TDP-43 nuclear loss in FTD/ALS causes widespread alternative polyadenylation changes

We thank the members of the Gitler lab and the Petrucelli lab for their helpful discussions and comments on the paper. We thank Z. Chen for helping with Aparent2. We also acknowledge the funding support from the following sources: a postdoctoral scholar award from the Phil and Penny Knight Initiative for Brain Resilience, Stanford University (to Y.Z.); a grant from the Larry L. Hillblom Foundation (to Y.Z.); the National Institutes of Health (NIH) Training Program in Aging Research (2T32AG047126-06A1 to T.A.); a grant from the Takeda Science Foundation (to T.A.); FightMND (to S.L.R.); a Stanford School of Medicine Dean's postdoctoral fellowship (to C.L.); the Milton Safenowitz Postdoctoral Fellowship Program (to C.G.); the NIH (U54NS123743, R35NS097273 and P01NS084974) and Target ALS (to L.P.); the NIH (U54NS123743 and RF1NS120992 to M.P.); and the NIH (R35NS137159, U54NS123743 and R01AG064690) and Target ALS (to A.D.G.). A.D.G. is an investigator at Chan Zuckerberg Biohub-San Francisco. Some of the computing for this project was performed on the Sherlock cluster. We would like to thank Stanford University and the Stanford Research Computing Center for providing computational resources and support that contributed to these research results. Part of the graphics was created with BioRender.com (Fig. 6e and Supplementary Fig. 1c). The funders had no role in study design, data collection and analysis, decision to publish or preparation of the manuscript.