摘要
Systemic acquired resistance （SAR） is a form of broad-spectrum resistance induced in response to local infections that protects uninfected parts against subsequent secondary infections by related or unrelated pathogens. SAR signaling requires two parallel branches, one regulated by salicylic acid （SA）. and theother by azelaic acid （AzA） and glycerol-3-phosphate （G3P）. AzA and G3P function downstream of the free radicals nitric oxide （NO） and reactive oxygen species （ROS）. During SAR, SA, AzA and G3P accumulate in the infected leaves, but only a small portion of these is transported to distal uninfected leaves. SA is preferen- tially transported via the apoplast, whereas phloem loading of AzA and G3P occurs via the symplast. The symplastic transport of AzA and G3P is regulated by gating of the plasmodesmata （PD）. The PD localizing proteins, PDLP1 and PDLP5, regulate SAR by regulating PD gating as well as the subcellular partitioning of a SAR-associated protein.
Systemic acquired resistance （SAR） is a form of broad-spectrum resistance induced in response to local infections that protects uninfected parts against subsequent secondary infections by related or unrelated pathogens. SAR signaling requires two parallel branches, one regulated by salicylic acid （SA）. and theother by azelaic acid （AzA） and glycerol-3-phosphate （G3P）. AzA and G3P function downstream of the free radicals nitric oxide （NO） and reactive oxygen species （ROS）. During SAR, SA, AzA and G3P accumulate in the infected leaves, but only a small portion of these is transported to distal uninfected leaves. SA is preferen- tially transported via the apoplast, whereas phloem loading of AzA and G3P occurs via the symplast. The symplastic transport of AzA and G3P is regulated by gating of the plasmodesmata （PD）. The PD localizing proteins, PDLP1 and PDLP5, regulate SAR by regulating PD gating as well as the subcellular partitioning of a SAR-associated protein.
基金
supported by funding from the National Science Foundation (0749731 and 051909)
