Lamins: ‘structure goes cycling’

Abstract

Nuclear intermediate filaments formed by A- and B-type lamins are central components of the nucleoskeleton and are required for the architecture and integrity of the nucleus. There is growing evidence that lamins are also involved in regulatory pathways controlling cell proliferation and differentiation. Lamins affect the activity of several transcription factors, such as retinoblastoma protein and c-Fos, and signalling pathways, such as the ERK1/2 (extracellular-signal-regulated kinase 1/2) and Notch pathways, which are key regulators of cell-cycle progression and differentiation. During mitosis, lamins are dynamically reorganized and play active roles in spindle matrix formation and in post-mitotic nuclear reassembly. Several of the cell-cycle-regulating functions of lamins may be impaired in the diseases linked to mutations in lamins and lamin-associated proteins, including striated muscle diseases, lipodystrophies and premature aging syndromes, and contribute to the tissue-specific disease pathologies.