ATF6通过诱导胃素和改变胆固醇动态,使虫的病原体感染成为可能
Kaylee A Vosbigian1, Sarah J Wright1, Brianna P Steiert1
1Department of Veterinary Microbiology and Pathology, College of Veterinary Sciences, Washington State University, Pullman, WA 99164.
概括
研究人员发现,的ATF6通路对于病原体的生存至关重要. 准这种途径和胃基因会破坏胆固醇平衡,抑制像莱姆病这样的传播疾病.
科学领域:
- 载体生物学 载体生物学
- 分子生物学分子生物学
- 传播的病原体
背景情况:
- 与脊椎动物宿主相比,内的病原体相互作用的了解很少.
- 展开蛋白反应 (UPR) 的ATF6分支在感染了Anaplasma phagocytophilum或Borrelia burgdorferi的身上被激活.
研究的目的:
- 研究ATF6通路在传播病原体生存中的作用.
- 为了确定ATF6调节基因及其功能在Ixodes scapularis的.
主要方法:
- 开发了一个自定义的R脚本 (ArthroQuest) 来分析tick促进器序列.
- 用 luciferase 试验,RNA 干扰和显微镜验证了作为 ATF6 标的胃蛋白.
- 评估了胃蛋白沉默对病原体殖民和胆固醇动态的影响.
主要成果:
- 在感染了A. phagocytophilum或B. burgdorferi的身上观察到ATF6激活.
- 禁用ATF6受限制的病原体生存.
- 斯托马丁被确定为ATF6向基因,参与胆固醇恒温.
- 静止胃氨酸减少了A. 细胞菌体的殖民化,并扰乱了细胞胆固醇动态.
- 阻断胃素通过限制胆固醇的可用性来抑制细菌的生长.
结论:
- 伊克索斯ATF6通路通过Stomatin调节的胆固醇平衡促进了载体能力.
- 胃的ATF6调节是血液养关节动物的独特特征.
- 研究非模型生物体的基本过程对于理解载体能力至关重要.
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