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The extent to which mutant mRNA\u2010driven disruptions contribute to HD pathogenesis, particularly in comparison to the dominant mechanisms related to the gain\u2010of\u2010function effects of the mutant polyQ protein, is still debatable. To evaluate this contribution in\u00a0vivo, we generated two mouse models through a knock\u2010in strategy at the\n                    <jats:italic>Rosa26<\/jats:italic>\n                    locus. These models expressed distinct variants of human mutant\n                    <jats:italic>HTT<\/jats:italic>\n                    cDNA fragment: a translated variant (HD\/100Q model, serving as a reference) and a nontranslated variant (HD\/100CAG model). The cohorts of animals were subjected to a broad spectrum of molecular, behavioral, and cognitive analysis for 21\u2009months. Behavioral testing revealed alterations in both models, with the HD\/100Q model exhibiting late disease phenotype. The rotarod, static rod, and open\u2010field tests showed some motor deficits in HD\/100CAG and HD\/100Q model mice during the light phase, while ActiMot indicated hyperkinesis during the dark phase. Both models also exhibited certain gene deregulations in the striatum that are related to disrupted pathways and phenotype alterations observed in HD. In conclusion, we provide in\u00a0vivo evidence for a minor contributory role of mutant RNA in HD pathogenesis. The separated effects resulting from the presence of mutant RNA in the HD\/100CAG model led to less severe but, to some extent, similar types of impairments as in the HD\/100Q model. Increased anxiety was one of the most substantial effects caused by mutant\n                    <jats:italic>HTT<\/jats:italic>\n                    RNA.\n                  <\/jats:p>","DOI":"10.1096\/fj.202401465r","type":"journal-article","created":{"date-parts":[[2024,11,28]],"date-time":"2024-11-28T00:30:20Z","timestamp":1732753820000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Insights into\n                    <scp>RNA<\/scp>\n                    \u2010mediated pathology in new mouse models of Huntington's disease"],"prefix":"10.1096","volume":"38","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2993-7000","authenticated-orcid":false,"given":"Magdalena","family":"Wozna\u2010Wysocka","sequence":"first","affiliation":[{"name":"Institute of Bioorganic Chemistry Polish Academy of Sciences  Poznan 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