Ma Zhongchen, Li Ruirui, Hu Ruirui, Deng Xiaoyu, Xu Yimei, Zheng Wei, Yi Jihai, Wang Yong, Chen Chuangfu
International Joint Research Center for Animal Health Breeding, College of Animal Science and Technology, Shihezi University, Shihezi, China.
Collaborative Innovation Center for Prevention and Control of High Incidence Zoonotic Infectious Diseases in Western China, College of Animal Science and Technology, Shihezi University, Shihezi, China.
Front Microbiol. 2020 Nov 12;11:599205. doi: 10.3389/fmicb.2020.599205. eCollection 2020.
To date, a variety of effector proteins have been found to mediate host cell secretion, autophagy, inflammation, and other signal pathways, but nuclear effector proteins have not yet been reported. We identified the first nucleomodulin, BspJ, and we screened out the BspJ interaction host proteins NME/NM23 nucleoside diphosphate kinase 2 (NME2) and creatine kinase B (CKB) through yeast two-hybrid and co-immunoprecipitation assays. These proteins are related to the host cell energy synthesis, metabolism, and apoptosis pathways. nucleomodulin BspJ will decrease the expression level of NME2 and CKB. In addition, BspJ gene deletion strains promoted the apoptosis of macrophages and reduced the intracellular survival of in host cells. In short, we found nucleomodulin BspJ may directly or indirectly regulate host cell apoptosis through the interaction with NME2 and CKB by mediating energy metabolism pathways in response to the intracellular circulation of infection, but the mechanism needs further study.
迄今为止，已发现多种效应蛋白可介导宿主细胞分泌、自噬、炎症及其他信号通路，但核效应蛋白尚未见报道。我们鉴定出首个核调节蛋白BspJ，并通过酵母双杂交和免疫共沉淀实验筛选出与BspJ相互作用的宿主蛋白NME/NM23核苷二磷酸激酶2（NME2）和肌酸激酶B（CKB）。这些蛋白与宿主细胞能量合成、代谢及凋亡途径相关。核调节蛋白BspJ会降低NME2和CKB的表达水平。此外，BspJ基因缺失菌株促进巨噬细胞凋亡，并降低其在宿主细胞内的存活能力。简而言之，我们发现核调节蛋白BspJ可能通过与NME2和CKB相互作用，介导能量代谢途径，直接或间接调节宿主细胞凋亡，以应对感染的细胞内循环，但具体机制仍需进一步研究。
