A rice tryptophan deficient dwarf mutant, tdd1, contains a reduced level of indole acetic acid and develops abnormal flowers and organless embryos
A rice tryptophan deficient dwarf mutant, tdd1, contains a reduced level of indole acetic acid and develops abnormal flowers and organless embryos
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DOI：
10.1111/j.1365-313x.2009.03952.x
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发表时间：
2009-10-01
期刊：
影响因子：
7.2
通讯作者：
Matsuoka, Makoto
中科院分区：
文献类型：
--
作者：
Sazuka, Takashi;Kamiya, Noriko;Matsuoka, Makoto
吲哚-3-乙酸（Indole-3-acetic acid，IAA）在植物生长发育中起着重要作用，但其在水稻中的生物合成途径、定位及功能尚不清楚。在这里，我们报告的分析水稻色氨酸-（Trp-）和IAA-缺陷型突变体，色氨酸缺陷型dwarf 1（tdd 1），这是胚胎致死的，因为未能开发大多数器官在胚胎发生过程中。tdd 1再生植株表现出矮化、窄叶、短根和畸形花等多效表型。TDD 1编码邻氨基苯甲酸合成酶β亚基同源蛋白，其催化Trp生物合成途径的第一步并在Trp依赖的IAA生物合成的上游起作用。TDD 1-uidA和DR 5-uidA在野生型植物中的表达在许多位点重叠，但在tdd 1中缺乏，表明TDD 1参与生长素的生物合成。在花和胚中的Trp和IAA水平在tdd 1中比野生型（WT）低得多。Trp营养完全挽救了突变体的表型，并且编码Trp依赖的IAA合成关键酶OsYUCCA 1的适度表达也挽救了株高和根长，表明tdd 1的异常表型主要是由Trp和IAA缺乏引起的。在tdd 1胚胎中，OSH 1和OsSCR的表达模式，这标志着假定的顶端区域和L2层，分别是相同的WT，这表明一种可能性，即不同的IAA水平所需的基本图案形成比器官形成或orthopathic基因补偿TDD 1缺陷在图案形成过程中。
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.