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A Central Regulatory System Largely Controls Transcriptional Activation and Repression Responses to Phosphate Starvation in Arabidopsis

机译：中央监管系统很大程度上控制拟南芥对磷酸饥饿的转录激活和抑制反应。

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Plants respond to different stresses by inducing or repressing transcription of partially overlapping sets of genes. In Arabidopsis, the PHR1 transcription factor (TF) has an important role in the control of phosphate (Pi) starvation stress responses. Using transcriptomic analysis of Pi starvation in phr1, and phr1 phr1-like (phl1) mutants and in wild type plants, we show that PHR1 in conjunction with PHL1 controls most transcriptional activation and repression responses to phosphate starvation, regardless of the Pi starvation specificity of these responses. Induced genes are enriched in PHR1 binding sequences (P1BS) in their promoters, whereas repressed genes do not show such enrichment, suggesting that PHR1(-like) control of transcriptional repression responses is indirect. In agreement with this, transcriptomic analysis of a transgenic plant expressing PHR1 fused to the hormone ligand domain of the glucocorticoid receptor showed that PHR1 direct targets (i.e., displaying altered expression after GR:PHR1 activation by dexamethasone in the presence of cycloheximide) corresponded largely to Pi starvation-induced genes that are highly enriched in P1BS. A minimal promoter containing a multimerised P1BS recapitulates Pi starvation-specific responsiveness. Likewise, mutation of P1BS in the promoter of two Pi starvation-responsive genes impaired their responsiveness to Pi starvation, but not to other stress types. Phylogenetic footprinting confirmed the importance of P1BS and PHR1 in Pi starvation responsiveness and indicated that P1BS acts in concert with other cis motifs. All together, our data show that PHR1 and PHL1 are partially redundant TF acting as central integrators of Pi starvation responses, both specific and generic. In addition, they indicate that transcriptional repression responses are an integral part of adaptive responses to stress.
机译：植物通过诱导或抑制部分重叠的基因转录来响应不同的胁迫。在拟南芥中，PHR1转录因子（TF）在控制磷酸盐（Pi）饥饿胁迫反应中具有重要作用。使用phr1和phr1 phr1样（phl1）突变体以及野生型植物中Pi饥饿的转录组学分析，我们显示PHR1与PHL1一起可控制大多数对磷酸盐饥饿的转录激活和抑制反应，而与Pi饥饿的特异性无关。这些回应。诱导的基因在其启动子中富含PHR1结合序列（P1BS），而被抑制的基因则未显示出这种富集现象，这表明PHR1（-like）对转录抑制反应的控制是间接的。与此相符的是，对表达PHR1融合至糖皮质激素受体激素配体结构域的转基因植物的转录组学分析显示，PHR1直接靶标（即在环己酰亚胺存在下地塞米松激活GR：PHR1后显示改变的表达）与Pi饥饿诱导的基因高度富含P1BS。包含多聚P1BS的最小启动子概括了Pi饥饿特异性反应。同样，两个Pi饥饿响应基因的启动子中P1BS的突变会削弱其对Pi饥饿的响应能力，但不会减弱对其他胁迫类型的响应。系统发育足迹证实了P1BS​​和PHR1在Pi饥饿反应中的重要性，并表明P1BS与其他顺式基序协同作用。总之，我们的数据表明，PHR1和PHL1是部分冗余的TF，充当Pi饥饿反应的中心整合者，包括特定的和通用的。另外，它们表明转录抑制反应是对压力的适应性反应的组成部分。

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