Morphogenetic movements during cranial neural tube closure in the chick embryo and the effect of homocysteine

Abstract

In order to unravel morphogenetic mechanisms involved in neural tube closure, critical cell movements that are fundamental to remodelling of the cranial neural tube in the chick embryo were studied in vitro by quantitative time-lapse video microscopy. Two main directions of movements were observed. The earliest was directed medially; these cells invaginated into a median groove and were the main contributors to the initial neural tube closure. Once the median groove was completed, cells changed direction and moved anteriorly to contribute to the anterior neural plate and head fold. This plate developed into the anterior neuropore, which started to close from the 4-somite stage onwards by convergence of its neural folds. Posteriorly, from the initial closure site onwards, the posterior neuropore started to close almost instantaneously by convergence of its neural folds. Homocysteine is adversely involved in human neural tube closure defects. After application of a single dose of homocysteine to chick embryos, a closure delay at the initial closure site and at the neuropores, flattening of the head fold and neural tube, and a halt of cell movements was seen. A possible interference of Hcy with actin microfilaments is discussed.

Cell delamination in the mesencephalic neural fold and its implication for the origin of ectomesenchyme

“…To test this idea, we labeled the non-neural ectoderm with DiI and recorded the movement of these cells during neural tube closure. Supplementary material Movie 1 shows the general lateral-to-medial movement of cells during neural tube closure, which is consistent with a previous study (Brouns et al, 2005), but more importantly, also shows that cells in the non-neural ectoderm undergo EMT and disperse into the embryo.…”

“…However, because of the topology of the chicken neural fold, it is not known whether the Snail2-expressing cells in the non-neural ectoderm also delaminate in chicken embryos or how this would occur. In a previous study, it was shown that there is a general lateral-to-medial movement during neural tube closure in the midbrain region (Brouns et al, 2005). To test this idea, we labeled the non-neural ectoderm with DiI and recorded the movement of these cells during neural tube closure.…”

“…However, subsequent studies dismissed the notion that there were two distinct waves of delaminating cells by conflating the definition of neural crest and neural fold (Hörstadius, 1950; Landacre, 1921). This was probably also complicated by the lateral-to-medial movement of cells during cranial neural tube closure (Brouns et al, 2005). Uncertainties remained as to whether cells were delaminating only from the neural epithelium or also from the overlying non-neural ectoderm, and this was true even in the trunk (Beard, 1888; Hörstadius, 1950).…”

Hyperhomocysteinemia in men with a reproductive history of fetal neural tube defects

“…Rosenquist et al [3] showed that hyperhomocysteinemia increases the number of NTDs in chick embryos. Brouns et al [4] demonstrated that homocysteine exposure can delay neural tube closure in avian embryos and speculated that hyperhomocysteinemia exerts a similar effect in the human fetus. Taparia et al [5] suggested that homocysteinemia indirectly influences NTD development.…”