Pujadas Liwag, Emily M.Wei, XiaolongAcosta, NicolasCarter, Lucas M.Yang, JiekunAlmassalha, Luay M.Jain, SurbhiDaneshkhah, AliRao, Suhas S. P.Seker-Polat, FidanMacQuarrie, Kyle L.Ibarra, JoeAgrawal, VasundharaAiden, Erez LiebermanKanemaki, Masato T.Backman, VadimAdli, Mazhar2024-08-022024-08-022024Pujadas Liwag, E. M., Wei, X., Acosta, N., Carter, L. M., Yang, J., Almassalha, L. M., Jain, S., Daneshkhah, A., Rao, S. S. P., Seker-Polat, F., MacQuarrie, K. L., Ibarra, J., Agrawal, V., Aiden, E. L., Kanemaki, M. T., Backman, V., & Adli, M. (2024). Depletion of lamins B1 and B2 promotes chromatin mobility and induces differential gene expression by a mesoscale-motion-dependent mechanism. Genome Biology, 25(1), 77. https://doi.org/10.1186/s13059-024-03212-yhttps://hdl.handle.net/1911/117582B-type lamins are critical nuclear envelope proteins that interact with the three-dimensional genomic architecture. However, identifying the direct roles of B-lamins on dynamic genome organization has been challenging as their joint depletion severely impacts cell viability. To overcome this, we engineered mammalian cells to rapidly and completely degrade endogenous B-type lamins using Auxin-inducible degron technology.engExcept where otherwise noted, this work is licensed under a Creative Commons Attribution (CC BY) license.  Permission to reuse, publish, or reproduce the work beyond the terms of the license or beyond the bounds of fair use or other exemptions to copyright law must be obtained from the copyright holder.Journal articles13059-024-03212-yhttps://doi.org/10.1186/s13059-024-03212-y