Shoot branching,determining plant architecture and crop yield,is critically controlled by strigolactones(SLs).However,how SLs inhibit shoot branching after its perception by the receptor complex remains largely obscur...Shoot branching,determining plant architecture and crop yield,is critically controlled by strigolactones(SLs).However,how SLs inhibit shoot branching after its perception by the receptor complex remains largely obscure.In this study,using the transcriptomic and genetic analyss as well as biochemical studies,we reveal the key role of BES1 in the SL-regulated shoot branching.Wedemonstrate that BES1 and D53-like SMXLs,the substrates of SL receptor complex D14–MAX2,interact with each other to inhibit BRC1 expression,which specifically triggers the SL-regulated transcriptional network in shoot branching.BES1 directly binds the BRC1 promoter and recruits SMXLs to inhibit BRC1 expression.Interestingly,despite being the shared component by SL and brassinosteroid(BR)signaling,BES1 gains signal specificity through different mechanisms in response to BR and SL signals.展开更多
基金Supported by NSFC 31430046(to X.W),31661143024(to X.W.)National Key Research and Development Plan 2016YFD0100403(to S.S.)+1 种基金the Ministry of Agriculture Innovation team plan(0120150092 to X.W.)the School Independent Scientific and Technological Innovation Foundation and Research Startup Foundation of Huazhong Agricultural University(2662015PY020 and 2014RC002 to X.W.).
文摘Shoot branching,determining plant architecture and crop yield,is critically controlled by strigolactones(SLs).However,how SLs inhibit shoot branching after its perception by the receptor complex remains largely obscure.In this study,using the transcriptomic and genetic analyss as well as biochemical studies,we reveal the key role of BES1 in the SL-regulated shoot branching.Wedemonstrate that BES1 and D53-like SMXLs,the substrates of SL receptor complex D14–MAX2,interact with each other to inhibit BRC1 expression,which specifically triggers the SL-regulated transcriptional network in shoot branching.BES1 directly binds the BRC1 promoter and recruits SMXLs to inhibit BRC1 expression.Interestingly,despite being the shared component by SL and brassinosteroid(BR)signaling,BES1 gains signal specificity through different mechanisms in response to BR and SL signals.
