Plasma membrane damage caused by listeriolysin O is not repaired through endocytosis of the membrane pore

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 disrupt cellular homeostasis. Yet, little is known about the specific role of distinct endocytic machineries in this pr...

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Main Authors: Lars Nygård Skalman, Mikkel R. Holst, Elin Larsson, Richard Lundmark
Format: Article
Language:English
Published: The Company of Biologists 2018-10-01
Series:Biology Open
Subjects:
LLO
Online Access:http://bio.biologists.org/content/7/10/bio035287
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spelling doaj-7295c383426c42528c838ab96fdd42732021-06-02T18:47:12ZengThe Company of BiologistsBiology Open2046-63902018-10-0171010.1242/bio.035287035287Plasma membrane damage caused by listeriolysin O is not repaired through endocytosis of the membrane poreLars Nygård Skalman0Mikkel R. Holst1Elin Larsson2Richard Lundmark3 Integrative Medical Biology, Umeå University, 901 87 Umeå, Sweden Integrative Medical Biology, Umeå University, 901 87 Umeå, Sweden Medical Biochemistry and Biophysics, Laboratory for Molecular Infection Medicine Sweden, Umeå University, 901 87 Umeå, Sweden Integrative Medical Biology, Umeå University, 901 87 Umeå, Sweden 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 disrupt 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.http://bio.biologists.org/content/7/10/bio035287Membrane poreRepairMembrane damageLLOListeriolysinCaveolaeClathrin-mediated endocytosis Clathrin-independent endocytosisCLIC
collection DOAJ
language English
format Article
sources DOAJ
author Lars Nygård Skalman
Mikkel R. Holst
Elin Larsson
Richard Lundmark
spellingShingle Lars Nygård Skalman
Mikkel R. Holst
Elin Larsson
Richard Lundmark
Plasma membrane damage caused by listeriolysin O is not repaired through endocytosis of the membrane pore
Biology Open
Membrane pore
Repair
Membrane damage
LLO
Listeriolysin
Caveolae
Clathrin-mediated endocytosis
Clathrin-independent endocytosis
CLIC
author_facet Lars Nygård Skalman
Mikkel R. Holst
Elin Larsson
Richard Lundmark
author_sort Lars Nygård Skalman
title Plasma membrane damage caused by listeriolysin O is not repaired through endocytosis of the membrane pore
title_short Plasma membrane damage caused by listeriolysin O is not repaired through endocytosis of the membrane pore
title_full Plasma membrane damage caused by listeriolysin O is not repaired through endocytosis of the membrane pore
title_fullStr Plasma membrane damage caused by listeriolysin O is not repaired through endocytosis of the membrane pore
title_full_unstemmed Plasma membrane damage caused by listeriolysin O is not repaired through endocytosis of the membrane pore
title_sort plasma membrane damage caused by listeriolysin o is not repaired through endocytosis of the membrane pore
publisher The Company of Biologists
series Biology Open
issn 2046-6390
publishDate 2018-10-01
description 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 disrupt 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.
topic Membrane pore
Repair
Membrane damage
LLO
Listeriolysin
Caveolae
Clathrin-mediated endocytosis
Clathrin-independent endocytosis
CLIC
url http://bio.biologists.org/content/7/10/bio035287
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AT elinlarsson plasmamembranedamagecausedbylisteriolysinoisnotrepairedthroughendocytosisofthemembranepore
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