Patterning of the chick forebrain anlage by the prechordal plate

Abstract

We analysed the role of the prechordal plate in forebrain development of chick embryos in vivo. After transplantation to uncommitted ectoderm a prechordal plate induces an ectopic, dorsoventrally patterned, forebrain-like vesicle. Grafting laterally under the anterior neural plate causes ventralization of the lateral side of the forebrain, as indicated by a second expression domain of the homeobox gene NKX2.1. Such a lateral ventralization cannot be induced by the secreted factor Sonic Hedgehog alone, as this is only able to distort the ventral forebrain medially. Removal of the prechordal plate does not reduce the rostrocaudal extent of the anterior neural tube, but leads to significant narrowing and cyclopia. Excision of the head process results in the caudal expansion of the NKX2.1 expression in the ventral part of the anterior neural tube, while PAX6 expression in the dorsal part remains unchanged. We suggest that there are three essential steps in early forebrain patterning, which culminate in the ventralization of the forebrain. First, anterior neuralization occurs at the primitive streak stage, when BMP-4-antagonizing factors emanate from the node and spread in a planar fashion to induce anterior neural ectoderm. Second, the anterior translocation of organizer-derived cells shifts the source of neuralizing factors anteriorly, where the relative concentration of BMP-4-antagonists is thus elevated, and the medial part of the prospective forebrain becomes competent to respond to ventralizing factors. Third, the forebrain anlage is ventralized by signals including Sonic Hedgehog, thereby creating a new identity, the prospective hypothalamus, which splits the eye anlage into two lateral domains.

Is There a Prechordal Region and an Acroterminal Domain in Amphioxus?

“…5a, b in Conklin [1932], von Kupffer [1894]; see also Lwoff [1894], Aasar [1931], Hill and Florian [1931], Adelmann [1932], De Lange [1936], Kopsch [1950]). Various authors have suggested that some mesodermal cells incorporate secondarily into the endodermal prechordal plate, implying a mixed endo-mesoderm or meso-endoderm [Adelmann, 1922[Adelmann, , 1926Seifert et al, 1993;Foley et al, 1997;Pera and Kessel, 1997;Nieuwkoop, 1999;Rowan et al, 1999]. However, in our opinion this point does not seem to be clearly established with appropriate labeling of mesodermal or endodermal elements.…”

“…However, some of the originally epithelial endodermal prechordal plate cells do instead make an epithelio-mesenchymal transition, and become in situ free prechordal cells that migrate thereafter dorsalwards in front of the rostromedian acroterminal domain of the hypothalamus, reaching septo-preoptic roof plate levels [Schulte-Merker et al, 1994;Thisse et al, 1994;Bally-Cuif et al, 1995]. Modern studies have revealed several selective gene markers typical of the early (plate-like) and late (freely migrating) prechordal plate cells [Goosecoid, Crescent, Hex, Bmp7, Nodal, Shh, and FoxA2;Pera and Kessel, 1997;Dale et al, 1999;Lopez-Sanchez et al, 2005].…”

Single-cell analysis of early chick hypothalamic development reveals that hypothalamic cells are induced from prethalamic-like progenitors

“…The earliest chick hypothalamic progenitors are floor-plate-like cells, termed rostral diencephalic ventral midline (RDVM) cells, that express SHH , BMP7 , and NKX2–1 ( Figure 1A ) ( Dale et al, 1997 , 1999 ; Ohyama et al, 2005 ). RDVM cells are induced around Hamburger–Hamilton stage 8 (HH8) through the combined action of Sonic hedgehog (SHH), Nodal, and bone morphogenetic protein (BMP) signals from prechordal mesendoderm ( Dale et al, 1999 ; Manning et al, 2006 ; Ohyama et al, 2005 ; Patten et al, 2003 ; Pera and Kessel, 1997 ). Some RDVM cells later upregulate TBX2 , BMP2 , and FGF10 in response to BMP signals ( Figure 1A ) ( Manning et al, 2006 ) and generate tuberal and mammillary hypothalamic progenitors ( Fu et al, 2017 ; Manning et al, 2006 ).…”

Amphiphilic zinc phthalocyanine photosensitizers: synthesis, photophysicochemical properties and in vitro studies for photodynamic therapy

“…Membranous organelles, including mitochondria, plasma membrane, and lysosomes, have been suggested to be the main sites of PDT damage. 3,4 Apoptosis after PDT has been demonstrated in vitro 5 and in vivo. 6 For this therapy, dyes such as hematoporphyrin derivatives are used.…”