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ArabidopsisFHY3andFAR1integratelightandstrigolactonesignalingtoregulatebranching
Firstauthor:YurongXie;Affiliations:CAASBiotechnologyResearchInstitute(农科院生物技术所):Beijing,China
Correspondingauthor:HaiyangWang
Branching/tilleringisanimportantparameterofplantarchitectureandistightlyregulatedbybothinternalfactors(suchasplanthormones)andexternalfactors(suchaslightconditions).Howthevarioussignalingpathwaysconvergetocoordinatelyregulatebranchingisnotwellunderstood.Here,wereportthatinArabidopsis,FHY3andFAR1,twohomologoustranscriptionfactorsessentialforphytochromeA-mediatedlightsignaling,andSMXL6/SMXL7/SMXL8,threekeyrepressorsofthestrigolactone(SL)signalingpathway,directlyinteractwithSPL9andSPL15andsuppresstheirtranscriptionalactivationofBRC1,akeyrepressorofbranching,thuspromotingbranching.Inaddition,FHY3andFAR1alsodirectlyup-regulatetheexpressionofSMXL6andSMXL7topromotebranching.SimulatedshadetreatmentreducestheaccumulationofFHY3protein,leadingtoincreasedexpressionofBRC1andreducedbranching.OurresultsestablishanintegratedmodeloflightandSLcoordinatelyregulatingBRC1expressionandbranchingthroughconvergingattheBRC1promoter.
分枝（branching）或分蘖（tillering）是植物株型结构的一个重要参数，并与植物激素等内部因素和光照条件等外部因素密切关联。不同的信号通路如何共同作用，协调调控分枝还有待深入的研究。本文中，作者发现拟南芥中两个同源转录因子FHY3与FAR1对于光敏色素A介导的光信号是必需的，并且三个独脚金内酯信号通路上的关键抑制因子SMXL6/SMXL7/SMXL8能够直接与SPL9和SPL15互作，抑制其对于分枝关键抑制基因BRC1的转录激活，从而促进植物分枝。另外，FHY3和FAR1还能直接上调SMXL6和SMXL7基因的表达水平，从而促进分枝。模拟阴影处理降低了FHY3蛋白的积累，导致BRC1基因的表达水平升高，减少了植株的分枝。本文的结果显示光与独脚金内酯同时通过BRC1基因的启动子作用于BRC1基因的表达调控，从而影响植物的分枝。
通讯：王海洋(