Arabidopsis PHL2 and PHR1 Act Redundantly as the Key Components of the Central Regulatory System Controlling Transcriptional Responses to Phosphate Starvation
Arabidopsis PHL2 and PHR1 Act Redundantly as the Key Components of the Central Regulatory System Controlling Transcriptional Responses to Phosphate Starvation
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拟南芥 PHL2 和 PHR1 作为控制磷酸盐饥饿转录反应的中央调控系统的关键组成部分发挥冗余作用
DOI：
10.1104/pp.15.01336
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发表时间：
2016-01-01
期刊：
影响因子：
7.4
通讯作者：
Liu, Dong
中科院分区：
文献类型：
--
作者：
Sun, Lichao;Song, Li;Liu, Dong
当面临无机磷（Pi）饥饿时，植物激活一系列适应性反应以维持其生长。这些反应在很大程度上是在转录水平上控制的。拟南芥（Arabidopsis thaliana）PHOSPHATE RESPONSE 1（PHR 1）及其同源物PHR 1-like 1（PHL 1）属于MYB-CC转录因子家族，是植物磷胁迫下转录调控系统的重要组成部分。然而，PHR 1和PHL 1的敲除仅导致Pi饥饿诱导的基因的转录的部分损失，这表明在该调节系统中存在其他关键组分。在这项工作中，我们使用的转录磷饥饿诱导的酸性磷酸酶，AtPAP 10，研究植物转录响应磷饥饿的分子机制。我们首先确定了AtPAP 10启动子上的DNA序列，该序列对AtPAP 10的转录至关重要。然后，我们证明了PHL 2和PHL 3，MYB-CC家族的另外两个成员，特异性地结合到该DNA序列并激活AtPAP 10的转录。与PHR 1和PHL 1不同，PHL 2和PHL 3的转录和蛋白质积累被Pi饥饿上调。RNA测序分析表明，大多数Pi饥饿诱导的基因的转录在phl 2突变体中受损，表明PHL 2也是中央调控系统的关键组成部分。最后，我们发现PHL 2，也许还有PHL 3，与PHR 1冗余地调节植物对Pi饥饿的转录反应。
When confronted with inorganic phosphate (Pi) starvation, plants activate an array of adaptive responses to sustain their growth. These responses, in a large extent, are controlled at the transcriptional level. Arabidopsis (Arabidopsis thaliana) PHOSPHATE RESPONSE1 (PHR1) and its close homolog PHR1-like 1 (PHL1) belong to a 15-member family of MYB-CC transcription factors and are regarded as the key components of the central regulatory system controlling plant transcriptional responses to Pi starvation. The knockout of PHR1 and PHL1, however, causes only a partial loss of the transcription of Pi starvation-induced genes, suggesting the existence of other key components in this regulatory system. In this work, we used the transcription of a Pi starvation-induced acid phosphatase, AtPAP10, to study the molecular mechanism underlying plant transcriptional responses to Pi starvation. We first identified a DNA sequence on the AtPAP10 promoter that is critical for the transcription of AtPAP10. We then demonstrated that PHL2 and PHL3, two other members of the MYB-CC family, specifically bind to this DNA sequence and activate the transcription of AtPAP10. Unlike PHR1 and PHL1, the transcription and protein accumulation of PHL2 and PHL3 are upregulated by Pi starvation. RNA-sequencing analyses indicated that the transcription of most Pi starvation-induced genes is impaired in the phl2 mutant, indicating that PHL2 is also a key component of the central regulatory system. Finally, we showed that PHL2, and perhaps also PHL3, acts redundantly with PHR1 to regulate plant transcriptional response to Pi starvation.