{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,5,7]],"date-time":"2026-05-07T11:14:10Z","timestamp":1778152450805,"version":"3.51.4"},"posted":{"date-parts":[[2025,8,6]]},"group-title":"Developmental Biology","reference-count":104,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2025,8,6]],"date-time":"2025-08-06T00:00:00Z","timestamp":1754438400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,5,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:p>\n                  Delineating the genetic and environmental instigators of congenital heart disease (CHD), affecting up to 1% of newborns, will improve preventative, diagnostic, and therapeutic efforts to mitigate disease outcomes. Although mutations in\n                  <jats:italic>NAA15<\/jats:italic>\n                  , which encodes the auxiliary subunit of N-alpha-acetyltransferase A (NatA), are associated with CHD in humans, vertebrate animal models of\n                  <jats:italic>NAA15<\/jats:italic>\n                  -related heart disease have yet to be described. Therefore, we isolated zebrafish strains carrying null mutations in paralogs\n                  <jats:italic>naa15a<\/jats:italic>\n                  and\n                  <jats:italic>naa15b,<\/jats:italic>\n                  which we co-localized to the early larval myocardium. Double knockout (DKO)\n                  <jats:italic>naa15<\/jats:italic>\n                  -deficient larvae exhibited diminutive, lowly contractile, and bradycardic ventricles composed of fewer and smaller cardiomyocytes (CMs) incapable of proliferation. On a subcellular level, mutant CMs exhibited moderately disorganized myofibrils. CM-specific re-expression of\n                  <jats:italic>naa15a<\/jats:italic>\n                  partially rescued the contractility and growth deficits, revealing an indispensable myocardial function. Ubiquitous mis-expression of human\n                  <jats:italic>NAA15<\/jats:italic>\n                  achieved complete rescue, enabling functional testing of human\n                  <jats:italic>NAA15<\/jats:italic>\n                  variants. Animals with a reduced dosage (RD) of\n                  <jats:italic>naa15<\/jats:italic>\n                  survived to adulthood and shared phenotypes with DKO larvae, including smaller ventricular chambers and CMs, which exhibited mosaic myofibril disarray. Deep quantitative proteomic profiling of WT and\n                  <jats:italic>\n                    naa15\n                    <jats:sup>RD<\/jats:sup>\n                  <\/jats:italic>\n                  adult hearts revealed differential expression of multiple protein classes, including several subunits of mitochondrial respiratory complex I, a component of the electron transport chain. Accordingly, we documented reduced mitochondrial content and function in the myocardium of\n                  <jats:italic>naa15<\/jats:italic>\n                  -deficient larvae. Taken together, our data reveal myocardial functional and structural abnormalities associated with mitochondrial dysfunction in a vertebrate animal model of\n                  <jats:italic>NAA15<\/jats:italic>\n                  -related heart disease.\n                <\/jats:p>","DOI":"10.1101\/2025.08.04.668548","type":"posted-content","created":{"date-parts":[[2025,8,6]],"date-time":"2025-08-06T20:50:10Z","timestamp":1754513410000},"source":"Crossref","is-referenced-by-count":0,"title":["Mitochondrial dysfunction underlies cardiac contractility and growth defects in a zebrafish model of\n                  <i>NAA15<\/i>\n                  -related heart disease"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6080-8701","authenticated-orcid":false,"given":"Warlen P.","family":"Piedade","sequence":"first","affiliation":[{"name":"Division of Basic and Translational Cardiovascular Research, Department of Cardiology, Boston Children\u2019s Hospital, Boston, MA, 02115"},{"name":"Harvard Medical School, Boston, MA, 02115"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1177-4848","authenticated-orcid":false,"given":"Olivia","family":"Weeks","sequence":"additional","affiliation":[{"name":"Division of Basic and Translational Cardiovascular Research, Department of Cardiology, Boston Children\u2019s Hospital, Boston, MA, 02115"},{"name":"Harvard Medical School, Boston, MA, 02115"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hannah R.","family":"Moran","sequence":"additional","affiliation":[{"name":"Harvard Medical School, Boston, MA, 02115"},{"name":"Department of Medicine, Brigham and Women\u2019s Hospital, Boston, MA, 02115"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9385-3739","authenticated-orcid":false,"given":"Alexander A.","family":"Akerberg","sequence":"additional","affiliation":[{"name":"Division of Basic and Translational 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02115"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0062-9867","authenticated-orcid":false,"given":"Hasmik","family":"Keshishian","sequence":"additional","affiliation":[{"name":"Proteomics Platform, Broad Institute of MIT and Harvard, Cambridge, MA. 02140"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Patrick","family":"Hart","sequence":"additional","affiliation":[{"name":"Proteomics Platform, Broad Institute of MIT and Harvard, Cambridge, MA. 02140"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7203-4299","authenticated-orcid":false,"given":"Steven A.","family":"Carr","sequence":"additional","affiliation":[{"name":"Proteomics Platform, Broad Institute of MIT and Harvard, Cambridge, MA. 02140"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Calum A.","family":"MacRae","sequence":"additional","affiliation":[{"name":"Harvard Medical School, Boston, MA, 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