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虞美人花粉中自交不亲和反应的信号与靶点。

Signals and targets of the self-incompatibility response in pollen of Papaver rhoeas.

作者信息

Rudd Jason J, Franklin-Tong Vernonica E

机构信息

School of Biosciences, University of Birmingham, Edgbaston B15 2TT, UK.

出版信息

J Exp Bot. 2003 Jan;54(380):141-8. doi: 10.1093/jxb/erg001.

DOI:10.1093/jxb/erg001
PMID:12456764
Abstract

Self-incompatibility (SI) in Papaver rhoeas involves an allele-specific recognition between stigmatic S-proteins and pollen, resulting in inhibition of incompatible pollen. A picture of some of the signalling events and mechanisms involved in this specific inhibition of pollen tube growth is beginning to be built up. This highly specific response triggers a Ca(2+)-dependent signalling cascade in incompatible pollen when a stigmatic S-protein interacts with it. Rapid increases in cytosolic free Ca(2+) concentration (Ca(2+)) can now be attributed (at least in part) to Ca(2+) influx. The rapid loss of the pollen apical Ca(2+) gradient within approximately 1-2 min is accompanied by the inhibition of pollen tube tip growth. Concomitant with this time-frame, hyper-phosphorylation of p26, a soluble pollen phosphoprotein is detected. Characterization of p26 reveals that it is a soluble inorganic pyrophosphatase, which suggests a possible direct functional role in pollen tube growth. Slightly later, a putative MAP kinase (p52) is thought to be activated. Finally, preliminary evidence that programmed cell death (PCD) may be triggered in this response is described. A key target for these signals, the actin cytoskeleton, has also been identified. In this article the current understanding of some of the components of this signalling cascade and how they are beginning to throw some light on possible mechanisms involved in this SI-induced inhibition of pollen tube growth, is discussed.

摘要

虞美人的自交不亲和性(SI)涉及柱头S蛋白与花粉之间的等位基因特异性识别,从而导致不亲和花粉受到抑制。关于这种对花粉管生长的特异性抑制所涉及的一些信号事件和机制的图景正逐渐形成。当柱头S蛋白与不亲和花粉相互作用时,这种高度特异性的反应会在不亲和花粉中触发一个依赖于Ca(2+)的信号级联反应。胞质游离Ca(2+)浓度(Ca(2+))的快速增加现在可以归因于(至少部分归因于)Ca(2+)内流。在大约1 - 2分钟内花粉顶端Ca(2+)梯度的快速丧失伴随着花粉管顶端生长的抑制。与此同时,在这个时间范围内,检测到一种可溶性花粉磷蛋白p26的过度磷酸化。对p26的表征表明它是一种可溶性无机焦磷酸酶,这表明它在花粉管生长中可能具有直接的功能作用。稍晚些时候,一种假定的丝裂原活化蛋白激酶(p52)被认为被激活。最后,描述了关于这种反应可能触发程序性细胞死亡(PCD)的初步证据。这些信号的一个关键靶点——肌动蛋白细胞骨架也已被确定。在本文中,我们讨论了对这个信号级联反应中一些成分的当前理解,以及它们如何开始揭示这种由自交不亲和性诱导的花粉管生长抑制所涉及的可能机制。

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