SlSGRL, a tomato SGR-like protein, promotes chlorophyll degradation downstream of the ABA signaling pathway
SlSGRL, a tomato SGR-like protein, promotes chlorophyll degradation downstream of the ABA signaling pathway
复制标题
SlSGRL 是一种番茄 SGR 样蛋白，可促进 ABA 信号通路下游的叶绿素降解
DOI：
10.1016/j.plaphy.2020.10.028
复制
发表时间：
2020-12-01
影响因子：
6.5
通讯作者：
Lv, Wei
中科院分区：
文献类型：
--
作者：
Yang, Minmin;Zhu, Shaobo;Lv, Wei
叶绿素 (chl) 降解在绿色植物生长和发育过程中起着至关重要的作用，包括营养代谢、果实和种子成熟以及光毒解毒。 STAY-GREEN (SGR) 是一种参与叶绿素降解的植物特异性调节剂。先前的研究表明，SlSGR1 在番茄（Solarium lycopersicum）果实成熟过程中叶绿素降解和番茄红素积累中发挥作用。然而，人们对SlSGR-LIKE (SlSGRL)基因知之甚少，该基因是SlSGR1的同源物。我们克隆了 SlSGRL 基因并创建了过表达 (OE) SlSGRL 的转基因番茄植物。表达分析表明 SlSGRL 被脱落酸 (ABA) 上调。我们的数据表明，在 ABA 处理下，SlSGRL-OE 品系比野生型 (WT) 品系表现出更早的叶片黄化。酵母双杂交 (Y2H) 测定表明，SlSGRL 与脱镁叶绿素脱镁叶绿酸水解酶 (SlPPH) 和光捕获复合物 a2 (SlLHCa2) 相互作用，促进叶绿素降解。进一步分析表明，ABA-INSENSITIVE5 (SlABI5) 和 SlABI5-LIKE 通过直接结合包含 ABRE 顺式元件的 SlSGRL 启动子序列（-611 至 -582）来调节 SlSGRL 表达。我们提出，SlSGRL 受 SlABI5/SlABI5-LIKE 调节，主要通过与 SlPPH 和 SlLHCa2 相互作用参与 ABA 诱导的 Chl 降解。
Chlorophyll (chl) degradation plays a vital role during green plant growth and development, including nutrient metabolism, fruit and seed maturation, and phototoxic detoxification. STAY-GREEN (SGR) is a plant-specific regulator involved in chl degradation. Previous studies showed that SlSGR1 functioned in chl degradation and lycopene accumulation during fruit ripening of tomato (Solarium lycopersicum). However, little is known about SlSGR-LIKE (SlSGRL) gene, which is a homolog of SlSGR1. We cloned the SlSGRL gene and created transgenic tomato plants overexpressing (OE) SlSGRL. Expression analysis showed that SlSGRL was up-regulated by abscisic acid (ABA). Our data showed that SlSGRL-OE lines exhibited earlier leaf yellowing than wild-type (WT) lines under ABA treatment. Yeast two-hybrid (Y2H) assay revealed that SlSGRL interacted with pheophytin pheophorbide hydrolase (SlPPH) and light-harvesting complex a2 (SlLHCa2) to promote the chl degradation. Further analysis demonstrated that ABA-INSENSITIVE5 (SlABI5) and SlABI5-LIKE regulated SlSGRL expression by directly binding to the sequence (-611 to -582) of the SlSGRL promoter that included an ABRE cis-element. We proposed that SlSGRL, which was regulated by SlABI5/SlABI5-LIKE, mainly acted in ABA-induced chl degradation via interacting with SlPPH and SlLHCa2.