Arabidopsis Type-III Phosphatidylinositol 4-Kinases β1 and β2 are Upstream of the Phospholipase C Pathway Triggered by Cold Exposure
Arabidopsis Type-III Phosphatidylinositol 4-Kinases β1 and β2 are Upstream of the Phospholipase C Pathway Triggered by Cold Exposure
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DOI：
10.1093/pcp/pcs011
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发表时间：
2012-03-01
影响因子：
4.9
通讯作者：
Puyaubert, Juliette
中科院分区：
文献类型：
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作者：
Delage, Elise;Ruelland, Eric;Puyaubert, Juliette
磷脂酰肌醇-4-磷酸（PtdIns 4P）是植物中最丰富的肌醇磷脂，是磷脂酰肌醇-4，5-二磷酸[PtdIns（4，5）P-2]的前体。这种脂质是磷酸肌醇依赖性磷脂酶C（PI-PLC）的底物，产生二酰基甘油（DAG），后者可磷酸化为磷脂酸（PtdOH）。在植物中，有人提出PtdIns 4P也可能是PI-PLC的直接底物。无论PtdIns 4P是PtdIns（4，5）P-2的前体还是PI-PLC的底物，其通过磷脂酰肌醇-4-激酶（PI 4Ks）的产生是产生由PI-PLC水解的磷酸肌醇的第一步。PI 4K可分为II型和III型。在植物中，PI-PLC上游的PI 4K的身份是未知的。在拟南芥中，冷触发PI-PLC激活，导致PtdOH产生，这是由PtdIns 4P和PtdIns（4，5）P-2的减少引起的。在悬浮细胞中，PtdIns 4P的减少和PtdOH的增加，在响应冷受损30 μ M渥曼青霉素，III型PI 4K抑制剂。III型PI 4K包括AtPI 4KIII α 1、β 1和β 2同种型。在这项工作中，我们表明，PtdOH从PI-PLC途径产生的是显着降低在一个pi 4kIII β 1 β 2双突变体暴露于冷应激。在单个pi 4kIII β 1和pi 4kIII β 2突变体中未检测到这种降低，表明AtPI 4KIII β 1和AtPI 4KIII β 2都可以作用于PI-PLC的上游。虽然几个短期到长期的冷反应是不变的pi 4kIII β 1 β 2，冷诱导的几个基因受损的双突变体和它的发芽是超敏感的冷却。我们还提供了证据表明，从头合成PtdIns 4P的PI 4Ks发生在并行PI-PLC激活。
Phosphatidylinositol-4-phosphate (PtdIns4P) is the most abundant phosphoinositide in plants and the precursor of phosphatidylinositol-4,5-bisphosphate [PtdIns(4,5)P-2]. This lipid is the substrate of phosphoinositide-dependent phospholipase C (PI-PLC) that produces diacylglycerol (DAG) which can be phosphorylated to phosphatidic acid (PtdOH). In plants, it has been suggested that PtdIns4P may also be a direct substrate of PI-PLC. Whether PtdIns4P is the precursor of PtdIns(4,5)P-2 or a substrate of PI-PLC, its production by phosphatidylinositol-4-kinases (PI4Ks) is the first step in generating the phosphoinositides hydrolyzed by PI-PLC. PI4Ks can be divided into type-II and type-III. In plants, the identity of the PI4K upstream of PI-PLC is unknown. In Arabidopsis, cold triggers PI-PLC activation, resulting in PtdOH production which is paralleled by decreases in PtdIns4P and PtdIns(4,5)P-2. In suspension cells, both the PtdIns4P decrease and the PtdOH increase in response to cold were impaired by 30 mu M wortmannin, a type-III PI4K inhibitor. Type-III PI4Ks include AtPI4KIII alpha 1, beta 1 and beta 2 isoforms. In this work we show that PtdOH resulting from the PI-PLC pathway is significantly lowered in a pi4kIII beta 1 beta 2 double mutant exposed to cold stress. Such a decrease was not detected in single pi4kIII beta 1 and pi4kIII beta 2 mutants, indicating that AtPI4KIII beta 1 and AtPI4KIII beta 2 can both act upstream of the PI-PLC. Although several short-term to long-term responses to cold were unchanged in pi4kIII beta 1 beta 2, cold induction of several genes was impaired in the double mutant and its germination was hypersensitive to chilling. We also provide evidence that de novo synthesis of PtdIns4P by PI4Ks occurs in parallel to PI-PLC activation.