Geitmann A, Snowman B N, Emons A M, Franklin-Tong V E
Experimental Plant Morphology and Cell Biology, Wageningen University, The Netherlands.
Plant Cell. 2000 Jul;12(7):1239-51. doi: 10.1105/tpc.12.7.1239.
Self-incompatibility (SI) is a genetically controlled process used to prevent self-pollination. In Papaver rhoeas, the induction of SI is triggered by a Ca(2)+-dependent signaling pathway that results in the rapid and S allele-specific inhibition of pollen tube tip growth. Tip growth of cells is dependent on a functioning actin cytoskeleton. We have investigated the effect of self-incompatibility (S) proteins on the actin cytoskeleton in poppy pollen tubes. Here, we report that the actin cytoskeleton of incompatible pollen tubes is rapidly and dramatically rearranged during the SI response, not only in our in vitro SI system but also in vivo. We demonstrate that nonspecific inhibition of growth does not result in similar actin rearrangements. Because the SI-induced alterations are not observed if growth stops, this clearly demonstrates that these alterations are triggered by the SI signaling cascade rather than merely resulting from the consequent inhibition of growth. We establish a detailed time course of events and discuss the mechanisms that might be involved. Our data strongly implicate a role for the actin cytoskeleton as a target for signaling pathways involved in the SI response of P. rhoeas.
自交不亲和性（SI）是一种由基因控制的防止自花授粉的过程。在虞美人中，SI的诱导由一条依赖Ca(2)+的信号通路触发，该通路导致花粉管顶端生长迅速且具有S等位基因特异性的抑制。细胞的顶端生长依赖于功能正常的肌动蛋白细胞骨架。我们研究了自交不亲和性（S）蛋白对罂粟花粉管中肌动蛋白细胞骨架的影响。在此，我们报告，不仅在我们的体外SI系统中，而且在体内，不亲和花粉管的肌动蛋白细胞骨架在SI反应过程中会迅速且显著地重新排列。我们证明，生长的非特异性抑制不会导致类似的肌动蛋白重排。因为如果生长停止就观察不到SI诱导的变化，这清楚地表明这些变化是由SI信号级联反应触发的，而不仅仅是由于随后的生长抑制导致的。我们确定了详细的事件时间进程，并讨论了可能涉及的机制。我们的数据有力地表明，肌动蛋白细胞骨架作为参与虞美人SI反应的信号通路的靶点发挥作用。
