Wilmowicz Emilia, Kućko Agata, Pokora Wojciech, Kapusta Małgorzata, Jasieniecka-Gazarkiewicz Katarzyna, Tranbarger Timothy John, Wolska Magdalena, Panek Katarzyna
Department of Plant Physiology and Biotechnology, Nicolaus Copernicus University, 1 Lwowska Street, 87-100 Toruń, Poland.
Department of Plant Physiology, Institute of Biology, Warsaw University of Life Sciences-SGGW (WULS-SGGW), Nowoursynowska 159 Street, 02-776 Warsaw, Poland.
Int J Mol Sci. 2021 Mar 16;22(6):3001. doi: 10.3390/ijms22063001.
Yellow lupine is a great model for abscission-related research given that excessive flower abortion reduces its yield. It has been previously shown that the EPIP peptide, a fragment of LlIDL (INFLORESCENCE DEFICIENT IN ABSCISSION) amino-acid sequence, is a sufficient molecule to induce flower abortion, however, the question remains: What are the exact changes evoked by this peptide locally in abscission zone (AZ) cells? Therefore, we used EPIP peptide to monitor specific modifications accompanied by early steps of flower abscission directly in the AZ. EPIP stimulates the downstream elements of the pathway- and MITOGEN-ACTIVATED PROTEIN KINASE6 and induces cellular symptoms indicating AZ activation. The EPIP treatment disrupts redox homeostasis, involving the accumulation of HO and upregulation of the enzymatic antioxidant system including superoxide dismutase, catalase, and ascorbate peroxidase. A weakening of the cell wall structure in response to EPIP is reflected by pectin demethylation, while a changing pattern of fatty acids and acyl lipids composition suggests a modification of lipid metabolism. Notably, the formation of a signaling molecule-phosphatidic acid is induced locally in EPIP-treated AZ. Collectively, all these changes indicate the switching of several metabolic and signaling pathways directly in the AZ in response to EPIP, which inevitably leads to flower abscission.
鉴于过多的花脱落会降低产量,黄羽扇豆是脱落相关研究的理想模型。先前的研究表明,EPIP肽是LlIDL(脱落缺陷花序)氨基酸序列的一个片段,是诱导花脱落的充分分子,然而,问题仍然存在:这种肽在脱落区(AZ)细胞中局部引发的确切变化是什么?因此,我们使用EPIP肽直接在AZ中监测伴随花脱落早期步骤的特定修饰。EPIP刺激该途径的下游元件以及丝裂原活化蛋白激酶6,并诱导表明AZ激活的细胞症状。EPIP处理破坏了氧化还原稳态,包括HO的积累和酶促抗氧化系统(包括超氧化物歧化酶、过氧化氢酶和抗坏血酸过氧化物酶)的上调。果胶去甲基化反映了细胞壁结构对EPIP的响应减弱,而脂肪酸和酰基脂质组成的变化模式表明脂质代谢发生了改变。值得注意的是,在经EPIP处理的AZ中局部诱导了信号分子磷脂酸的形成。总的来说,所有这些变化表明,响应EPIP,AZ中几种代谢和信号通路发生了切换,这不可避免地导致花脱落。