College of Agronomy, Gansu Provincial Key Laboratory of Aridland Crop Science, Gansu Key Laboratory of Crop Improvement and Germplasm Enhancement, Gansu Agricultural University, Lanzhou, 730070, China.
College of Horticulture, Gansu Agricultural University, Lanzhou, China.
Planta. 2019 Jul;250(1):199-217. doi: 10.1007/s00425-019-03163-w. Epub 2019 Apr 11.
The present study is the first to integrate physiological and proteomic data providing information on Fe, Mn and Zn deficiency-responsive mechanisms of potato plants in vitro. Micronutrient deficiency is an important limiting factor for potato production that causes substantial tuber yield and quality losses. To under the underlying molecular mechanisms of potato in response to Fe, Mn and Zn deficiency, a comparative proteomic approach was applied. Leaf proteome change of in vitro-propagated potato plantlets subjected to a range of Fe-deficiency treatments (20, 10 and 0 μM Na-Fe-EDTA), Mn-deficiency treatments (1 and 0 μM MnCl·4HO) and Zn-deficiency treatment (0 μM ZnCl) using two-dimensional gel electrophoresis was analyzed. Quantitative image analysis showed a total of 146, 55 and 42 protein spots under Fe, Mn and Zn deficiency with their abundance significantly altered (P < 0.05) more than twofold, respectively. By MALDI-TOF/TOF MS analyses, the differentially abundant proteins were found mainly involved in bioenergy and metabolism, photosynthesis, defence, redox homeostasis and protein biosynthesis/degradation under the metal deficiencies. Signaling, transport, cellular structure and transcription-related proteins were also identified. The hierarchical clustering results revealed that these proteins were involved in a dynamic network in response to Fe, Mn and Zn deficiency. All these metal deficiencies caused cellular metabolic remodeling to improve metal acquisition and distribution in potato plants. The reduced photosynthetic efficiency occurred under each metal deficiency, yet Fe-deficient plants showed a more severe damage of photosynthesis. More defence mechanisms were induced by Fe deficiency than Mn and Zn deficiency, and the antioxidant systems showed different responses to each metal deficiency. Reprogramming of protein biosynthesis/degradation and assembly was more strongly required for acclimation to Fe deficiency. The signaling cascades involving auxin and NDPKs might also play roles in micronutrient stress signaling and pinpoint interesting candidates for future studies. Our results first provide an insight into the complex functional and regulatory networks in potato plants under Fe, Mn and Zn deficiency.
本研究首次整合了生理学和蛋白质组学数据，提供了有关体外马铃薯植物铁、锰和锌缺乏响应机制的信息。微量元素缺乏是马铃薯生产的一个重要限制因素，会导致大量块茎产量和质量损失。为了了解马铃薯对铁、锰和锌缺乏的潜在分子机制，应用了比较蛋白质组学方法。通过二维凝胶电泳分析了在一系列铁缺乏处理（20、10 和 0 μM Na-Fe-EDTA）、锰缺乏处理（1 和 0 μM MnCl·4HO）和锌缺乏处理（0 μM ZnCl）下，体外繁殖的马铃薯苗叶片蛋白质组的变化。定量图像分析显示，在铁、锰和锌缺乏下，共有 146、55 和 42 个蛋白质斑点，其丰度显著改变（P < 0.05）超过两倍。通过 MALDI-TOF/TOF MS 分析，发现差异丰度蛋白主要参与生物能量和代谢、光合作用、防御、氧化还原稳态和蛋白质生物合成/降解，这些蛋白在金属缺乏下丰度发生了改变。还鉴定了信号转导、运输、细胞结构和转录相关蛋白。层次聚类结果表明，这些蛋白质参与了对铁、锰和锌缺乏的动态网络反应。所有这些金属缺乏导致细胞代谢重塑，以改善马铃薯植物对金属的获取和分布。每种金属缺乏都会导致光合作用效率降低，但缺铁植物的光合作用损伤更为严重。与锰和锌缺乏相比，缺铁会诱导更多的防御机制，抗氧化系统对每种金属缺乏的反应也不同。铁缺乏时对蛋白质生物合成/降解和组装的重编程要求更强，以适应缺铁。涉及生长素和 NDPKs 的信号级联反应可能也在微量元素胁迫信号中发挥作用，并为未来的研究指明了有趣的候选者。我们的研究结果首次提供了对铁、锰和锌缺乏下马铃薯植物复杂功能和调控网络的深入了解。
