{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T01:13:51Z","timestamp":1788225231145,"version":"build-2803163510"},"reference-count":48,"publisher":"American Society for Microbiology","issue":"5","license":[{"start":{"date-parts":[[2023,10,17]],"date-time":"2023-10-17T00:00:00Z","timestamp":1697500800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2023,10,17]],"date-time":"2023-10-17T00:00:00Z","timestamp":1697500800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/501100001691","name":"MEXT | Japan Society for the Promotion of Science","doi-asserted-by":"crossref","award":["19K07558"],"award-info":[{"award-number":["19K07558"]}],"id":[{"id":"10.13039\/501100001691","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100001691","name":"MEXT | Japan Society for the Promotion of Science","doi-asserted-by":"crossref","award":["20H3415"],"award-info":[{"award-number":["20H3415"]}],"id":[{"id":"10.13039\/501100001691","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Microbiol Spectr"],"published-print":{"date-parts":[[2023,10,17]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    <jats:italic toggle=\"yes\">Chlamydia trachomatis<\/jats:italic>\n                    infection can be regulated by autophagy-related (\n                    <jats:italic toggle=\"yes\">ATG<\/jats:italic>\n                    ) genes. Here, we found that the depletion of\n                    <jats:italic toggle=\"yes\">ATG9A<\/jats:italic>\n                    , one of the core\n                    <jats:italic toggle=\"yes\">ATG<\/jats:italic>\n                    genes, in HeLa cells suppressed\n                    <jats:italic toggle=\"yes\">C. trachomatis<\/jats:italic>\n                    growth in the inclusion. The growth was restored by re-expressing\n                    <jats:italic toggle=\"yes\">ATG9A<\/jats:italic>\n                    or an\n                    <jats:italic toggle=\"yes\">ATG9A<\/jats:italic>\n                    mutant impairing lipid scramblase activity in\n                    <jats:italic toggle=\"yes\">ATG9A<\/jats:italic>\n                    -knockout (KO) cells. Moreover, the depletion of lipid transfer proteins ATG2A\/B, responsible for isolation membrane expansion together with ATG9A, did not significantly alter the growth, suggesting that the non-autophagic function of ATG9A supports\n                    <jats:italic toggle=\"yes\">C. trachomatis<\/jats:italic>\n                    infection.\n                    <jats:italic toggle=\"yes\">ATG9A<\/jats:italic>\n                    -KO cells showed no infection-induced redistribution of the Golgi from the perinuclear region to inclusion, which was restored by re-expressing the mutant but not the\n                    <jats:italic toggle=\"yes\">ATG9A<\/jats:italic>\n                    mutant lacking an N-terminal adapter protein-binding domain. Re-expression of the N-terminal deletion mutant in\n                    <jats:italic toggle=\"yes\">ATG9A<\/jats:italic>\n                    -KO cells did not rescue\n                    <jats:italic toggle=\"yes\">C. trachomatis<\/jats:italic>\n                    growth, suggesting the importance of this domain for its growth. Although\n                    <jats:italic toggle=\"yes\">ATG9A<\/jats:italic>\n                    -KO cells showed enhanced TBK1 activation, interferon (IFN)-\u03b2 was not significantly increased, excluding the possibility that upregulation of stimulator of IFN genes (STING) signaling suppressed bacterial growth. Taken together, these findings suggest that the proper trafficking, rather than the isolation membrane expansion function, of ATG9A assists\n                    <jats:italic toggle=\"yes\">C. trachomatis<\/jats:italic>\n                    growth in the inclusion.\n                  <\/jats:p>\n                  <jats:sec>\n                    <jats:title>IMPORTANCE<\/jats:title>\n                    <jats:p>\n                      <jats:italic toggle=\"yes\">ATG9A<\/jats:italic>\n                      is an autophagy-related gene that functions during the isolation membrane expansion process to form autophagosomes, but it also has other functions independent of autophagy. In this study, we employed\n                      <jats:italic toggle=\"yes\">ATG9A<\/jats:italic>\n                      -deficient HeLa cells and found that the absence of\n                      <jats:italic toggle=\"yes\">ATG9A<\/jats:italic>\n                      negatively impacted proliferation of\n                      <jats:italic toggle=\"yes\">Chlamydia trachomatis<\/jats:italic>\n                      in inclusions. Furthermore, rescue experiments using\n                      <jats:italic toggle=\"yes\">ATG9A<\/jats:italic>\n                      mutants revealed that this action was mediated not by its autophagic function but by its binding ability to clathrin adapter proteins. These findings suggest that the proper trafficking of ATG9A assists\n                      <jats:italic toggle=\"yes\">C. trachomatis<\/jats:italic>\n                      growth in the inclusion.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/spectrum.02774-23","type":"journal-article","created":{"date-parts":[[2023,9,14]],"date-time":"2023-09-14T10:41:11Z","timestamp":1694688071000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":3,"title":["ATG9A supports\n                    <i>Chlamydia trachomatis<\/i>\n                    infection via autophagy-independent mechanisms"],"prefix":"10.1128","volume":"11","author":[{"given":"Michitaka","family":"Suzuki","sequence":"first","affiliation":[{"name":"Department of Anatomy and Histology, Fukushima Medical University School of Medicine","place":["Hikarigaoka, 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