{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T10:41:48Z","timestamp":1790505708505,"version":"4.1.0"},"reference-count":44,"publisher":"American Society for Microbiology","issue":"9","license":[{"start":{"date-parts":[[2007,9,1]],"date-time":"2007-09-01T00:00:00Z","timestamp":1188604800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Eukaryot Cell"],"published-print":{"date-parts":[[2007,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The\n            <jats:italic>alb1<\/jats:italic>\n            (\n            <jats:italic>pksP<\/jats:italic>\n            ) gene has been reported as a virulence factor controlling the pigmentation and morphology of conidia in\n            <jats:italic>Aspergillus fumigatus<\/jats:italic>\n            . A recent report suggested that\n            <jats:italic>laeA<\/jats:italic>\n            regulates\n            <jats:italic>alb1<\/jats:italic>\n            expression and conidial morphology but not pigmentation in the\n            <jats:italic>A. fumigatus<\/jats:italic>\n            strain AF293.\n            <jats:italic>laeA<\/jats:italic>\n            has also been reported to regulate the synthesis of secondary metabolites, such as gliotoxin. We compared the role of\n            <jats:italic>laeA<\/jats:italic>\n            in the regulation of conidial morphology and the expression of\n            <jats:italic>alb1<\/jats:italic>\n            and\n            <jats:italic>gliP<\/jats:italic>\n            in strains B-5233 and AF293, which differ in colony morphology and nutritional requirements. Deletion of\n            <jats:italic>laeA<\/jats:italic>\n            did not affect conidial morphology or pigmentation in these strains, suggesting that\n            <jats:italic>laeA<\/jats:italic>\n            is not involved in\n            <jats:italic>alb1<\/jats:italic>\n            regulation during conidial morphogenesis. Deletion of\n            <jats:italic>laeA<\/jats:italic>\n            , however, caused down-regulation of\n            <jats:italic>alb1<\/jats:italic>\n            during mycelial growth in a liquid medium. Transcription of\n            <jats:italic>gliP<\/jats:italic>\n            , involved in the synthesis of gliotoxin, was drastically reduced in B-5233\n            <jats:italic>laeA\u0394<\/jats:italic>\n            , and the gliotoxin level found in the culture filtrates was 20% of wild-type concentrations. While up-regulation of\n            <jats:italic>gliP<\/jats:italic>\n            in AF293 was comparable to that in B-5233, the relative mRNA level in AF293\n            <jats:italic>laeA\u0394<\/jats:italic>\n            was about fourfold lower than that in B-5233\n            <jats:italic>laeA\u0394<\/jats:italic>\n            . Strain B-5233\n            <jats:italic>laeA\u0394<\/jats:italic>\n            caused slower onset of fatal infection in mice relative to that with B-5233. Histopathology of sections from lungs of infected mice corroborated the survival data. Culture filtrates from B-5233\n            <jats:italic>laeA\u0394<\/jats:italic>\n            caused reduced death in thymoma cells and were less inhibitory to a respiratory burst of neutrophils than culture filtrates from B-5233. Our results suggest that while\n            <jats:italic>laeA<\/jats:italic>\n            is not involved in the regulation of\n            <jats:italic>alb1<\/jats:italic>\n            function in conidial morphology, it regulates the synthesis of gliotoxin and the virulence of\n            <jats:italic>A. fumigatus.<\/jats:italic>\n          <\/jats:p>","DOI":"10.1128\/ec.00140-07","type":"journal-article","created":{"date-parts":[[2007,7,14]],"date-time":"2007-07-14T01:10:41Z","timestamp":1184375441000},"page":"1552-1561","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":89,"title":["Role of\n            <i>laeA<\/i>\n            in the Regulation of\n            <i>alb1<\/i>\n            ,\n            <i>gliP<\/i>\n            , Conidial Morphology, and Virulence in\n            <i>Aspergillus fumigatus<\/i>"],"prefix":"10.1128","volume":"6","author":[{"given":"Janyce A.","family":"Sugui","sequence":"first","affiliation":[{"name":"Laboratory of Clinical Infectious Diseases"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julian","family":"Pardo","sequence":"additional","affiliation":[{"name":"Max Planck Institute of Immunology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yun C.","family":"Chang","sequence":"additional","affiliation":[{"name":"Laboratory of Clinical Infectious Diseases"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Arno","family":"Mu\u0308llbacher","sequence":"additional","affiliation":[{"name":"John Curtin School of Medical Research, Australian National University, Canberra, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kol A.","family":"Zarember","sequence":"additional","affiliation":[{"name":"Laboratory of Host Defense"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eva M.","family":"Galvez","sequence":"additional","affiliation":[{"name":"Institut fu\u0308r Physikalische Chemie, Freiburg Universita\u0308t, Freiburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lauren","family":"Brinster","sequence":"additional","affiliation":[{"name":"Office of Research Services, National Institutes of Health, Bethesda, Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patricia","family":"Zerfas","sequence":"additional","affiliation":[{"name":"Office of Research Services, National Institutes of Health, Bethesda, Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John I.","family":"Gallin","sequence":"additional","affiliation":[{"name":"Laboratory of Host Defense"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Markus M.","family":"Simon","sequence":"additional","affiliation":[{"name":"Max Planck Institute of Immunology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kyung J.","family":"Kwon-Chung","sequence":"additional","affiliation":[{"name":"Laboratory of Clinical Infectious Diseases"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1183\/09031936.95.08101681"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1080\/j.1365-280X.1999.00225.x"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1128\/EC.4.9.1574-1582.2005"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.00780-06"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.chembiol.2005.10.008"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1128\/EC.3.2.527-535.2004"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2958.2006.05330.x"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1128\/EC.00049-06"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1086\/513943"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1093\/infdis\/155.1.1"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1016\/0192-0561(86)90016-0"},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.65.12.5110-5117.1997"},{"key":"e_1_3_2_14_2","doi-asserted-by":"publisher","DOI":"10.3314\/jjmm.43.37"},{"key":"e_1_3_2_15_2","doi-asserted-by":"publisher","DOI":"10.1080\/13693780600835773"},{"key":"e_1_3_2_16_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2958.2006.05373.x"},{"key":"e_1_3_2_17_2","first-page":"201","year":"1992","unstructured":"Kwon-Chung, K. 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