Excess lamins delay the cell cycle.

On page 83, Dorner et al. report that overexpression of a lamina-associated protein slows cell proliferation and promotes differentiation in vitro. The findings suggest that laminopathy symptoms may not be due to structural weakness in the tissue, but rather to a failure of stem cells to properly regenerate damaged or aging tissues.

A-type lamins are found at the nuclear periphery and in the nucleoplasm of differentiated cells and have been implicated in cell cycle regulation and chromatin function. An associated protein, LAP2α, interacts with the hypophosphorylated form of Rb, which represses entry into S-phase by blocking activation of E2F target genes.

Dorner et al. found that cells treated with LAP2α RNAi proliferated more rapidly than untreated controls. Cells with excess LAP2α, however, paused at the G1-S transition, delayed reentry into the cell cycle after serum addition to previously...

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