zip I transcription factors, participate in Al resistance. In response to Al stress, AtHB7 and AtHB12 displayed different dynamic expression patterns. Although both AtHB7 and AtHB12 positively regulate root growth in the absence of Al stress, our results showed that AtHB7 antagonizes with AtHB12 to control root growth in response to Al stress. The athb7/12 double mutant displayed a wild-type phenotype under Al stress. Consistently, our physiological analysis showed that AtHB7 and AtHB12 oppositely regulate the capacity of cell wall to bind Al. Yeast two hybrid assays showed that AtHB7 and AtHB12 could form homo-dimers and hetero-dimers in vitro, suggesting the interaction between AtHB7 and AtHB12 in the regulation of root growth. The conclusion was that AtHB7 and AtHB12 oppositely regulate Al resistance by affecting Al accumulation in root cell wall.
Highlights
A major factor constraint crop production on acidic soils worldwide is aluminum (Al) toxicity [1]
The root transition zone (TZ), located between the apical meristem and basal elongation zone (EZ) in root apex, is the critical site of perception of Al toxicity, which has been reported in the model plant Arabidopsis (Arabidopsis thaliana), wheat (Triticum aestivum), maize (Zea mays), sorghum (Sorghum bicolor), and common bean (Phaseolus vulgaris) [6,7,8,9,10,11]
AtHB7 and AtHB12 Induced by Al Stress, Which Was Independent of SENSITIVE TO PROTON RHIZOTOXICITY1 (STOP1)
Summary
A major factor constraint crop production on acidic soils worldwide is aluminum (Al) toxicity [1]. In response to Al stress, both AtALMT1 (Al-activated Malate Transporter1) and AtMATE (Multidrug and Toxic Compound Extrusion) were significantly up-regulated at transcription levels, which caused the secretion of malic acid and cirtic acid into rhizosphere for Al chelation, and alleviated Al-induced inhibition of root elongation [29,30]. Since AtHB7 and AtHB12 as two members of HD-ZIP I subfamily play important roles in regulation of tolerance to abiotic stress and were significantly induced by Al, we speculated that these two transcription factors might relate to regulation of Al resistance. We showed that AtHB7 and AtHB12 acted in a cooperative manner under normal condition but in an antagonistic manner to regulate primary root growth under Al treatment
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