The IBR5 phosphatase promotes Arabidopsis auxin responses through a novel mechanism distinct from TIR1-mediated repressor degradation.
The IBR5 phosphatase promotes Arabidopsis auxin responses through a novel mechanism distinct from TIR1-mediated repressor degradation.
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DOI：
10.1186/1471-2229-8-41
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发表时间：
2008-04-18
影响因子：
5.3
通讯作者：
Bartel B
中科院分区：
文献类型：
--
作者：
Strader LC;Monroe-Augustus M;Bartel B
在拟南芥中，吲哚-3-丁酸应答酶(IBR5)是生长素应答的正性调节因子，被认为是一种双特异性蛋白磷酸酶。IBR5基因突变导致植株高度降低，维管发育缺陷，叶片锯齿增加，侧根减少，并对植物激素生长素和脱落酸产生抗性。然而，IBR5影响生长素反应的途径还不完全清楚。我们分析了ibr5的双突变体和其他抑制生长素反应的突变体，发现ibr5与生长素受体突变体TIR1相结合，相对于亲本之一，增强了生长素的抗性。像其他生长素反应突变体一样，ibr5中生长素反应报告的积累减少了。与其他生长素抗性突变体不同，AUX/IAA阻遏蛋白AXR3NT-GUS在ibr5中不稳定。同样，AUX/IAA抑制因子IAA28在ibr5中的含量低于野生型。过表达缺乏催化半胱氨酸残基的IBR5突变形式并不能完全挽救IBR5缺陷。我们的遗传和分子证据表明，IBR5是一种磷酸酶，它促进生长素反应，包括生长素诱导的转录，不同于TIR1生长素受体，并且不破坏AUX/IAA抑制蛋白的稳定。我们的数据与生长素反应转录可以在TIR1介导的抑制子降解下游调节的可能性是一致的。
In Arabidopsis, INDOLE-3-BUTYRIC ACID RESPONSE5 (IBR5), a putative dual-specificity protein phosphatase, is a positive regulator of auxin response. Mutations in IBR5 result in decreased plant height, defective vascular development, increased leaf serration, fewer lateral roots, and resistance to the phytohormones auxin and abscisic acid. However, the pathways through which IBR5 influences auxin responses are not fully understood. We analyzed double mutants of ibr5 with other mutants that dampen auxin responses and found that combining ibr5 with an auxin receptor mutant, tir1, enhanced auxin resistance relative to either parent. Like other auxin-response mutants, auxin-responsive reporter accumulation was reduced in ibr5. Unlike other auxin-resistant mutants, the Aux/IAA repressor reporter protein AXR3NT-GUS was not stabilized in ibr5. Similarly, the Aux/IAA repressor IAA28 was less abundant in ibr5 than in wild type. ibr5 defects were not fully rescued by overexpression of a mutant form of IBR5 lacking the catalytic cysteine residue. Our genetic and molecular evidence suggests that IBR5 is a phosphatase that promotes auxin responses, including auxin-inducible transcription, differently than the TIR1 auxin receptor and without destabilizing Aux/IAA repressor proteins. Our data are consistent with the possibility that auxin-responsive transcription can be modulated downstream of TIR1-mediated repressor degradation.
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影响因子：
11.6
作者：
del Pozo, JC;Dharmasiri, S;Estelle, M
通讯作者：
Estelle, M
DOI：
10.1073/pnas.162339999
发表时间：
2002-08-20
影响因子：
11.1
作者：
Gagne, JM;Downes, BP;Vierstra, RD
通讯作者：
Vierstra, RD
影响因子：
56.9
作者：
Bennett, MJ;Marchant, A;Feldmann, KA
通讯作者：
Feldmann, KA
影响因子：
7.2
作者：
Gupta, R;Huang, YF;Luan, S
通讯作者：
Luan, S
DOI：
10.1007/bf00331020
发表时间：
1986-01-01
期刊：
MOLECULAR AND GENERAL GENETICS
影响因子：
--
作者：
HAUGHN, GW;SOMERVILLE, C
通讯作者：
SOMERVILLE, C