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Research article

Revisiting the truncated lamin A produced by a commonly used strain of Lmna knockout mice

ORCID Icon, ORCID Icon, , ORCID Icon & ORCID Icon
Article: 2262308 | Received 05 Jul 2023, Accepted 08 Sep 2023, Published online: 27 Sep 2023

References

  • Sullivan T, Escalante-Alcalde D, Bhatt H, et al. Loss of A-type lamin expression compromises nuclear envelope integrity leading to muscular dystrophy. J Cell Bio. 1999;147(5):913–9. doi: 10.1083/jcb.147.5.913
  • Jahn D, Schramm S, Schnolzer M, et al. A truncated lamin A in the Lmna –/– mouse line: implications for the understanding of laminopathies. Nucleus. 2012;3(5):463–474. doi: 10.4161/nucl.21676
  • Fong LG, Ng JK, Meta M, et al. Heterozygosity for Lmna deficiency eliminates the progeria-like phenotypes in Zmpste24-deficient mice. Proc Natl Acad Sci U S A. 2004;101(52):18111–18116. doi: 10.1073/pnas.0408558102
  • Lammerding J, Fong LG, Ji JY, et al. Lamins a and C but not lamin B1 regulate nuclear mechanics. J Biol Chem. 2006;281(35):25768–25780. doi: 10.1074/jbc.M513511200
  • Jung HJ, Tatar A, Tu Y, et al. An absence of nuclear lamins in keratinocytes leads to ichthyosis, defective epidermal barrier function, and intrusion of nuclear membranes and endoplasmic reticulum into the nuclear chromatin. Mol Cell Biol. 2014;34(24):4534–4544. doi: 10.1128/MCB.00997-14
  • Chen NY, Kim P, Weston TA, et al. Fibroblasts lacking nuclear lamins do not have nuclear blebs or protrusions but nevertheless have frequent nuclear membrane ruptures. Proc Natl Acad Sci U S A. 2018;115(40):10100–10105. doi: 10.1073/pnas.1812622115
  • Chen NY, Kim PH, Tu Y, et al. Increased expression of LAP2β eliminates nuclear membrane ruptures in nuclear lamin-deficient neurons and fibroblasts. Proc Natl Acad Sci U S A. 2021;118(25): doi: 10.1073/pnas.2107770118
  • Yang SH, Bergo MO, Toth JI, et al. Blocking protein farnesyltransferase improves nuclear blebbing in mouse fibroblasts with a targeted Hutchinson-Gilford progeria syndrome mutation. Proc Natl Acad Sci U S A. 2005;102(29):10291–10296. doi: 10.1073/pnas.0504641102
  • Kim PH, Luu J, Heizer P, et al. Disrupting the LINC complex in smooth muscle cells reduces aortic disease in a mouse model of Hutchinson-Gilford progeria syndrome. Sci Transl Med. 2018;10(460): doi: 10.1126/scitranslmed.aat7163
  • Heizer PJ, Yang Y, Tu Y, et al. Deficiency in ZMPSTE24 and resulting farnesyl–prelamin A accumulation only modestly affect mouse adipose tissue stores. J Lipid Res. 2020;61(3):413–421. doi: 10.1194/jlr.RA119000593
  • Kim PH, Chen NY, Heizer PJ, et al. Nuclear membrane ruptures underlie the vascular pathology in a mouse model of Hutchinson-Gilford progeria syndrome. JCI Insight. 2021;6(16): doi: 10.1172/jci.insight.151515
  • Jung HJ, Nobumori C, Goulbourne CN, et al. Farnesylation of lamin B1 is important for retention of nuclear chromatin during neuronal migration. Proc Natl Acad Sci U S A. 2013;110(21):E1923–1932. doi: 10.1073/pnas.1303916110
  • Davies BS, Barnes RH 2nd, Tu Y, et al. An accumulation of non-farnesylated prelamin A causes cardiomyopathy but not progeria. Hum Mol Genet. 2010;19(13):2682–2694. doi: 10.1093/hmg/ddq158
  • Wolf CM, Wang L, Alcalai R, et al. Lamin A/C haploinsufficiency causes dilated cardiomyopathy and apoptosis-triggered cardiac conduction system disease. J Mol Cell Cardiol. 2008;44(2):293–303. doi: 10.1016/j.yjmcc.2007.11.008
  • Mehl JL, Earle A, Lammerding J, et al. Blockage of lamin-A/C loss diminishes the pro-inflammatory macrophage response. iScience. 2022;25(12):105528. doi: 10.1016/j.isci.2022.105528
  • Brayson D, Shanahan CM. Lamin A precursor localizes to the Z-disc of sarcomeres in the heart and is dynamically regulated in muscle cell differentiation. Philos Trans R Soc Lond B Biol Sci. 2022;377(1864):20210490. doi: 10.1098/rstb.2021.0490
  • Earle AJ, Kirby TJ, Fedorchak GR, et al. Mutant lamins cause nuclear envelope rupture and DNA damage in skeletal muscle cells. Nat Mater. 2020;19(4):464–473. doi: 10.1038/s41563-019-0563-5
  • Kubben N, Voncken JW, Konings G, et al. Post-natal myogenic and adipogenic developmental: defects and metabolic impairment upon loss of A-type lamins. Nucleus. 2011;2(3):195–207. doi: 10.4161/nucl.2.3.15731
  • Solovei I, Wang AS, Thanisch K, et al. LBR and lamin A/C sequentially tether peripheral heterochromatin and inversely regulate differentiation. Cell. 2013;152(3):584–598. doi: 10.1016/j.cell.2013.01.009