{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,27]],"date-time":"2026-10-27T19:38:53Z","timestamp":1793129933457,"version":"4.5.0"},"reference-count":106,"publisher":"American Society for Microbiology","issue":"10","license":[{"start":{"date-parts":[[2026,10,20]],"date-time":"2026-10-20T00:00:00Z","timestamp":1792454400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,10,20]],"date-time":"2026-10-20T00:00:00Z","timestamp":1792454400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["R01 AI149737"],"award-info":[{"award-number":["R01 AI149737"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000057","name":"National Institute of General Medical Sciences","doi-asserted-by":"publisher","award":["R35 GM149559"],"award-info":[{"award-number":["R35 GM149559"]}],"id":[{"id":"10.13039\/100000057","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["NIH R01 AI155664"],"award-info":[{"award-number":["NIH R01 AI155664"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000015","name":"U.S. Department of Energy","doi-asserted-by":"publisher","award":["DE-AC05-76RL01830"],"award-info":[{"award-number":["DE-AC05-76RL01830"]}],"id":[{"id":"10.13039\/100000015","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["mSystems"],"published-print":{"date-parts":[[2026,10,20]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      <jats:italic toggle=\"yes\">Mycobacterium abscessus<\/jats:italic>\n                      (\n                      <jats:italic toggle=\"yes\">Mab<\/jats:italic>\n                      ) is an opportunistic pathogen that can cause chronic, debilitating lung disease.\n                      <jats:italic toggle=\"yes\">Mab<\/jats:italic>\n                      is intrinsically resistant to most antibiotics, making\n                      <jats:italic toggle=\"yes\">Mab<\/jats:italic>\n                      infections challenging to manage and frequently incurable. During infection,\n                      <jats:italic toggle=\"yes\">Mab<\/jats:italic>\n                      adapts to survive various stresses, including hypoxia and nutrient starvation.\n                      <jats:italic toggle=\"yes\">In vitro<\/jats:italic>\n                      , these conditions drive\n                      <jats:italic toggle=\"yes\">Mab<\/jats:italic>\n                      into a drug-tolerant, non-replicating state. Changes in the\n                      <jats:italic toggle=\"yes\">Mab<\/jats:italic>\n                      proteome that result from entering a non-replicating state have been minimally described despite the clinical importance of this physiological state. Using\n                      <jats:italic toggle=\"yes\">Mab<\/jats:italic>\n                      reference strain ATCC 19977, we collected proteomic data comparing replicating to non-replicating states using a carbon starvation (CS) model of persistence. We identified 2,251 proteins overall (45% proteome coverage), and 17% of these proteins were found in only one of the two conditions. A third of identified proteins were significantly changed in abundance, indicating an extensive proteomic response to CS. The response regulator DosR and many DosRS-responsive proteins were significantly more abundant under CS, suggesting that this response regulator plays a key role in CS-induced\n                      <jats:italic toggle=\"yes\">Mab<\/jats:italic>\n                      persistence. Many aspects of cell wall biosynthesis were altered, including changes in glycolipid abundance under CS. Proteins involved in other key cellular processes such as secretion, oxidative phosphorylation, and nutrient metabolism were altered under CS. This proteomic analysis provides new insights and clarity into how the\n                      <jats:italic toggle=\"yes\">Mab<\/jats:italic>\n                      proteome is regulated during non-replicating persistence, a key consideration for understanding\n                      <jats:italic toggle=\"yes\">Mab<\/jats:italic>\n                      pathophysiology.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        <jats:italic toggle=\"yes\">Mycobacterium abscessus<\/jats:italic>\n                        (\n                        <jats:italic toggle=\"yes\">Mab<\/jats:italic>\n                        ) is a highly drug-resistant species of non-tuberculous mycobacteria (NTM). People most susceptible to pulmonary NTM infections are immunocompromised or have an existing lung disease, such as chronic obstructive pulmonary disease or cystic fibrosis. Infections with\n                        <jats:italic toggle=\"yes\">Mab<\/jats:italic>\n                        cause chronic lung disease that is challenging to manage. Patients typically must take multiple antibiotics daily for at least a year. Despite aggressive treatment regimens, cure rates remain low. One reason for this is\n                        <jats:italic toggle=\"yes\">Mab<\/jats:italic>\n                        \u2019s ability to enter dormancy during chronic infections. The authors provide a first description of the proteomic remodeling that occurs in\n                        <jats:italic toggle=\"yes\">Mab<\/jats:italic>\n                        in response to carbon starvation, which induces a non-replicating state. They report that a third of the proteome changes in response to carbon starvation, including pathways involved in cell envelope biosynthesis, energy production, and nutrient acquisition. The detailed description of these changes provides insights into the adaptations likely used by\n                        <jats:italic toggle=\"yes\">Mab<\/jats:italic>\n                        to survive during infection.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/msystems.00564-26","type":"journal-article","created":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T13:01:11Z","timestamp":1790168471000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["Carbon starvation of\n                    <i>Mycobacterium abscessus<\/i>\n                    induces a non-replicating state with extensive proteomic remodeling"],"prefix":"10.1128","volume":"11","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5842-0591","authenticated-orcid":false,"given":"Kaylyn 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