Over-expression of an AT-hook gene, AHL22, delays flowering and inhibits the elongation of the hypocotyl in Arabidopsis thaliana
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The Arabidopsis genome encodes 29 AHL (AT-hook motif nuclear localized) proteins, but the function for most of them remains unknown. We report here a study of the AHL22 gene, which was originally identified as a gain-of-function allele that enhanced the phenotype of the cry1 cry2 mutant. AHL22 is a nuclear protein with the binding activity for an AT-rich DNA sequence. AHL22 overexpression delayed flowering and caused a constitutive photomorphogenic phenotype. The loss-of-function AHL22 mutant showed no clear phenotype on flowering, but slightly longer hypocotyls. However, silencing four AHL genes (AHL22, AHL18, AHL27, and AHL29) resulted in early flowering and enhanced ahl22-1 mutant phenotype on the growth of hypocotyls, suggesting genetic redundancy of AHL22 with other AHL genes on these plant developmental events. Further analysis showed that AHL22 controlled flowering and hypocotyl elongation might result from primarily the regulation of FT and PIF4 expression, respectively.
KeywordsArabidopsis thaliana AT-hook Flowering time Hypocotyl Photomorphogenesis
Thanks to Drs. Bekir Ülker and Jane Parker for kindly providing pJawohl8-RNAi and pLeela vectors, and to Dr. Robert Koebner for his critical reading of the manuscript. This work was supported in part by the National ‘‘863’’ Program of China (2006AA10A111, 2006AA10Z107, and 2007AA10Z119), the National Key Basic Research ‘973’ Program of China (2004CB117206), the Key Technology R & D Program (2007BAD59B02), National Science Foundation of China (30671245), National Institute of Health (GM56265), and UCLA faculty research and Sol Leshin BGU-UCLA Academic Cooperation programs.
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