{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T20:08:50Z","timestamp":1792786130476,"version":"4.5.0"},"reference-count":59,"publisher":"Oxford University Press (OUP)","issue":"10","license":[{"start":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T00:00:00Z","timestamp":1790553600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100008530","name":"European Regional Development Fund","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100008530","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Spanish Ministerio de Ciencia e Innovaci\u00f3n","id":[{"id":"https:\/\/ror.org\/05r0vyz12","id-type":"ROR","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100011033","name":"Agencia Estatal de Investigaci\u00f3n","doi-asserted-by":"publisher","award":["PID2021- 124716OB-I00"],"award-info":[{"award-number":["PID2021- 124716OB-I00"]}],"id":[{"id":"10.13039\/501100011033","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Fundaci\u00f3 Sant Joan de D\u00e9u per la Recerca"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,9,30]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Ewing sarcoma (EwS) is an aggressive, human-exclusive tumor typically driven by the EWS::friend leukemia integration 1 (FLI1) fusion protein. To assess whether EWS::FLI1's neomorphic functions depend on evolutionarily recent cofactors, we expressed EWS::FLI1 in Saccharomyces cerevisiae, a minimal system in which the BAF complex is strongly diverged and ETS transcription factors (ETS-TFs), polycomb group (PcG) proteins, and CBP\/p300 are absent. We used co-IP\/mass spectrometry to map the yeast interactome, ChIP-seq to identify gDNA binding sequences, RNA-seq for gene expression, and engineered reporters to test conversion of GGAA tandem repeats (GGAA\u03bcSat) into neoenhancers. We found that the yeast EWS::FLI1 interactome was limited and distinct from its human counterpart, sharing core machinery (RNA polymerase II, FACT) but lacking BAF\/SWI\u2013SNF and spliceosome complexes, and showing enrichment for SAGA. EWS::FLI1 binds to hundreds of yeast genomic sites with preference for putative ETS-TF consensus sequences and CA dinucleotide repeats, and redirects RNA polymerase II to EWS::FLI1-bound loci. Yet, EWS::FLI1-expressing cells presented only minimal transcriptional dysregulation, in contrast to the extensive changes observed in human and Drosophila cells. Finally, EWS::FLI1 successfully converted silent GGAA\u03bcSat sequences into active enhancers in yeast. This remarkable result occurs despite the absence of homologs for key human activators, such as CBP\/p300, suggesting that EWS::FLI1 can mobilize functionally related, nonhomologous pathways to establish neoenhancers at GGAA\u03bcSat sites. Altogether, our results indicate that EWS::FLI1's core ability to drive GGAA\u03bcSat-dependent gene expression is a conserved, ancient property, while GGAA\u03bcSat-independent extensive transcriptome reprogramming depends on animal-specific cofactors and pathways.<\/jats:p>","DOI":"10.1093\/pnasnexus\/pgag329","type":"journal-article","created":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T08:21:02Z","timestamp":1790583662000},"source":"Crossref","is-referenced-by-count":0,"title":["Ancient and animal-specific regulatory modes of EWS::FLI1 revealed by a minimal yeast model"],"prefix":"10.1093","volume":"5","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5987-2570","authenticated-orcid":false,"given":"Diego","family":"Vel\u00e1zquez","sequence":"first","affiliation":[{"name":"Institute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology , Barcelona 08028 ,","place":["Spain"]},{"name":"Developmental Tumor Biology Laboratory, Institut de Recerca Sant Joan de De\u0301u, Esplugues de Llobregat , Barcelona 08950 ,","place":["Spain"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3426-4234","authenticated-orcid":false,"given":"Cristina","family":"Molnar","sequence":"additional","affiliation":[{"name":"Institute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology , Barcelona 08028 ,","place":["Spain"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3789-4514","authenticated-orcid":false,"given":"Jose","family":"Reina","sequence":"additional","affiliation":[{"name":"Institute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology , Barcelona 08028 ,","place":["Spain"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jaume","family":"Mora","sequence":"additional","affiliation":[{"name":"Developmental Tumor Biology Laboratory, Institut de Recerca Sant Joan de De\u0301u, Esplugues de Llobregat , Barcelona 08950 ,","place":["Spain"]},{"name":"Pediatric Cancer Center Barcelona (PCCB), Hospital Sant Joan de De\u0301u, Esplugues de Llobregat , Barcelona 08950 ,","place":["Spain"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5259-3608","authenticated-orcid":false,"given":"Cayetano","family":"Gonzalez","sequence":"additional","affiliation":[{"name":"Institute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology , Barcelona 08028 ,","place":["Spain"]},{"name":"Instituci\u00f3 Catalana de Recerca i Estudis Avan\u00e7ats (ICREA) , Barcelona 08010 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