The involvement of 1-aminocyclopropane-1-carboxylic acid synthase isogene, Pp-ACS1, in peach fruit softening

The involvement of 1-aminocyclopropane-1-carboxylic acid synthase isogene, Pp-ACS1, in peach fruit softening
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DOI:
10.1093/jxb/erj097
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发表时间:
2006-03-01
影响因子:
6.9
通讯作者:
Yamaguchi, M
Yamaguchi, M
中科院分区:
生物学1区
文献类型:
--
作者:
Tatsuki, M;Haji, T;Yamaguchi, M

文献摘要

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乙烯促进果实成熟,包括软化。融肉桃(Prunus persica (L). Batsch)品种“Akatsuki”的果实产生的乙烯含量不断增加,在成熟阶段果肉硬度迅速软化。另一方面,石硬桃品种“Yumying”、“Odoroki”和“Manami”的果实在果实成熟和储存过程中不会软化,并且产生很少的乙烯。为了阐明石硬桃抑制乙烯产生的机制,检查了四种乙烯生物合成酶的表达模式:ACC合酶(Pp-ACS1、Pp-ACS2和Pp-ACS3)和ACC氧化酶(Pp-ACO1)。融肉品种‘Akatsuki’采收后Pp-ACS1 mRNA显着诱导,产生大量乙烯。另一方面,在石硬桃中,Pp-ACS1 mRNA在成熟阶段没有被诱导,乙烯的产生受到抑制。由于Pp-ACS1 mRNA在“有明”的衰老花、受伤叶和受伤未成熟果实中正常诱导,因此Pp-ACS1仅在成熟阶段受到抑制,并不是Pp-ACS1的缺陷。这些结果表明,石硬桃品种果实软化的抑制是由乙烯产生水平低引起的,这取决于 Pp-ACS1 表达的抑制。
Ethylene promotes fruit ripening, including softening. The fruit of melting-flesh peach (Prunus persica (L). Batsch) cultivar 'Akatsuki' produces increasing levels of ethylene, and the flesh firmness softens rapidly during the ripening stage. On the other hand, the fruit of stony hard peach cultivars 'Yumyeong', 'Odoroki', and 'Manami' does not soften and produces little ethylene during fruit ripening and storage. To clarify the mechanism of suppression of ethylene production in stony hard peaches, the expression patterns of four ethylene biosynthesis enzymes were examined: ACC synthases (Pp-ACS1, Pp-ACS2, and Pp-ACS3) and ACC oxidase (Pp-ACO1). In the melting-flesh cultivar 'Akatsuki', Pp-ACS1 mRNA was dramatically induced after harvesting, and a large amount of ethylene was produced. On the other hand, in stony hard peaches, Pp-ACS1 mRNA was not induced during the ripening stage, and ethylene production was inhibited. Since Pp-ACS1 mRNA was induced normally in senescing flowers, wounded leaves, and wounded immature fruit of 'Yumyeong', Pp-ACS1 was suppressed only at the ripening stage, and was not a defect in Pp-ACS1. These results indicate that the suppression of fruit softening in stony hard peach cultivars was caused by a low level of ethylene production, which depends on the suppressed expression of Pp-ACS1.