Mitochondria shed their outer membrane in response to infection-induced stress.
Science
; 375(6577): eabi4343, 2022 Jan 14.
Article
em En
| MEDLINE
| ID: mdl-35025629
ABSTRACT
The outer mitochondrial membrane (OMM) is essential for cellular homeostasis. Yet little is known of the mechanisms that remodel it during natural stresses. We found that large "SPOTs" (structures positive for OMM) emerge during Toxoplasma gondii infection in mammalian cells. SPOTs mediated the depletion of the OMM proteins mitofusin 1 and 2, which restrict parasite growth. The formation of SPOTs depended on the parasite effector TgMAF1 and the host mitochondrial import receptor TOM70, which is required for optimal parasite proliferation. TOM70 enabled TgMAF1 to interact with the host OMM translocase SAM50. The ablation of SAM50 or the overexpression of an OMM-targeted protein promoted OMM remodeling independently of infection. Thus, Toxoplasma hijacks the formation of SPOTs, a cellular response to OMM stress, to promote its growth.
Texto completo:
1
Coleções:
01-internacional
Contexto em Saúde:
3_ND
Base de dados:
MEDLINE
Assunto principal:
Toxoplasma
/
Proteínas de Protozoários
/
Membranas Mitocondriais
/
Proteínas do Complexo de Importação de Proteína Precursora Mitocondrial
Limite:
Animals
/
Humans
Idioma:
En
Revista:
Science
Ano de publicação:
2022
Tipo de documento:
Article