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Anillin localization defect in cardiomyocyte binucleation.

Research paper by Felix B FB Engel, Michael M Schebesta, Mark T MT Keating

Indexed on: 08 Aug '06Published on: 08 Aug '06Published in: Journal of Molecular and Cellular Cardiology



Abstract

Heart growth is augmented during early development by cardiomyocyte proliferation. In contrast, heart growth during postnatal life occurs by increasing cell size. Postnatal cardiomyocytes can undergo DNA synthesis, mitosis and binucleation. However, they lose the ability to complete cytokinesis. The underlying mechanism is poorly understood. It has been suggested that incomplete disassembly of contractile elements prohibits cytokinesis. Here, we show that serum-induced binucleation results in the normal disassembly of the contractile apparatus. In contrast, analysis of Aurora B and Anillin localization demonstrates that binucleation is characterized by asymmetric constriction, delay of furrow constriction and defective mid-body formation. Anillin fails to focus at the cortex in anaphase and shows an expanded localization around the mid-body during cytokinesis. p38 inhibition rescues the mid-body formation defect. We show that p38 accumulates during cytokinesis at the mid-body and suggest that p38 activity has a regulatory role in cytokinesis. Microarray analysis reveals that p38 inhibition upregulates core components of the central spindle. Taken together, our results demonstrate that postnatal cardiomyocytes form a cleavage furrow and that binucleation is associated with an Anillin localization defect.