Cell- autonomous immunity is widespread in plant - fungus interactions and terminates fungal pathogenesis either at the cell surface or after pathogen entry. Although post- invasive resistance responses typically coincide with a self- contained cell death of plant cells undergoing attack by parasites, these cells survive pre- invasive defence. Mutational analysis in Arabidopsis identified PEN1 syntaxin as one component of two pre- invasive resistance pathways against ascomycete powdery mildew fungi(1-3). Here we show that plasma- membrane- resident PEN1 promiscuously forms SDS- resistant soluble N- ethylmaleimide sensitive factor attachment protein receptor ( SNARE) complexes together with the SNAP33 adaptor and a subset of vesicle- associated membrane proteins ( VAMPs). PEN1- dependent disease resistance acts in vivo mainly through two functionally redundant VAMP72 subfamily members, VAMP721 and VAMP722. Unexpectedly, the same two VAMP proteins also operate redundantly in a default secretory pathway, suggesting dual functions in separate biological processes owing to evolutionary co- option of the default pathway for plant immunity. The disease resistance function of the secretory PEN1 - SNAP33 - VAMP721/ 722 complex and the pathogen- induced subcellular dynamics of its components are mechanistically reminiscent of immunological synapse formation in vertebrates, enabling execution of immune responses through focal secretion.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据