Asset Details
Do you wish to reserve the book?
Plasma membrane damage caused by Listeriolysin O is not repaired through endocytosis of the membrane pore
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Plasma membrane damage caused by Listeriolysin O is not repaired through endocytosis of the membrane pore
Do you wish to request the book?
Plasma membrane damage caused by Listeriolysin O is not repaired through endocytosis of the membrane pore
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Plasma membrane damage caused by Listeriolysin O is not repaired through endocytosis of the membrane pore
2018
Overview
Endocytic mechanisms have been suggested to be important for plasma membrane repair in response to pore-forming toxins such as Listeriolysin O (LLO), which form membrane pores that disrupts cellular homeostasis. Yet, little is known about the specific role of distinct endocytic machineries in this process. Here, we have addressed the importance of key endocytic pathways, and developed reporter systems for real-time imaging of the endocytic response to LLO pore formation. We found that loss of clathrin-independent endocytic pathways negatively influenced the efficiency of membrane repair. However, we did not detect any increased activity of these pathways, or co-localisation with the toxin or markers of membrane repair, suggesting that they were not directly involved in removal of LLO pores from the plasma membrane. In fact, markers of clathrin-independent carriers (CLICs) were rapidly disassembled in the acute phase of membrane damage due to Ca2+ influx, followed by a reassembly about 2 min after pore formation. We propose that these endocytic mechanisms might influence membrane repair by regulating the plasma membrane composition and tension, but not via direct internalisation of LLO pores.
