{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,4,9]],"date-time":"2026-04-09T13:23:05Z","timestamp":1775740985288,"version":"3.50.1"},"posted":{"date-parts":[[2026,3,17]]},"group-title":"Neuroscience","reference-count":118,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,3,17]],"date-time":"2026-03-17T00:00:00Z","timestamp":1773705600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,4,7]]},"abstract":"<jats:p>\n                  Binge-eating disorder (BED) is the most common eating disorder worldwide and carries life-altering comorbidities. While genetic and environmental risk factors have been identified, the mechanisms that determine inter-individual susceptibility to BED remain largely unknown. Here, we demonstrate that developmental dosage of the DNA hydroxymethylase\n                  <jats:italic>Tet1<\/jats:italic>\n                  defines stable inter-individual differences in binge-eating susceptibility. In mice, midbrain dopaminergic neurons of the ventral tegmental area (VTA\n                  <jats:sup>DA<\/jats:sup>\n                  ) are essential for the induction of addictive binge-eating behavior, express high levels of\n                  <jats:italic>Tet1<\/jats:italic>\n                  , and undergo rapid and widespread DNA hydroxymethylation remodeling upon experimental binge eating. Strikingly,\n                  <jats:italic>Tet1<\/jats:italic>\n                  haploinsufficiency creates pronounced inter-individual variation in binge-eating susceptibility even among genetically identical mice, which we trace to reduced connectivity between the prelimbic medial prefrontal cortex (mPFC\n                  <jats:sup>PL<\/jats:sup>\n                  ) and the VTA. Chemogenetic inhibition of mPFC\n                  <jats:sup>PL<\/jats:sup>\n                  \u2192VTA projections reduces binge-eating susceptibility, whereas EGR1-guided re-activation of TET1 in VTA dopaminergic neurons restores susceptibility, supporting a causal role for this axis. Importantly,\n                  <jats:italic>TET1<\/jats:italic>\n                  promoter methylation in patients associates with binge-eating behavior and reward-circuit function, suggesting conservation of this regulatory network in humans. Collectively, these findings identify\n                  <jats:italic>Tet1<\/jats:italic>\n                  dosage as a novel regulator of binge-eating susceptibility and provide a mechanistic basis for how inter-individual differences in behavior are established.\n                <\/jats:p>","DOI":"10.64898\/2026.03.14.711800","type":"posted-content","created":{"date-parts":[[2026,3,18]],"date-time":"2026-03-18T04:15:16Z","timestamp":1773807316000},"source":"Crossref","is-referenced-by-count":0,"title":["Midbrain\n                  <i>Tet1<\/i>\n                  dosage defines inter-individual binge-eating susceptibility"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6884-7046","authenticated-orcid":false,"given":"Tim","family":"Gruber","sequence":"first","affiliation":[{"name":"Department of Epigenetics, Van Andel Institute, Grand Rapids, MI, USA"},{"name":"Department of Metabolism and Nutritional Programming, Van Andel Institute, Grand Rapids, MI, 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