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. 2025 Aug 12;36(9):ar111. doi: 10.1091/mbc.E25-02-0057

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© 2025 Alabi et al. This article is distributed by The American Society for Cell Biology under license from the author(s). It is available to the public under an Attribution 4.0 International Creative Commons CC-BY 4.0 License (https://creativecommons.org/licenses/by/4.0/).

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FIGURE 1: — Auxin-inducible degradation of lamin A/C, LB1, and LB2 in DLD1 cells. (A) Relative expression levels of LMNA, LMNB1, and LMNB2 genes in DLD1 cells. (B) Schematic of two-component auxin-inducible degron system, consisting of (i) N-terminal bi-allelic insertion of an mNeonGreen fluorescent protein and a microAID tag into the LMNA, LMNB1, or LMNB2 loci; and (ii) stable expression of the OsTir1 ligase into the RCC1 locus. (C–E) Immunoblots showing degradation of LA/C (C), LB1 (D), and LB2 (E) compared with untagged DLD1 parental cell line after 16 h of auxin treatment. (F) Quantification of nuclear envelope protein abundance by LC-MS/MS in nuclear extracts from mNG-AID-LA/C, mNG-AID-LB1, and mNG-AID-LB2 cells treated with auxin for 16 h. (G) Number of genes significantly differentially expressed (p_adj < 0.05) at least 2-fold in mNG-AID-LA/C, mNG-AID-LB1, and mNG-AID-LB2 cells after 16 or 96 h of auxin treatment compared with untreated mNG-AID-LA/C, mNG-AID-LB1, and mNG-AID-LB2 cells.