{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T15:21:41Z","timestamp":1785424901181,"version":"3.56.0"},"posted":{"date-parts":[[2026,6,16]]},"group-title":"Genetics","reference-count":0,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,6,16]],"date-time":"2026-06-16T00:00:00Z","timestamp":1781568000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"NSF","award":["2145195"],"award-info":[{"award-number":["2145195"]}]},{"name":"NIH","award":["R35GM124701"],"award-info":[{"award-number":["R35GM124701"]}]},{"name":"NIH","award":["R35GM139595"],"award-info":[{"award-number":["R35GM139595"]}]},{"name":"NIH","award":["F32GM156085"],"award-info":[{"award-number":["F32GM156085"]}]},{"name":"NIGMS","award":["P20GM103474"],"award-info":[{"award-number":["P20GM103474"]}]},{"award":["202324717"],"award-info":[{"award-number":["202324717"]}],"id":[{"id":"https:\/\/ror.org\/02hxgd925","id-type":"ROR","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,6,16]]},"abstract":"<jats:p>\n                  Maternally transmitted\n                  <jats:italic>Wolbachia<\/jats:italic>\n                  often cause cytoplasmic incompatibility (CI), a sperm modification that kills host embryos lacking the endosymbiont. CI produces defects in paternal chromosome replication, condensation, and segregation during the first zygotic cell cycle, but a significant fraction of embryos progress normally through this and subsequent cycles and only exhibit defects at later developmental stages. These results, together with documented CI-induced epigenetic chromatin modifications, suggest heritable chromatin modifications are responsible for the developmentally delayed defects. Here, we conducted a Position-Effect Variegation (PEV) screen in\n                  <jats:italic>Drosophila melanogaster<\/jats:italic>\n                  using\n                  <jats:italic>\n                    In(1)w\n                    <jats:sup>m4<\/jats:sup>\n                  <\/jats:italic>\n                  to test for persistent effects on heterochromatin-mediated silencing in adults that survived CI. We show that\n                  <jats:italic>Wolbachia<\/jats:italic>\n                  acts as a variegation suppressor, or\n                  <jats:italic>Su(var)<\/jats:italic>\n                  , increasing eye pigment when present in CI-inducing fathers, a reproducible effect observed across several maternal genotypes that differed in CI strength. That is, passage of the\n                  <jats:italic>\n                    In(1)w\n                    <jats:sup>m4<\/jats:sup>\n                  <\/jats:italic>\n                  through\n                  <jats:italic>Wolbachia<\/jats:italic>\n                  -infected males limits the spread of heterochromatin into the neighboring euchromatin in the progeny. This effect is consistent with disruption of heterochromatin establishment at the mid-blastula transition, when stochastic spreading of heterochromatin determines whether the displaced\n                  <jats:italic>white<\/jats:italic>\n                  gene is silenced. Surprisingly, maternal\n                  <jats:italic>Wolbachia<\/jats:italic>\n                  did not revert the PEV modification, and in one genotype,\n                  <jats:italic>Wolbachia<\/jats:italic>\n                  increased suppression. Together, our results demonstrate that\n                  <jats:italic>Wolbachia<\/jats:italic>\n                  -mediated chromatin effects persist to adulthood, are not corrected by CifA-dependent rescue, and can be compounded by maternal\n                  <jats:italic>Wolbachia<\/jats:italic>\n                  . These findings establish that rescue is incomplete at the level of heterochromatin-mediated silencing and suggest that CI-specific and constitutive\n                  <jats:italic>Wolbachia<\/jats:italic>\n                  chromatin effects may operate through at least partially independent pathways.\n                <\/jats:p>","DOI":"10.64898\/2026.06.12.731975","type":"posted-content","created":{"date-parts":[[2026,6,17]],"date-time":"2026-06-17T02:50:21Z","timestamp":1781664621000},"source":"Crossref","is-referenced-by-count":0,"title":["<i>Wolbachia<\/i>\n                  -induced cytoplasmic incompatibility produces heritable chromatin modifications that suppress position-effect variegation"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0009-0004-9994-9503","authenticated-orcid":false,"given":"Hunter J","family":"Hill","sequence":"first","affiliation":[{"name":"University of Montana;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William","family":"Sullivan","sequence":"additional","affiliation":[{"name":"University of California, Santa Cruz"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8269-7731","authenticated-orcid":false,"given":"Brandon S.","family":"Cooper","sequence":"additional","affiliation":[{"name":"University of Montana;"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"54368","container-title":[],"original-title":[],"link":[{"URL":"https:\/\/syndication.highwire.org\/content\/doi\/10.64898\/2026.06.12.731975","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,6,17]],"date-time":"2026-06-17T02:50:21Z","timestamp":1781664621000},"score":1,"resource":{"primary":{"URL":"http:\/\/biorxiv.org\/lookup\/doi\/10.64898\/2026.06.12.731975"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2026,6,16]]},"references-count":0,"URL":"https:\/\/doi.org\/10.64898\/2026.06.12.731975","relation":{},"subject":[],"published":{"date-parts":[[2026,6,16]]},"subtype":"preprint"}}