Sazuka Takashi, Kamiya Noriko, Nishimura Takeshi, Ohmae Kozue, Sato Yutaka, Imamura Kohei, Nagato Yasuo, Koshiba Tomokazu, Nagamura Yoshiaki, Ashikari Motoyuki, Kitano Hidemi, Matsuoka Makoto
Bioscience and Biotechnology Center, Nagoya University, Nagoya, Aichi, Japan.
Plant J. 2009 Oct;60(2):227-41. doi: 10.1111/j.1365-313X.2009.03952.x. Epub 2009 Jun 15.
Indole-3-acetic acid (IAA) plays a critical role in many aspects of plant growth and development; however, complete pathways of biosynthesis, localization and many aspects of functions of IAA in rice remain unclear. Here, we report the analysis of a rice tryptophan- (Trp-) and IAA-deficient mutant, tryptophan deficient dwarf1 (tdd1), which is embryonic lethal because of a failure to develop most organs during embryogenesis. Regenerated tdd1 plants showed pleiotropic phenotypes: dwarfing, narrow leaves, short roots and abnormal flowers. TDD1 encodes a protein homologous to anthranilate synthase beta-subunit, which catalyses the first step of the Trp biosynthesis pathway and functions upstream of Trp-dependent IAA biosynthesis. TDD1-uidA and DR5-uidA expression overlapped at many sites in WT plants but was lacking in tdd1, indicating that TDD1 is involved in auxin biosynthesis. Both Trp and IAA levels in flowers and embryos were much lower in tdd1 than in wild type (WT). Trp feeding completely rescued the mutant phenotypes and moderate expression of OsYUCCA1, which encodes a key enzyme in Trp-dependent IAA biosynthesis, also rescued plant height and root length, indicating that the abnormal phenotypes of tdd1 are caused predominantly by Trp and IAA deficiency. In tdd1 embryos, the expression patterns of OSH1 and OsSCR, which mark the presumptive apical region and the L2 layer, respectively, are identical to those in WT, suggesting a possibility either that different IAA levels are required for basic pattern formation than for organ formation or that an orthologous gene compensates for TDD1 deficiency during pattern formation.
吲哚 - 3 - 乙酸(IAA)在植物生长和发育的许多方面发挥着关键作用;然而,水稻中IAA的生物合成、定位以及功能的许多方面的完整途径仍不清楚。在此,我们报道了对一个水稻色氨酸(Trp)和IAA缺陷型突变体——色氨酸缺陷矮化1(tdd1)的分析,该突变体由于在胚胎发生过程中大多数器官无法发育而胚胎致死。再生的tdd1植株表现出多效性表型:矮化、叶片狭窄、根系短小和花异常。TDD1编码一种与邻氨基苯甲酸合酶β亚基同源的蛋白质,它催化Trp生物合成途径的第一步,并在依赖Trp的IAA生物合成上游起作用。TDD1 - uidA和DR5 - uidA的表达在野生型(WT)植株的许多位点重叠,但在tdd1中缺失,表明TDD1参与生长素生物合成。tdd1中花和胚胎中的Trp和IAA水平均远低于野生型(WT)。色氨酸饲喂完全挽救了突变体表型,并且编码依赖Trp的IAA生物合成关键酶的OsYUCCA1的适度表达也挽救了株高和根长,表明tdd1的异常表型主要是由Trp和IAA缺乏引起的。在tdd1胚胎中,分别标记假定顶端区域和L2层的OSH1和OsSCR的表达模式与WT中的相同,这表明要么基本模式形成所需的IAA水平与器官形成所需的不同,要么在模式形成过程中一个直系同源基因补偿了TDD1的缺陷。