De Nisco Nicole J, Orth Kim, VanHook Annalisa M
Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Sci Signal. 2017 May 16;10(479):eaan5621. doi: 10.1126/scisignal.aan5621.
This Podcast features a conversation with Kim Orth and Nicole De Nisco, authors of a Research Resource that appears in the 16 May 2017 issue of , about how the marine bacterium rewires host cell signaling networks. thrives in warm brackish waters and infects both shellfish and finfish. This bacterium causes gastroenteritis when humans consume contaminated seafood that is raw or undercooked. delivers virulence factors into host cells through two different type 3 secretion systems (T3SSes). Whereas T3SS2 mediates gastroenteritis, T3SS1 is required for the bacterium to survive in its natural environment and delivers virulence factors that target conserved cellular processes. De Nisco examined transcriptional changes in human cells infected with a strain of that lacked T3SS2 but had an intact T3SS1. They found that the virulence factors delivered through T3SS1 initially induced transcriptional changes that promoted cell survival, then later repressed prosurvival signaling to induce cell death.Listen to Podcast.
本期播客呈现了一段对金·奥思(Kim Orth)和妮可·德·尼斯科(Nicole De Nisco)的访谈,他们是一篇研究资源的作者,该资源发表于2017年5月16日的《 》杂志,内容是关于海洋细菌如何重塑宿主细胞信号网络。这种细菌在温暖的咸淡水中大量繁殖,会感染贝类和有鳍鱼类。当人类食用未经煮熟或未煮熟的受污染海鲜时,这种细菌会引发肠胃炎。该细菌通过两种不同的3型分泌系统(T3SSes)将毒力因子传递到宿主细胞中。虽然T3SS2介导肠胃炎,但T3SS1是该细菌在其自然环境中生存所必需的,并且传递针对保守细胞过程的毒力因子。德·尼斯科研究了感染了一种缺乏T3SS2但T3SS1完整的菌株的人类细胞中的转录变化。他们发现,通过T3SS1传递的毒力因子最初会诱导促进细胞存活的转录变化,随后会抑制促存活信号以诱导细胞死亡。收听播客。