{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,29]],"date-time":"2026-08-29T01:13:24Z","timestamp":1787966004784,"version":"build-2784847793"},"reference-count":60,"publisher":"American Society for Microbiology","issue":"8","license":[{"start":{"date-parts":[[2026,8,4]],"date-time":"2026-08-04T00:00:00Z","timestamp":1785801600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,8,4]],"date-time":"2026-08-04T00:00:00Z","timestamp":1785801600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["AI132422"],"award-info":[{"award-number":["AI132422"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["AI155473"],"award-info":[{"award-number":["AI155473"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["AI187284"],"award-info":[{"award-number":["AI187284"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Microbiol Spectr"],"published-print":{"date-parts":[[2026,8,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      Intrinsic and acquired antibiotic resistance in\n                      <jats:italic toggle=\"yes\">Mycobacterium abscessus<\/jats:italic>\n                      present unique challenges in treatment of its infections, which are rapidly emerging as a significant public health threat. The majority of clinically relevant antibiotics used against\n                      <jats:italic toggle=\"yes\">M. abscessus<\/jats:italic>\n                      infections target the ribosome, which undergoes remodeling and hibernation in\n                      <jats:italic toggle=\"yes\">Mycobacterium smegmatis<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">Mycobacterium tuberculosis<\/jats:italic>\n                      in response to zinc-limiting conditions. Ribosome remodeling involves replacement of multiple zinc-binding C+ ribosomal proteins with a CXXC motif by their respective C\u2212 paralogs lacking the motif, whereas ribosome hibernation involves recruitment of mycobacterial protein Y (Mpy) to the mRNA decoding center on the 30S subunit. Here, we report that zinc-responsive ribosome remodeling and hibernation are conserved in\n                      <jats:italic toggle=\"yes\">M. abscessus<\/jats:italic>\n                      . We further demonstrate that Mpy binding suppresses translation and preserves ribosome abundance under zinc-limited conditions, while conferring tolerance to the aminoglycoside amikacin. Systematic biochemical analyses demonstrate that amino acid residues of Mpy that are critical for its interaction with the ribosome are also essential for Mpy stability in the cytosol. Together, these findings demonstrate amikacin tolerance as an important outcome of ribosome hibernation in\n                      <jats:italic toggle=\"yes\">M. abscessus<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>IMPORTANCE<\/jats:title>\n                    <jats:p>\n                      <jats:italic toggle=\"yes\">Mycobacterium abscessus<\/jats:italic>\n                      causes life-threatening infections in people with underlying health conditions. The treatment regimens for\n                      <jats:italic toggle=\"yes\">M. abscessus<\/jats:italic>\n                      infections are months-long and include several ribosome-targeting antibiotics, such as amikacin. The long regimens are primarily attributed to intrinsic drug resistance in the pathogen. However, mechanisms of resistance for several of the antibiotics remain unclear. Here, we show that ribosome hibernation in\n                      <jats:italic toggle=\"yes\">M. abscessus<\/jats:italic>\n                      by Mpy under zinc-starved conditions, which likely prevail in hosts, is a key determinant of amikacin tolerance. Thus, Mpy is a potential target for potentiating amikacin activity against\n                      <jats:italic toggle=\"yes\">M. abscessus<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/spectrum.00378-26","type":"journal-article","created":{"date-parts":[[2026,7,6]],"date-time":"2026-07-06T13:25:49Z","timestamp":1783344349000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":1,"title":["Ribosome hibernation in zinc-starved\n                    <i>Mycobacterium abscessus<\/i>\n                    confers amikacin tolerance"],"prefix":"10.1128","volume":"14","author":[{"given":"Ryan Z.","family":"Treen","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/04hf5kq57","id-type":"ROR","asserted-by":"publisher"}],"name":"Division of Genetics, Wadsworth Center, NY State Department of Health","place":["Albany, 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