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1The contractile cortical actomyosin cytoskeleton (or cortex) in interphase cells confers rigidity 2 to cells, but also lead to shape dynamics. Regulation of its thickness, although well studied in 3 rounded cells, is less explored in well-spread cells. In this paper, we quantify the variations in 4 thickness and study the contribution of actin polymerization, myosin II activity and spread area 5 of cells. We report an increase in cortex thickness and its variations on disrupting actin network 6 by actin depolymerizing agents or reducing contractility by inhibiting motor activity of myosin

1 Dilated Cardiomyopathy (DCM) is one of the different types of laminopathies caused by the 2 mutations in A-type lamins in somatic cells. The involuntary cyclic stretching of cardiac 3 muscle cells, as observed in normal physiological conditions is perturbed in DCM which 4 afflict patients globally. As A-type lamins are principal components in nuclear mechanics, we 5 have investigated the effect of the DCM causing mutants-K97E, E161K and R190W on 6 nuclear stretching and deformation by static and dynamic strain inducing experiments. All 7 the mutants exhibited differential nuclear structural aberrations along with a tilt in the 8 nuclear axis compared to the direction of the cell axis and a significant decrease in the lamina 9 thickness which reflected the lower mechanical rigidity. These phenotypes could potentially 10 lead to defects in nuclear anchorage to the actin filaments thereby resulting in the misshapen 11 and misaligned nucleus. 12 13 14