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Autophagy Volume 18, 2022 - Issue 2
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Autophagic Punctum

Innate host defense mechanisms SAC bacteria by regulating phosphoinositide kinases and phosphatases

Kimberly L. Careya Infectious Disease and Microbiome Program, Broad Institute of MIT and Harvard, Cambridge, MA, USACorrespondence[email protected]
ORCID Iconhttps://orcid.org/0000-0002-0836-8710View further author information
ORCID Icon,
Kai Liub Center for Computational and Integrative Biology, Department of Molecular Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USAView further author information
&
Ramnik J. Xaviera Infectious Disease and Microbiome Program, Broad Institute of MIT and Harvard, Cambridge, MA, USA;b Center for Computational and Integrative Biology, Department of Molecular Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA;c Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA;d Klarman Cell Observatory, Broad Institute of MIT and Harvard, Cambridge, MA, USAORCID Iconhttps://orcid.org/0000-0002-5630-5167View further author information
ORCID Icon
Pages 452-454 | Received 27 Oct 2021, Accepted 01 Nov 2021, Published online: 23 Nov 2021

Figures & data

Figure 1. Function of SACM1L PtdIns4P phosphatase in autophagy. Loss of SACM1L leads to the accumulation of PtdIns4P on cellular membranes, including autophagosomes, and a defect in xenophagy-dependent restriction of intracellular bacterial replication. Fusion of lysosomes with nonselective autophagosomes, as well as those induced through selective mitophagy and aggrephagy, are unaffected by loss of SACM1L expression. Salmonella-secreted effector and PtdIns4Pbinding protein SteA contributes to the xenophagy defect by blocking lysosomal fusion, and thus, shifting the balance in favor of bacterial replication. Loss of both SACM1L and Salmonella SteA restores the host defense mechanism.

Figure 1. Function of SACM1L PtdIns4P phosphatase in autophagy. Loss of SACM1L leads to the accumulation of PtdIns4P on cellular membranes, including autophagosomes, and a defect in xenophagy-dependent restriction of intracellular bacterial replication. Fusion of lysosomes with nonselective autophagosomes, as well as those induced through selective mitophagy and aggrephagy, are unaffected by loss of SACM1L expression. Salmonella-secreted effector and PtdIns4Pbinding protein SteA contributes to the xenophagy defect by blocking lysosomal fusion, and thus, shifting the balance in favor of bacterial replication. Loss of both SACM1L and Salmonella SteA restores the host defense mechanism.

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