{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,10,24]],"date-time":"2026-10-24T10:31:55Z","timestamp":1792837915982,"version":"4.5.0"},"posted":{"date-parts":[[2026,7,17]]},"group-title":"Genetics","reference-count":61,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,7,17]],"date-time":"2026-07-17T00:00:00Z","timestamp":1784246400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"name":"NIH","award":["R03TR004645"],"award-info":[{"award-number":["R03TR004645"]}]},{"name":"NIH","award":["T32 GM152342"],"award-info":[{"award-number":["T32 GM152342"]}]},{"name":"NIH","award":["T32 GM008042"],"award-info":[{"award-number":["T32 GM008042"]}]},{"name":"NIH","award":["T32GM008243"],"award-info":[{"award-number":["T32GM008243"]}]},{"DOI":"10.13039\/501100011096","name":"DOST-PCHRD","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100011096","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,7,17]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                <jats:p>\n                  Bohring-Opitz syndrome (BOS, OMIM#605309) is a rare neurodevelopmental disorder caused by heterozygous and truncating variants in\n                  <jats:italic>ASXL1 (Additional Sex Combs Like 1<\/jats:italic>\n                  ), a chromatin-associated epigenetic regulator that forms the catalytic PR-DUB complex with BAP1. Truncating\n                  <jats:italic>ASXL1<\/jats:italic>\n                  variants are also recurrent somatic drivers in myeloid leukemia, yet the metabolic consequences of these mutations remain undefined. Using patient derived dermal fibroblasts, we show that truncating\n                  <jats:italic>ASXL1<\/jats:italic>\n                  variants drive a Warburg-like metabolic state characterized by increased glycolytic flux, and accumulation of pyruvate and lactate. Truncated ASXL1 and BAP1 show aberrant co-occupancy at an H3K4me3-marked intronic regulatory element within\n                  <jats:italic>MPC2<\/jats:italic>\n                  intron 1, with broadened ASXL1 occupancy extending beyond BRD4-defined regulatory boundaries while BRD4 positioning remains unchanged, consistent with aberrant PR-DUB complex spreading beyond its normally constrained chromatin territory. This altered occupancy is accompanied by modest but significant reduction in\n                  <jats:italic>MPC2<\/jats:italic>\n                  transcript abundance and a disproportionately larger reduction in MPC1 and MPC2 protein levels, indicating that transcriptional dysregulation at this intronic element is amplified at the protein level through post-transcriptional mechanisms including impaired MPC1\/MPC2 heterodimer stability. Pharmacologic MPC inhibition recapitulates both the metabolic and Wnt signaling phenotypes of BOS cells, while canonical Wnt activation increases glycolytic flux without reducing MPC abundance, establishing mitochondrial pyruvate restriction as causally upstream of signaling dysregulation. These findings define a previously unrecognized chromatin-to-metabolism axis connecting gain-of-function\n                  <jats:italic>ASXL1<\/jats:italic>\n                  truncation to mitochondrial pyruvate transport, identifying MPC as a central mediator of epigenetic-metabolic crosstalk in both a rare developmental syndrome and\n                  <jats:italic>ASXL1<\/jats:italic>\n                  -mutant myeloid malignancy.\n                <\/jats:p>\n                <jats:sec>\n                  <jats:title>Graphical Abstract<\/jats:title>\n                  <jats:p>\n                    <jats:fig id=\"ufig1\" position=\"float\" orientation=\"portrait\" fig-type=\"figure\">\n                      <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"737346v1_ufig1\" position=\"float\" orientation=\"portrait\"\/>\n                    <\/jats:fig>\n                  <\/jats:p>\n                  <jats:p>Truncating and heterozygous ASXL1 variants cause a neurodevelopmental syndrome called Bohring-Opitz syndrome. (1) At an epigenetic level, we have shown that Truncating ASXL1 variants drive more open chromatin and aberrant activation of key developmental pathways. (2) Truncating ASXL1 mutations are sufficient to drive Decreased MPC1 and MPC2 protein levels. (3) Decreased MPC1 or MPC2 level or function are sufficient to drive increased glycolysis which is observed in BOS cells. (4) Truncating ASXL1 mutations drive Increased Wnt signaling via MPC depletion. * Increased Wnt signaling (4) is also sufficient to drive increased glycolysis (3), however Increased Wnt signaling does not drive Decreased MPC1 and MPC2 levels (2).<\/jats:p>\n                <\/jats:sec>","DOI":"10.64898\/2026.07.13.737346","type":"posted-content","created":{"date-parts":[[2026,7,18]],"date-time":"2026-07-18T04:10:28Z","timestamp":1784347828000},"source":"Crossref","is-referenced-by-count":1,"title":["Truncating\n                  <i>ASXL1<\/i>\n                  variants rewire cellular metabolism via mitochondrial pyruvate carrier repression"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7102-6879","authenticated-orcid":false,"given":"Isabella","family":"Lin","sequence":"first","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, UCLA, Los Angeles, CA, USA"},{"name":"Department of Computational Medicine, 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