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The ethylene biosynthetic and perception machinery is differentially expressed during endosperm and embryo development in maize

机译:玉米胚乳和胚发育过程中乙烯生物合成和感知机制差异表达

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摘要

The maize endosperm undergoes programmed cell death late in its development so that, with the exception of the aleurone layer, the tissue is dead by the time the kernel matures. Although ethylene is known to regulate the onset of endosperm cell death, the temporal and spatial control of the ethylene biosynthetic and perception machinery during maize endosperm development has not been examined. In this study, we report the isolation of the maize gene families for ACC synthase, ACC oxidase, the ethylene receptor, and EIN2 and EIL, which act downstream of the receptor. We show that ACC oxidase is expressed primarily in the endosperm, and only at low levels in the developing embryo late in its development. ACC synthase is expressed throughout endosperm development but, in contrast to ACC oxidase, it is transiently expressed to a significantly higher level in the developing embryo at a time that corresponds with the onset of endosperm cell death. Only two ethylene receptor gene families were identified in maize, in contrast to the five types previously identified in Arabidopsis. Members of both ethylene receptor families were expressed to substantially higher levels in the developing embryo than in the endosperm, as were members of the EIN2 and EIL gene families. These results suggest that the endosperm and embryo both contribute to the synthesis of ethylene, and they provide a basis for understanding why the developing endosperm is especially sensitive to ethylene-induced cell death while the embryo is protected.
机译:玉米胚乳在发育后期经历了程序性的细胞死亡,因此,除了糊粉层以外,在籽粒成熟时组织已经死亡。尽管已知乙烯可调节胚乳细胞死亡的发作,但尚未检查玉米胚乳发育过程中乙烯生物合成和感知机制的时间和空间控制。在这项研究中,我们报告了玉米基因家族的ACC合酶,ACC氧化酶,乙烯受体以及在受体下游起作用的EIN2和EIL的分离。我们表明,ACC氧化酶主要在胚乳中表达,并且在发育后期的胚胎中仅以低水平表达。 ACC合酶在整个胚乳发育过程中表达,但与ACC氧化酶相反,它在发育胚中瞬时表达至显着较高的水平,这与胚乳细胞死亡的发作时间相对应。与先前在拟南芥中鉴定的五种类型相反,在玉米中仅鉴定出两个乙烯受体基因家族。 EIN2和EIL基因家族的成员在发育中的胚中表达的乙烯受体均高于胚乳中的水平。这些结果表明胚乳和胚胎都有助于乙烯的合成,并且它们为理解为什么发育中的胚乳对乙烯诱导的细胞死亡特别敏感而胚胎受到保护提供了基础。

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