Scribe.Lecture 31.docx

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Department
Cell and Systems Biology
Course Code
CSB328H1
Professor
William Navarre

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Lecture 31 2 1. key step in the evolution of salmonella from ancestral salmonella was the T3SS 1. to transfer protein into host cell 2. S. bongori rarely infects humans 3. S. enteric & S. bongori acquired diff T3SS 4. SPI-2 SS didn’t look anything like the SPI-1 SS 5. there are 7 subspecies of S. enteric 6. subspecies I encode pathogens that infect humans 7. salmonella typhi has strictly human hosts 8. typhimurium – food poisoning 9. Dublin – acquired through contaminated meat 10. see first acquisition of SPI-1, SPI-2 3 11. the diff T3SS (SPI-1, SPI-2) were acquired to do diff things 12. used at diff times during infection 13. SPI-1 & SPI-2 are never expressed at the same time (turned off when the other is turned on) 10 14. salmonella invasion by the T3SS 15. bacteria strip away the microvilli and drive massive ruffle at cell surface 16. drive actin polymerization w/in the cell and drives ruffling to start uptake by vacuoles 17. when inside vacuole, can replicate 11 18. once inside cell, a vacuole goes through an ordered maturation sequence 19. salmonella blocks the maturation and stays in a permanent features of early endosome, then quickly modify the T3 effectors, sets up a niche where they can replicate and produce Sif structures and prevents lysosome fusion 12 20. invasion of host cell is driving by the SPI-1 T3SS 21. injects a cocktail of diff effectors into host cell 22. in some cell types like macrophages, the bacteria can inject one effector (SipB) to directly kill them 1. rapid 23. 4 diff effectors can modulate actin rearrangement to drive the ruffling mechanism to drive uptake into a vacuole 1. salmonella directly manipulates host cell actin rearragnemtns 1. once inside, they turn off actin rearrangement 2. too much actin is bad, host can detect when actin is being modulated 24. salmonella forces their uptake into host (other pathogens wait around to be passively taken up by host) 14 25. there is also SPI-1 independent uptake 26. some effectors can modulate gene expression in host 27. some control SVC maturation & positioning 28. some kill cells (sometimes want to kill cells, sometimes want to modulate, and not kill cells) 28 29. early on, bacteria move in vacuoles towards the nucleus 1. at 8 h, right at nucleus, right at golgi 30. later during infection, they start to move to periphery (by 24 h, at periphery) 1. outward mvmt allows bacteria to spread themselves out 31. pathogen goal: get in towards nucleus, replicate, then get out and move to next cell 29 32. key function of SPI-2 T3SS is spreading from cell to cell 33. PipB2, a kinesin recruitor (that is re
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