Foo Eloise, Bullier Erika, Goussot Magali, Foucher Fabrice, Rameau Catherine, Beveridge Christine Anne
Australian Research Council Centre of Excellence for Integrative Legume Research, University of Queensland, St. Lucia, Queensland, 4072, Australia.
Plant Cell. 2005 Feb;17(2):464-74. doi: 10.1105/tpc.104.026716. Epub 2005 Jan 19.
In Pisum sativum, the RAMOSUS genes RMS1, RMS2, and RMS5 regulate shoot branching via physiologically defined mobile signals. RMS1 is most likely a carotenoid cleavage enzyme and acts with RMS5 to control levels of an as yet unidentified mobile branching inhibitor required for auxin inhibition of branching. Our work provides molecular, genetic, and physiological evidence that RMS1 plays a central role in a shoot-to-root-to-shoot feedback system that regulates shoot branching in pea. Indole-3-acetic acid (IAA) positively regulates RMS1 transcript level, a potentially important mechanism for regulation of shoot branching by IAA. In addition, RMS1 transcript levels are dramatically elevated in rms3, rms4, and rms5 plants, which do not contain elevated IAA levels. This degree of upregulation of RMS1 expression cannot be achieved in wild-type plants by exogenous IAA application. Grafting studies indicate that an IAA-independent mobile feedback signal contributes to the elevated RMS1 transcript levels in rms4 plants. Therefore, the long-distance signaling network controlling branching in pea involves IAA, the RMS1 inhibitor, and an IAA-independent feedback signal. Consistent with physiological studies that predict an interaction between RMS2 and RMS1, rms2 mutations appear to disrupt this IAA-independent regulation of RMS1 expression.
在豌豆中,RMS1、RMS2和RMS5基因通过生理上确定的移动信号调节茎枝分枝。RMS1很可能是一种类胡萝卜素裂解酶,与RMS5共同作用,控制生长素抑制分枝所需的一种尚未确定的移动分枝抑制剂的水平。我们的研究提供了分子、遗传和生理学证据,表明RMS1在调节豌豆茎枝分枝的茎-根-茎反馈系统中起核心作用。吲哚-3-乙酸(IAA)正向调节RMS1转录水平,这是IAA调节茎枝分枝的一个潜在重要机制。此外,RMS1转录水平在rms3、rms4和rms5植株中显著升高,这些植株中IAA水平并未升高。通过外源施加IAA,野生型植株无法达到RMS1表达上调的这种程度。嫁接研究表明,一种不依赖IAA的移动反馈信号导致rms4植株中RMS1转录水平升高。因此,控制豌豆分枝的长距离信号网络涉及IAA、RMS1抑制剂和一种不依赖IAA的反馈信号。与预测RMS2和RMS1之间存在相互作用的生理学研究一致,rms2突变似乎破坏了这种对RMS1表达的不依赖IAA的调节。