Kumar Rakesh, Mukherjee Prasun K
School of Life Sciences, Jawaharlal Nehru University, New Delhi, 110067 India.
Nuclear Agriculture and Biotechnology Division, Bhabha Atomic Research Centre, Trombay, Mumbai, 400085 India.
3 Biotech. 2021 Mar;11(3):144. doi: 10.1007/s13205-021-02652-8. Epub 2021 Feb 26.
The filamentous fungi spp. are widely used for plant growth promotion and disease control. They form stable symbiosis-like relationship with roots. Unlike plant pathogens and mycorrhizae, the molecular events leading to the development of this association is not well understood. Pathogens deploy effector proteins to suppress or evade plant defence. Indirect evidences suggest that spp. can also deploy effector-like proteins to suppress plant defence favouring colonization of roots. Here, using computer simulation, we provide evidence that may deploy analogues of host defence proteins to "neutralize" its own effector protein to minimize damage to host tissues, as one of the mechanisms to achieve a stable symbiotic relationship with plants. We provide evidence that Bys1 protein has a structure similar to plant PR5/thaumatin-like protein and can bind Alt a 1 with a very high affinity, which might lead to the inactivation of its own effector protein. We have, for the first time, predicted a fungal protein that is a competitive inhibitor of a fungal effector protein deployed by many pathogenic fungi to suppress plant defence, and this protein/gene can potentially be used to enhance plant defence through transgenic or other approaches.
The online version contains supplementary material available at 10.1007/s13205-021-02652-8.
丝状真菌属被广泛用于促进植物生长和控制病害。它们与根系形成类似稳定共生的关系。与植物病原体和菌根不同,导致这种关联发展的分子事件尚未得到充分理解。病原体利用效应蛋白来抑制或逃避植物防御。间接证据表明,该属真菌也可利用类效应蛋白来抑制植物防御,从而有利于根系定殖。在此,我们通过计算机模拟提供证据表明,该真菌可能利用宿主防御蛋白的类似物来“中和”自身的效应蛋白,以尽量减少对宿主组织的损害,这是与植物建立稳定共生关系的机制之一。我们提供证据表明,该真菌的Bys1蛋白具有与植物PR5/类thaumatin蛋白相似的结构,并且能够以非常高的亲和力结合Alt a 1,这可能导致其自身效应蛋白失活。我们首次预测了一种真菌蛋白,它是许多致病真菌用于抑制植物防御的一种真菌效应蛋白的竞争性抑制剂,并且这种蛋白/基因有可能通过转基因或其他方法用于增强植物防御。
在线版本包含可在10.1007/s13205-021-0265-8获取的补充材料。