ABI1 protein phosphatase 2C is a negative regulator of abscisic acid signaling
ABI1 protein phosphatase 2C is a negative regulator of abscisic acid signaling
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DOI：
10.1105/tpc.11.10.1897
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发表时间：
1999-10-01
期刊：
影响因子：
11.6
通讯作者：
Giraudat, J
中科院分区：
文献类型：
--
作者：
Gosti, F;Beaudoin, N;Giraudat, J
植物激素脱落酸（阿坝）是种子成熟和萌发的关键调节剂，并介导对环境胁迫的适应性反应。在拟南芥中，ABI 1基因编码蛋白丝氨酸/苏氨酸磷酸酶（PP 2C）的2C类的成员，和abi 1 -1突变显着降低种子和营养组织中的阿坝响应。然而，这种突变是显性的，并且是ABI 1基因唯一可用的突变等位基因。因此，目前还不清楚ABI 1是否有助于阿坝信号传导，以及如果ABI 1确实调节阿坝反应，它是阿坝作用的正调节剂还是负调节剂。在这项研究中，我们分离出7个新的等位基因的ABI 1基因的abi 1 -1突变体的基因内回复突变。与ABA抗性突变体abi 1 -1相比，这些回复突变体对阿坝抑制种子萌发和幼苗根系生长的作用比野生型更敏感。它们还显示种子休眠和干旱适应性反应的增加，这表明对内源阿坝的反应更高。回复突变等位基因隐性野生型ABI 1等位基因在提高阿坝的敏感性，表明这种ABA超敏感表型的结果从ABI 1的功能丧失。这七个抑制突变是ABI 1的PP 2C结构域的保守区域中的错义突变，并且每个相应的回复突变等位基因编码在体外酶促测定中缺乏任何可检测到的PP 2C活性的ABI 1蛋白。这些结果表明，ABI 1 PP 2C活性的丧失导致对阿坝的响应性增强。因此，野生型ABI 1磷酸酶是阿坝反应的负调节因子。
The plant hormone abscisic acid (ABA) is a key regulator of seed maturation and germination and mediates adaptive responses to environmental stress. In Arabidopsis, the ABI1 gene encodes a member of the 2C class of protein serine/threonine phosphatases (PP2C), and the abi1-1 mutation markedly reduces ABA responsiveness in both seeds and vegetative tissues. However, this mutation is dominant and has been the only mutant allele available for the ABI1 gene. Hence, it remained unclear whether ABI1 contributes to ABA signaling, and in case ABI1 does regulate ABA responsiveness, whether it is a positive or negative regulator of ABA action. In this study, we isolated seven novel alleles of the ABI1 gene as intragenic revertants of the abi1-1 mutant. In contrast to the ABA-resistant abi1-1 mutant, these revertants were more sensitive than the wild type to the inhibition of seed germination and seedling root growth by applied ABA. They also displayed increases in seed dormancy and drought adaptive responses that are indicative of a higher responsiveness to endogenous ABA. The revertant alleles were recessive to the wild-type ABI1 allele in enhancing ABA sensitivity, indicating that this ABA-supersensitive phenotype results from a loss of function in ABI1. The seven suppressor mutations are missense mutations in conserved regions of the PP2C domain of ABI1, and each of the corresponding revertant alleles encodes an ABI1 protein that lacked any detectable PP2C activity in an in vitro enzymatic assay. These results indicate that a loss of ABI1 PP2C activity leads to an enhanced responsiveness to ABA. Thus, the wild-type ABI1 phosphatase is a negative regulator of ABA responses.