Ohto Masa-Aki, Hayashi Shingo, Sawa Shinichiro, Hashimoto-Ohta Akiko, Nakamura Kenzo
Division of Developmental Biology, National Institute for Basic Biology, Myodaiji-cho, Okazaki, 444-8585 Japan.
Plant Cell Physiol. 2006 Dec;47(12):1603-11. doi: 10.1093/pcp/pcl027. Epub 2006 Oct 27.
Sugar regulates a variety of genes and controls plant growth and development similarly to phytohormones. As part of a screen for Arabidopsis mutants with defects in sugar-responsive gene expression, we identified a loss-of-function mutation in the HOOKLESS1 (HLS1) gene. HLS1 was originally identified to regulate apical hook formation of dark-grown seedlings (Lehman et al., 1996, Cell 85: 183-194). In hls1, sugar-induced gene expression in excised leaf petioles was more sensitive to exogenous sucrose than that in the wild type. Exogenous IAA partially repressed sugar-induced gene expression and concomitantly activated some auxin response genes such as AUR3 encoding GH3-like protein. The repression and the induction of gene expression by auxin were attenuated and enhanced, respectively, by the hls1 mutation. These results suggest that HLS1 plays a negative role in sugar and auxin signaling. Because AUR3 GH3-like protein conjugates free IAA to amino acids (Staswick et al., 2002, Plant Cell 14: 1405-1415; Staswick et al., 2005, Plant Cell 17: 616-627), enhanced expression of GH3-like genes would result in a decrease in the free IAA level. Indeed, hls1 leaves accumulated a reduced level of free IAA, suggesting that HLS1 may be involved in negative feedback regulation of IAA homeostasis through the control of GH3-like genes. We discuss the possible mechanisms by which HLS1 is involved in auxin signaling for sugar- and auxin-responsive gene expression and in IAA homeostasis.
糖与植物激素类似,可调控多种基因并控制植物的生长和发育。作为筛选糖响应基因表达存在缺陷的拟南芥突变体的一部分,我们鉴定出了HOOKLESS1(HLS1)基因的功能缺失突变。HLS1最初被鉴定为调控暗生长幼苗的顶端弯钩形成(Lehman等人,1996年,《细胞》85卷:183 - 194页)。在hls1突变体中,离体叶柄中糖诱导的基因表达对外源蔗糖比野生型更敏感。外源吲哚 - 3 - 乙酸(IAA)部分抑制了糖诱导的基因表达,并同时激活了一些生长素响应基因,如编码GH3类蛋白的AUR3。生长素对基因表达的抑制和诱导分别因hls1突变而减弱和增强。这些结果表明,HLS1在糖和生长素信号传导中起负向作用。由于AUR3 GH3类蛋白将游离IAA与氨基酸结合(Staswick等人,2002年,《植物细胞》14卷:1405 - 1415页;Staswick等人,2005年,《植物细胞》17卷:616 - 627页),GH3类基因表达增强会导致游离IAA水平降低。实际上,hls1叶片中游离IAA的积累水平降低,这表明HLS1可能通过控制GH3类基因参与IAA稳态的负反馈调节。我们讨论了HLS1参与糖和生长素响应基因表达的生长素信号传导以及IAA稳态的可能机制。