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植物血球蛋白调节一氧化氮依赖的脱落酸合成和乙烯诱导的玉米体细胞胚胎发育中的程序性细胞死亡。

Phytoglobins regulate nitric oxide-dependent abscisic acid synthesis and ethylene-induced program cell death in developing maize somatic embryos.

机构信息

Department of Plant Science, University of Manitoba, Winnipeg, MB, R3T 2N2, Canada.

Department of Botany, Faculty of Science, Tanta University, Tanta, 31527, Egypt.

出版信息

Planta. 2018 Jun;247(6):1277-1291. doi: 10.1007/s00425-018-2862-5. Epub 2018 Feb 17.

DOI:10.1007/s00425-018-2862-5
PMID:29455261
Abstract

During maize somatic embryogenesis, suppression of phytoglobins (Pgbs) reduced ABA levels leading to ethylene-induced programmed cell death in the developing embryos. These effects modulate embryonic yield depending on the cellular localization of specific phytoglobin gene expression. Suppression of Zea mays phytoglobins (ZmPgb1.1 or ZmPgb1.2) during somatic embryogenesis induces programmed cell death (PCD) by elevating nitric oxide (NO). While ZmPgb1.1 is expressed in many embryonic domains and its suppression results in embryo abortion, ZmPgb1.2 is expressed in the basal cells anchoring the embryos to the embryogenic tissue. Down-regulation of ZmPgb1.2 is required to induce PCD in these anchor cells allowing the embryos to develop further. Exogenous applications of ABA could reverse the effects caused by the suppression of either of the two ZmPgbs. A depletion of ABA, ascribed to a down-regulation of biosynthetic genes, was observed in those embryonic domains where the respective ZmPgbs were repressed. These effects were mediated by NO. Depletion in ABA content increased the transcription of genes participating in the synthesis and response of ethylene, as well as the accumulation of ethylene, which influenced embryogenesis. Somatic embryo number was reduced by high ethylene levels and increased with pharmacological treatments suppressing ethylene synthesis. The ethylene inhibition of embryogenesis was linked to the production of reactive oxygen species (ROS) and the execution of PCD. Integration of ABA and ethylene in the ZmPgb regulation of embryogenesis is proposed in a model where NO accumulates in ZmPgb-suppressing cells, decreasing the level of ABA. Abscisic acid inhibits ethylene biosynthesis and the NO-mediated depletion of ABA relieves this inhibition causing ethylene to accumulate. Elevated ethylene levels trigger production of ROS and induce PCD. Ethylene-induced PCD in the ZmPgb1.1-suppressing line [ZmPgb1.1 (A)] leads to embryo abortion, while PCD in the ZmPgb1.2-suppressing line [ZmPgb1.2 (A)] results in the elimination of the anchor cells and the successful development of the embryos.

摘要

在玉米体细胞胚胎发生过程中,抑制植物血球素(Pgbs)会降低 ABA 水平,导致发育中的胚胎发生乙烯诱导的程序性细胞死亡。这些效应根据特定植物血球素基因表达的细胞定位来调节胚胎产量。在体细胞胚胎发生过程中抑制玉米植物血球素(ZmPgb1.1 或 ZmPgb1.2)会通过升高一氧化氮(NO)诱导程序性细胞死亡(PCD)。虽然 ZmPgb1.1 在许多胚胎区域表达,其抑制导致胚胎流产,但 ZmPgb1.2 在锚定胚胎到胚胎组织的基础细胞中表达。下调 ZmPgb1.2 是诱导这些锚定细胞中 PCD 的必要条件,从而使胚胎进一步发育。ABA 的外源应用可以逆转抑制两种 ZmPgbs 中的任何一种所引起的效应。在相应的 ZmPgbs 被抑制的那些胚胎区域观察到 ABA 的消耗,归因于生物合成基因的下调。这些效应是由 NO 介导的。ABA 含量的减少增加了参与乙烯合成和反应的基因的转录,以及乙烯的积累,这影响了胚胎发生。高乙烯水平会减少体细胞胚胎的数量,并通过抑制乙烯合成的药理学处理增加数量。乙烯对胚胎发生的抑制与活性氧(ROS)的产生和 PCD 的执行有关。在一个模型中提出了 ABA 和乙烯在 ZmPgb 调节胚胎发生中的整合,其中 NO 在抑制 ZmPgb 的细胞中积累,降低 ABA 水平。ABA 抑制乙烯生物合成,NO 介导的 ABA 消耗解除这种抑制,导致乙烯积累。乙烯水平的升高引发 ROS 的产生并诱导 PCD。ZmPgb1.1 抑制系[ZmPgb1.1(A)]中乙烯诱导的 PCD 导致胚胎流产,而 ZmPgb1.2 抑制系[ZmPgb1.2(A)]中 PCD 导致锚定细胞消除和胚胎成功发育。

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