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IbinA and IbinB are related short peptides with robust expression upon microbial challenge in\n                      <jats:italic>Drosophila melanogaster<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      <jats:italic>Ibin<\/jats:italic>\n                      genes are ubiquitously present in flies of the\n                      <jats:italic>Drosophila<\/jats:italic>\n                      subgenus\n                      <jats:italic>Sophophora<\/jats:italic>\n                      , replacing the likely evolutionarily older, related gene,\n                      <jats:italic>Mibin<\/jats:italic>\n                      , which is found across a much wider range of cyclorrhaphan flies and is also upregulated following infection. We observed no direct bactericidal or bacteriostatic activity for IbinA or IbinB in vitro. Using single and double\n                      <jats:italic>Ibin<\/jats:italic>\n                      mutant\n                      <jats:italic>Drosophila<\/jats:italic>\n                      lines, we examined their roles in development and during microbial infections.\n                      <jats:italic>IbinA<\/jats:italic>\n                      is expressed in early pupae, and a lack of\n                      <jats:italic>IbinA<\/jats:italic>\n                      and\n                      <jats:italic>IbinB<\/jats:italic>\n                      leads to temperature-dependent formation of melanized tissue during metamorphosis, frequently around the trachea. IbinA and IbinB have distinct effects on susceptibility to microbial infection. For example, flies lacking\n                      <jats:italic>IbinB<\/jats:italic>\n                      had improved survival when challenged with\n                      <jats:italic>Listeria monocytogenes<\/jats:italic>\n                      , an intracellular pathogen, whereas a lack of\n                      <jats:italic>IbinA<\/jats:italic>\n                      alone had no effect. RNA sequencing following\n                      <jats:italic>L. monocytogenes<\/jats:italic>\n                      infection showed enhanced Toll target gene expression in flies lacking\n                      <jats:italic>IbinB<\/jats:italic>\n                      , suggesting that IbinB acts as a negative regulator of the Toll pathway. In contrast,\n                      <jats:italic>IbinA<\/jats:italic>\n                      mutants had decreased Toll target gene expression. Correspondingly,\n                      <jats:italic>IbinB<\/jats:italic>\n                      mutant flies had improved, and\n                      <jats:italic>Ibin<\/jats:italic>\n                      A compromised survival in septic fungal infection, where the Toll pathway has a major role.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Our study provides insight into the roles of IbinA and IbinB in regulation of the immune response in\n                      <jats:italic>Drosophila<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s12915-025-02501-7","type":"journal-article","created":{"date-parts":[[2026,1,9]],"date-time":"2026-01-09T08:36:18Z","timestamp":1767947778000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["IbinA and IbinB regulate the Toll pathway-mediated immune response in Drosophila melanogaster"],"prefix":"10.1186","volume":"24","author":[{"given":"Matthew K.","family":"Maasdorp","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Susanna","family":"Valanne","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laura","family":"Vesala","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Petra","family":"Vornanen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elina","family":"Haukkavaara","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tea","family":"Tuomela","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aino","family":"Malin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tiina S.","family":"Salminen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dan","family":"Hultmark","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5776-164X","authenticated-orcid":false,"given":"Mika","family":"R\u00e4met","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,1,9]]},"reference":[{"key":"2501_CR1","doi-asserted-by":"publisher","first-page":"697","DOI":"10.1146\/annurev.immunol.25.022106.141615","volume":"25","author":"B Lemaitre","year":"2007","unstructured":"Lemaitre B, Hoffmann J. 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