Strigolactones (SLs), or their metabolites, were recently identified as endogenous inhibitors of shoot branch- ing. However, certain key features and dynamics of SL action remained to be physiologically characterize...Strigolactones (SLs), or their metabolites, were recently identified as endogenous inhibitors of shoot branch- ing. However, certain key features and dynamics of SL action remained to be physiologically characterized. Here we show that successive direct application of SL to axillary buds at every node along the stem can fully inhibit branching. The SL inhibition of early outgrowth did not require inhibitory signals from other growing buds or the shoot tip. In add- ition to this very early or initial suppression of outgrowth, we also found SL to be effective, up to a point, at moderating the continuing growth of axillary branches. The effectiveness of SL at affecting bud and branch growth correlated with the ability of SL to regulate expression of PsBRC1. PsBRC1 is a transcription factor that is expressed strongly in axillary buds and is required for SL inhibition of shoot branching. Consistent with a dynamic role of the hormone, SL inhibition of bud growth did not prevent buds from later responding to a decapitation treatment, even though SL treatment immediately after decapitation inhibits the outgrowth response. Also, as expected from the hypothesized branching control network in plants, treatment of exogenous SL caused feedback down-regulation of SL biosynthesis genes within 2 h. Altogether, these results reveal new insights into the dynamics of SL function and support the premise that SLs or SL-derived metabolites function dynamically as a shoot branching hormone and that they act directly in axillary buds.展开更多
文摘Strigolactones (SLs), or their metabolites, were recently identified as endogenous inhibitors of shoot branch- ing. However, certain key features and dynamics of SL action remained to be physiologically characterized. Here we show that successive direct application of SL to axillary buds at every node along the stem can fully inhibit branching. The SL inhibition of early outgrowth did not require inhibitory signals from other growing buds or the shoot tip. In add- ition to this very early or initial suppression of outgrowth, we also found SL to be effective, up to a point, at moderating the continuing growth of axillary branches. The effectiveness of SL at affecting bud and branch growth correlated with the ability of SL to regulate expression of PsBRC1. PsBRC1 is a transcription factor that is expressed strongly in axillary buds and is required for SL inhibition of shoot branching. Consistent with a dynamic role of the hormone, SL inhibition of bud growth did not prevent buds from later responding to a decapitation treatment, even though SL treatment immediately after decapitation inhibits the outgrowth response. Also, as expected from the hypothesized branching control network in plants, treatment of exogenous SL caused feedback down-regulation of SL biosynthesis genes within 2 h. Altogether, these results reveal new insights into the dynamics of SL function and support the premise that SLs or SL-derived metabolites function dynamically as a shoot branching hormone and that they act directly in axillary buds.