Cell Population Growth and Area Expansion in Early Chick Embryos During Normal and Abnormal Morphogenesis in vitro

Abstract

The exponential growth and cell population during the early embryogenesis of chick, cultured in vitro correlates with a linear increase in the blastoderm area. To understand the relationship between these parameters and normal morphogenesis, we have used a known teratogen, trypan blue, as a probe. A method is developed in which each new embryonic structure is assigned a rank value of 1 and the total number of ranks allows quantification of development and establishment of a numerical relationship between the size of the cell population, blastoderm area and the morphological development. The teratogen inhibits cell population growth, morphogenetic movements and shaping of organ primordia, but not the epiboly and differentiation of cells which have already invaginated and positioned during primitive streak formation. In contrast, the cell population growth, but not the blastoderm area-expansion, is correlated with the extent of abnormal development. A graphic analysis of the rank order, log cell number and blastoderm area reveals that these three parameters coordinately regulate morphogenesis. It is suggested that head fold formation is the key event regulating the progress of early morphogenesis.

Post‐nodal mesoblast caudalizes the host axis and inhibits cell population growth, and induces new primitive streaks in chick embryos

“…Yamada (1994Yamada ( , 1995 has hypothesized that the antero-posterior specification in the mesoderm and the ectoderm is a combined effect of a positive cell cycle control during dorsalization and a positive cell cycle regulation during caudalization. Thus, caudalization is indeed regulated by a negative cell cycle control (Ghatpande et al 1991Modak et al 1993;Joshi 1999;present data). In contrast, examination of the chronology of neural induction (Joshi 1999;Deshmukh et al 2001;Joshi-Banka et al 2001;Chatterjee et al unpubl.…”

“…The PN region of the full primitive streak contains presumptive postero‐lateral mesoblast (Rawles 1936; Rudnick 1948; Spratt 1952; Aberchrombie & Bellairs 1954; Nicolet 1970, 1971; Khan & Mulherkar 1974, 1978). In this study, we showed that increasing the number of PN grafts transplanted in the anterior half of the area pellucida inhibited cell population growth and development of the anterior axial structures, and promoted caudalization of the host axis similar to the effects of LiCl, Trypan blue and RA (Ghatpande et al 1991, 1993; Modak et al 1993). Furthermore, the head was either of reduced size or absent, and the forebrain and midbrain, but not the tail region, were truncated.…”

“…The lengths of the host axes (anterior extremity of the telencephalon to the anterior end of the regressing streak), the head regions (from the anterior tip of the telencephalon and the posterior extremity of the rhombencephalon) and the remaining tail portions were measured in control and experimental embryos, with a micrometer. Outlines of the area pellucida, opaca and vasculosa were recorded and the surface areas (mm 2 ) at the beginning and end of culture were determined by planimetry (Ghatpande et al 1991, 1993). Host ectoblast reaction to the graft was examined both ventrally and dorsally as previously described (Guttikar et al 1993).…”

“…During early morphogenesis of the chick, the cell population growth controls blastoderm expansion (Ghatpande et al 1993; Sonawane 2000). Lithium chloride (LiCl), Trypan blue, isonicotinic acid hydrazide and retinoic acid (RA) affect both processes adversely by caudalizing the host axis, although these reagents target different biochemical processes (Nicolet 1965; Joshi et al 1990; Ghatpande et al 1991, 1993; Modak et al 1993). Therefore, caudalization has been suggested to be under a negative cell cycle control (Ghatpande et al 1991, 1993; Modak et al 1993; Yamada 1994, 1995).…”

Hypoxia induces cardiac malformations via A1 adenosine receptor activation in chicken embryos

“…Total cell proliferation in early chicken embryos can be determined by counting cells in the whole embryo (Ghatpande et al, 1990, 1991). We counted cells as described by Ghatpande et al (1990).…”