Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.23.218347v1?rss=1 Authors: Coffey, S. R., Andrew, M., Ging, H., Hamilton, J., Flower, M., Kovalenko, M., Bragg, R. M., Cantle, J. P., McHugh, C. A., Carrillo, J. M., Rodier, J.-A., Marchionini, D. M., Wilkinson, H. A., Kwak, S., Howland, D. S., Bennett, C. F., Mouro Pinto, R., Auburger, G., Zeitlin, S. O., Kordasiewicz, H. B., Tabrizi, S. J., Wheeler, V. C., Carroll, J. B. Abstract: Expanded trinucleotide repeats cause many human diseases, including Huntington's disease (HD). Recent studies indicate that somatic instability of these repeats contributes to pathogenesis in several expansion disorders. We find that lowering huntingtin protein (HTT) levels reduces somatic instability of both the Htt and Atxn2 CAG tracts in knockin mouse models, and the HTT CAG tract in human iPSC-derived neurons, revealing an unexpected role for HTT in regulating somatic instability. Copy rights belong to original authors. Visit the link for more info