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拟南芥几丁质合成酶 CalS1/8 在胁迫过程中调节质膜通道的通透性。

Arabidopsis callose synthases CalS1/8 regulate plasmodesmal permeability during stress.

机构信息

Department of Plant and Soil Sciences, Delaware Biotechnology Institute, University of Delaware, Newark, Delaware 19711, USA.

出版信息

Nat Plants. 2016 Apr 11;2(5):16034. doi: 10.1038/nplants.2016.34.

Abstract

Plants need to cope with biotic and abiotic stress through well-coordinated cell-to-cell communication to survive as sedentary organisms. Environmental challenges such as wounding, low temperature, oxidative states and pathogen infection are known to affect the symplasmic molecular exchange between plant cells determined by plasmodesmal permeability. However, the signalling pathways and mechanisms by which different environmental stressors affect plasmodesmal permeability are not well understood. Here we show that regulating callose accumulation at plasmodesmal channels is a common strategy to alter plasmodesmal permeability under both pathogen infection and mechanical wounding stress. We have identified Arabidopsis callose synthase 1 (CalS1) and CalS8 as key genes involved in this process, and have integrated these new players into both known and novel signalling pathways that control responses to biotic and abiotic stress. Our studies provide experimental data that indicate the presence of specialized pathways tuned to respond to particular stressors, and new insights into how plants regulate plasmodesmata in response to environmental assaults.

摘要

植物作为固着生物,需要通过细胞间的良好协调来应对生物和非生物胁迫。已知环境挑战,如创伤、低温、氧化状态和病原体感染,会影响由胞质通道通透性决定的植物细胞之间的胞质分子交换。然而,不同环境胁迫因子影响胞质通道通透性的信号通路和机制尚不清楚。在这里,我们表明,调节质膜通道处的胼胝质积累是在病原体感染和机械创伤胁迫下改变胞质通道通透性的一种常见策略。我们已经鉴定出拟南芥几丁质合酶 1(CalS1)和 CalS8 是参与这一过程的关键基因,并将这些新的参与者整合到控制生物和非生物胁迫反应的已知和新的信号通路中。我们的研究提供了实验数据,表明存在专门的途径来响应特定的胁迫因子,并深入了解植物如何调节质膜通道以应对环境攻击。

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