Senescence mechanisms

Senescence mechanisms
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DOI:
10.1111/j.1399-3054.1997.tb01059.x
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发表时间:
1997-12-01
影响因子:
6.4
通讯作者:
John, I
John, I
中科院分区:
生物学2区
文献类型:
--
作者:
Noodén, LD;Guiamét, JJ;John, I

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植物的衰老通常被视为导致死亡的内部程序性退化。这是一个发生在许多不同组织中的发育过程:;并服务于不同的目的。一般来说,细胞凋亡是指少量动物细胞的程序性死亡,在细胞水平上表现出一些特殊的特征。一些衰老的植物细胞表现出一些典型的细胞凋亡症状,而另一些则没有。本综述将主要关注叶片衰老,最终目的是解释整个植物的衰老(即单果衰老)。传统上,关于衰老机制的想法分为两大类:营养缺乏(例如饥​​饿)和遗传编程(即促进衰老和抑制衰老的基因)。大量证据表明,营养缺乏并不是衰老程序的核心组成部分,而越来越多的证据支持遗传编程。由于叶绿素 (Chi) 和叶绿体 (CP) 分解非常显着,因此叶片衰老通常以 Chi 损失来衡量。尽管CP分解可能不是叶细胞死亡的直接原因,但它作为其他地方使用的营养来源确实很重要,例如,对于单果植物中生殖结构的发育,并且这种损失限制了同化能力。 CP按顺序拆除。单个蛋白质复合物似乎被一次性全部取出,而不是一次取出一个亚基。去除任何成分,例如“气”,似乎都会破坏整个复合体的稳定。特别有趣的是,衰老的 CP 会分泌含 Chi 的小球,这表明一些 CP 成分在 CP 之外被分解。衰老似乎是由细胞核强加给CP的,除了大豆中的cytG之外,所有已知的衰老改变基因都是细胞核基因。只有大豆中的 d(1)d(2) 突变才能阻止广泛的叶片衰老过程。确切地说,导致细胞死亡的原因尚不清楚。然而,选择性硫醇蛋白酶抑制剂 E-64 确实可以延迟死亡,这表明蛋白酶发挥着关键作用。
Senescence in plants is usually viewed as an internally programmed degeneration leading to death. It is a developmental process that occurs in many different tissues :; and serves different purposes. Generally, apoptosis refers to programmed death of small numbers of animal cells, and it shows some special features at the cell level. Some senescing plant cells show some symptoms typical of apoptosis, while others do not. This review will focus primarily on leaf senescence with ultimate aim of explaining whole plant senescence (i.e., monocarpic senescence). Traditionally, the ideas on senescence mechanisms fall into two major groupings, nutrient deficiencies (e.g., starvation) and genetic programming (i.e., senescence-promoting and senescence-inhibiting genes). Considerable evidence indicates that nutrient deficiencies are not central senescence program components, while increasing evidence supports genetic programming. Because chlorophyll (Chi) and chloroplast (CP) breakdown are so prominent, leaf senescence is generally measured in terms of Chi loss. Although CP breakdown may not be the proximate cause of leaf cell death, it certainly is important as a source of nutrients for use elsewhere, e.g., for developing reproductive structures in monocarpic plants, and this loss limits assimilatory capacity. The CP is dismantled in an orderly sequence. Individual protein complexes seem to be taken out all at once, not one subunit at a time. Removal of any component, e.g., Chi, seems to destabilize the whole complex. It is of special interest that senescing CPs secrete Chi-containing globules indicating that some CP components are broken down outside the CP. Senescence appears to be imposed on the CP by the nucleus, and all the known senescence-altering genes except one, cytG in soybean, are nuclear. Only the d(1)d(2) mutation(s) in soybean prevents a broad range of leaf senescence processes. Exactly, what causes cell death is unclear; however, the selective thiol protease inhibitor, E-64, does delay death, and this suggests that proteases play a key role.