Suzuki Masashi, Yamazaki Chiaki, Mitsui Marie, Kakei Yusuke, Mitani Yuka, Nakamura Ayako, Ishii Takahiro, Soeno Kazuo, Shimada Yukihisa
Kihara Institute for Biological Research, Yokohama City University, 641-12 Maioka-cho, Totsuka-ku, Yokohama, Kanagawa, 244-0813, Japan.
Plant Cell Rep. 2015 Aug;34(8):1343-52. doi: 10.1007/s00299-015-1791-z. Epub 2015 Apr 23.
The IPyA pathway, the major auxin biosynthesis pathway, is transcriptionally regulated through a negative feedback mechanism in response to active auxin levels. The phytohormone auxin plays an important role in plant growth and development, and levels of active free auxin are determined by biosynthesis, conjugation, and polar transport. Unlike conjugation and polar transport, little is known regarding the regulatory mechanism of auxin biosynthesis. We discovered that expression of genes encoding indole-3-pyruvic acid (IPyA) pathway enzymes is regulated by elevated or reduced active auxin levels. Expression levels of TAR2, YUC1, YUC2, YUC4, and YUC6 were downregulated in response to synthetic auxins [1-naphthaleneacetic acid (NAA) and 2,4-dichlorophenoxyacetic acid (2,4-D)] exogenously applied to Arabidopsis thaliana L. seedlings. Concomitantly, reduced levels of endogenous indole-3-acetic acid (IAA) were observed. Alternatively, expression of these YUCCA genes was upregulated by the auxin biosynthetic inhibitor kynurenine in Arabidopsis seedlings, accompanied by reduced IAA levels. These results indicate that expression of YUCCA genes is regulated by active auxin levels. Similar results were also observed in auxin-overproduction and auxin-deficient mutants. Exogenous application of IPyA to Arabidopsis seedlings preincubated with kynurenine increased endogenous IAA levels, while preincubation with 2,4-D reduced endogenous IAA levels compared to seedlings exposed only to IPyA. These results suggest that in vivo conversion of IPyA to IAA was enhanced under reduced auxin levels, while IPyA to IAA conversion was depressed in the presence of excess auxin. Based on these results, we propose that the IPyA pathway is transcriptionally regulated through a negative feedback mechanism in response to active auxin levels.
吲哚-3-丙酮酸(IPyA)途径是主要的生长素生物合成途径,它通过负反馈机制响应活性生长素水平进行转录调控。植物激素生长素在植物生长发育中起重要作用,活性游离生长素的水平由生物合成、共轭作用和极性运输决定。与共轭作用和极性运输不同,关于生长素生物合成的调控机制知之甚少。我们发现,编码吲哚-3-丙酮酸(IPyA)途径酶的基因表达受活性生长素水平升高或降低的调控。将合成生长素[1-萘乙酸(NAA)和2,4-二氯苯氧乙酸(2,4-D)]外源施加于拟南芥幼苗后,TAR2、YUC1、YUC2、YUC4和YUC6的表达水平下调。同时,观察到内源吲哚-3-乙酸(IAA)水平降低。另外,在拟南芥幼苗中,生长素生物合成抑制剂犬尿氨酸上调了这些YUCCA基因的表达,同时IAA水平降低。这些结果表明,YUCCA基因的表达受活性生长素水平的调控。在生长素过量产生和生长素缺陷型突变体中也观察到了类似结果。将IPyA外源施加于用犬尿氨酸预孵育的拟南芥幼苗,可提高内源IAA水平,而与仅暴露于IPyA的幼苗相比,用2,4-D预孵育可降低内源IAA水平。这些结果表明,在生长素水平降低的情况下,IPyA在体内向IAA的转化增强,而在生长素过量时,IPyA向IAA的转化受到抑制。基于这些结果,我们提出IPyA途径通过负反馈机制响应活性生长素水平进行转录调控。