Abstract:
:Optic atrophy 1 (OPA1) is a mitochondrial inner membrane protein that has an important role in mitochondrial fusion and structural integrity. Dysfunctional OPA1 mutations cause atrophy of the optic nerve leading to blindness. Here, we show that OPA1 has an important role in the innate immune system. Using conditional knockout mice lacking Opa1 in neutrophils (Opa1N∆), we report that lack of OPA1 reduces the activity of mitochondrial electron transport complex I in neutrophils. This then causes a decline in adenosine-triphosphate (ATP) production through glycolysis due to lowered NAD+ availability. Additionally, we show that OPA1-dependent ATP production in these cells is required for microtubule network assembly and for the formation of neutrophil extracellular traps. Finally, we show that Opa1N∆ mice exhibit a reduced antibacterial defense capability against Pseudomonas aeruginosa.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Amini P,Stojkov D,Felser A,Jackson CB,Courage C,Schaller A,Gelman L,Soriano ME,Nuoffer JM,Scorrano L,Benarafa C,Yousefi S,Simon HUdoi
10.1038/s41467-018-05387-ysubject
Has Abstractpub_date
2018-07-27 00:00:00pages
2958issue
1issn
2041-1723pii
10.1038/s41467-018-05387-yjournal_volume
9pub_type
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