Effects of Colchicine on the Formation and Looping of the Tubular Heart of the Embryonic Chick

Abstract

The role of microtubules in the early development of the chick embryo heart was studied. The microtubules were disrupted by treatment of the embryos with colchicine. The embryos were divided for study into three groups: (I) before the fusion of the paired cardiac primordia; (II) before the starting of the cardiac loop, and (III) during the formation of the looping process. Colchicine did not impair the fusion of the paired heart primordia nor the acquisition of an asymmetric C-shaped form. However, the normal counterclockwise movement of the heart loop was prevented. From these results we conclude that the formation of the tubular heart and its looping are independent of the integrity of the microtubular system. Under the effects of colchicine the developing myocytes rounded up bulging into the pericardial cavity. The cell contours became scarcely discernible and the individual cell surfaces gave rise to blebs and ruffles of different sizes. In older embryos, clefts of different sizes appeared between the myocardial cells. The effects of colchicine on the pulsatile activity of the heart were recorded. These effects, as well as those on the cell surface characteristics, were found to be age dependent. The more mature the hearts were, the more resistant to colchicine they became. The developmental significance of the results reported here is discussed.

Cardiac looping may be driven by compressive loads resulting from unequal growth of the heart and pericardial cavity. Observations on a physical simulation model

“…We should note, however, that not all available data seem to support the idea of an intrinsic, cell shape-driven bending mechanism. Hill and Lemanski (1979) could not observe a progression of heart looping in in vitro cultures of amphibian embryonic heart loops, and data from colchicine-treated chick embryos suggest that the cell shape changes observed during ventral bending are merely the result and not the cause of the bending process (Icardo and Ojeda, 1984). …”

Mechanotransduction: the role of mechanical stress, myocyte shape, and cytoskeletal architecture on cardiac function

“…After looping, myocardium on the concave side remains thick and columnar, versus the flatter convex side [122]. Although these regional changes in cell shape could be a passive response to extrinsic forces, heart tubes bend even when removed from the embryo [124], indicating that looping is caused by a local, intrinsic mechanism, which was later found to be actin filament growth [98,102,112,123,146]. Together, these studies suggest that actin dynamics actively induce heart tube looping by flattening cells exclusively on the convex side, illustrating how localized remodeling of cell shape contributes to the emergence of gross morphological form.…”

Biophysical mechanisms of cardiac looping

“…Disrupting microtubules with colchicine causes MY cells to round up but does not affect c-looping (Icardo and Ojeda, 1984;Itasaki et al, 1991). However, the form of the heart is perturbed during s-looping (Icardo and Ojeda, 1984). 15.…”