Increased expression of MAP KINASE KINASE7 causes deficiency in polar auxin transport and leads to plant architectural abnormality in Arabidopsis
Increased expression of MAP KINASE KINASE7 causes deficiency in polar auxin transport and leads to plant architectural abnormality in Arabidopsis
复制标题
DOI：
10.1105/tpc.105.037846
复制
发表时间：
2006-02-01
期刊：
影响因子：
11.6
通讯作者：
Li, JY
中科院分区：
文献类型：
--
作者：
Dai, Y;Wang, HZ;Li, JY
生长素极性运输（PAT）在植物生长发育的许多方面起着重要的调节作用。我们报告了一个半显性拟南芥bushy和dwarf 1（bud 1）突变体的特性。分子遗传学分析表明，bud 1表型是拟南芥MAP激酶激酶7（MKK 7）表达增加的结果，MKK 7是植物丝裂原活化蛋白激酶激酶D组的成员。我们发现BUD 1/MKK 7是一种功能性激酶，激酶活性对其生物学功能至关重要。与野生型相比，芽1植物侧根明显减少，脉序模式简单，向重力性测定中的弯曲更快和更大。此外，芽1植物在高温（29摄氏度）和光照下具有较短的下胚轴，这是生长素作用缺陷的特征。氚标记吲哚乙酸转运的测定结果表明，在bud 1中MKK 7表达的增加或在MKK 7反义转基因植株中表达的抑制导致生长素转运的缺乏或增强，表明MKK 7负调控PAT。这一结论进一步证实了由bud 1和生长素相关突变体axr 3 -3，tir 1 -1，doc 1 -1和atmdr 1 -1杂交产生的双突变体的遗传和表型分析。
Polar auxin transport ( PAT) plays a crucial role in the regulation of many aspects of plant growth and development. We report the characterization of a semidominant Arabidopsis thaliana bushy and dwarf1 (bud1) mutant. Molecular genetic analysis indicated that the bud1 phenotype is a result of increased expression of Arabidopsis MAP KINASE KINASE7 (MKK7), a member of plant mitogen-activated protein kinase kinase group D. We showed that BUD1/MKK7 is a functional kinase and that the kinase activity is essential for its biological functions. Compared with the wild type, the bud1 plants develop significantly fewer lateral roots, simpler venation patterns, and a quicker and greater curvature in the gravitropism assay. In addition, the bud1 plants have shorter hypocotyls at high temperature (29 degrees C) under light, which is a characteristic feature of defective auxin action. Determination of tritium-labeled indole-3-acetic acid transport showed that the increased expression of MKK7 in bud1 or the repressed expression in MKK7 antisense transgenic plants causes deficiency or enhancement in auxin transport, indicating that MKK7 negatively regulates PAT. This conclusion was further substantiated by genetic and phenotypic analyses of double mutants generated from crosses between bud1 and the auxin-related mutants axr3-3, tir1-1, doc1-1, and atmdr1-1.