scholarly journals Sox2 gene regulation via the D1 enhancer in embryonic neural tube and neural crest by the combined action of SOX2 and ZIC2

2020 ◽  
Vol 25 (4) ◽  
pp. 242-256 ◽  
Author(s):  
Hideaki Iida ◽  
Yoko Furukawa ◽  
Machiko Teramoto ◽  
Hitomi Suzuki ◽  
Tatsuya Takemoto ◽  
...  
1937 ◽  
Vol 14 (2) ◽  
pp. 232-239 ◽  
Author(s):  
C. H. WADDINGTON

1. The presumptive ear ectoderm, removed from its normal site and transplanted to the amnio-cardiac vesicle, does not develop into an otic placode unless it comes from an embryo with more than nine pairs of somites. 2. The ectoderm which grows over the place from which the presumptive ear ectoderm is removed is induced to form an otic placode, the size of the placode being smaller the older the embryo at the time of operation. 3. If the wall of the neural tube, including the neural crest, is removed from the region of the ear in embryos younger than the nine-somite stage, an ear may nevertheless be formed. Since the ear ectoderm at this stage is not capable of differentiating when isolated, this result shows that inducing agencies other than the neural material are active at this stage. In some of the operated embryos, the acoustico-facialis ganglion was completely lacking, so this structure cannot be the sole organizer of the ear, as Szepsenwol suggested. 4. If both the wall of the neural tube and the presumptive ear ectoderm are removed, no ear is formed even in stages younger than the nine-somite stage, so that it appears that the non-neural inducing agents are more effective when working on presumptive ectoderm of this age than when working on non-presumptive ectoderm. This suggests that the ear ectoderm is beginning to be determined some time before it acquires the capacity for independent differentiation. 5. The wall of the neural tube, from the ear region, can induce a small ear when grafted under the ectoderm of the anterior part of the head. 6. The evidence suggests that the induction of the ear in normal development is due to the combined action of several structures, of which the wall of the neural tube, and the tissues derived from it (ganglia), is one but not the only one.


2007 ◽  
Vol 27 (1) ◽  
pp. 45-52
Author(s):  
Koh-ichi Atoh ◽  
Manae S. Kurokawa ◽  
Hideshi Yoshikawa ◽  
Chieko Masuda ◽  
Erika Takada ◽  
...  

genesis ◽  
2021 ◽  
Author(s):  
Alexandra J. Palmer ◽  
Dawn Savery ◽  
Valentina Massa ◽  
Andrew J. Copp ◽  
Nicholas D. E. Greene

Development ◽  
1990 ◽  
Vol 109 (1) ◽  
pp. 75-80 ◽  
Author(s):  
M. Maden ◽  
D.E. Ong ◽  
F. Chytil

We have analysed the distribution of cellular retinol-binding protein (CRBP) and cellular retinoic acid-binding protein (CRABP) in the day 8.5-day 12 mouse and rat embryo. CRBP is localised in the heart, gut epithelium, notochord, otic vesicle, sympathetic ganglia, lamina terminalis of the brain, and, most strikingly, in a ventral stripe across the developing neural tube in the future motor neuron region. This immunoreactivity remains in motor neurons and, at later stages, motor axons are labelled in contrast to unlabelled sensory axons. CRABP is localised to the neural crest cells, which are particularly noticeable streaming into the branchial arches. At later stages, neural crest derivatives such as Schwann cells, cells in the gut wall and sympathetic ganglia are immunoreactive. An additional area of CRABP-positive cells are neuroblasts in the mantle layer of the neural tube, which subsequently appear to be the axons and cell bodies of the commissural system. Since retinol and retinoic acid are the endogenous ligands for these binding proteins, we propose that retinoids may play a role in the development and differentiation of the mammalian nervous system and may interact with certain homoeobox genes whose transcripts have also been localised within the nervous system.


Development ◽  
1990 ◽  
Vol 109 (2) ◽  
pp. 411-423 ◽  
Author(s):  
T.P. Rothman ◽  
N.M. Le Douarin ◽  
J.C. Fontaine-Perus ◽  
M.D. Gershon

The technique of back-transplantation was used to investigate the developmental potential of neural crest-derived cells that have migrated to and colonized the avian bowel. Segments of quail bowel (removed at E4) were grafted between the somites and neural tube of younger (E2) chick host embryos. Grafts were placed at a truncal level, adjacent to somites 14–24. Initial experiments, done in vitro, confirmed that crest-derived cells are capable of migrating out of segments of foregut explanted at E4. The foregut, which at E4 has been colonized by cells derived from the vagal crest, served as the donor tissue. Comparative observations were made following grafts of control tissues, which included hindgut, lung primordia, mesonephros and limb bud. Additional experiments were done with chimeric bowel in which only the crest-derived cells were of quail origin. Targets in the host embryos colonized by crest-derived cells from the foregut grafts included the neural tube, spinal roots and ganglia, peripheral nerves, sympathetic ganglia and the adrenals, but not the gut. Donor cells in these target organs were immunostained by the monoclonal antibody, NC-1, indicating that they were crest-derived and developing along neural or glial lineages. Some of the crest-derived cells (NC-1-immunoreactive) that left the bowel and reached sympathetic ganglia, but not peripheral nerves or dorsal root ganglia, co-expressed tyrosine hydroxylase immunoreactivity, a neural characteristic never expressed by crest-derived cells in the avian gut. None of the cells leaving enteric back-grafts produced pigment. Cells of mesodermal origin were also found to leave donor explants and aggregate in dermis and feather germs near the grafts. These observations indicate that crest-derived cells, having previously migrated to the bowel, retain the ability to migrate to distant sites in a younger embryo. The routes taken by these cells appear to reflect, not their previous migratory experience, but the level of the host embryo into which the graft is placed. Some of the population of crest-derived cells that leave the back-transplanted gut remain capable of expressing phenotypes that they do not express within the bowel in situ, but which are appropriate for the site in the host embryo to which they migrate.


1995 ◽  
Vol 16 (12) ◽  
pp. 475-476
Author(s):  
Lisa Menasse-Palmer ◽  
Anna Bogdanow ◽  
Robert W. Marion

Choanal atresia is an abnormality of canalization during development of the nasal passages. It involves bone and/or soft tissue and may result in either partial (choanal stenosis) or complete obstruction of the posterior nasal airway. The most widely accepted mechanism for the development of choanal atresia is the persistence of the oronasal membrane beyond the sixth week of gestation, but abnormal migration of cephalic neural crest cells following neural tube closure also has been implicated. The incidence of choanal atresia is 1 in 7000 to 8000 live births. It is more common in females (2:1), more likely to be bony or cartilaginous than membranous (9:1), and more commonly unilateral and right-sided (2:1).


Development ◽  
1968 ◽  
Vol 19 (2) ◽  
pp. 109-119
Author(s):  
Judith Shulman Weis

In teleost fishes, unlike many other vertebrates, the spinal cord originates as a solid structure, the neural keel, which subsequently hollows out. Unlike vertebrates in which the neural tube is formed from neural folds, and where the neural crest arises from wedge-shaped masses of tissue connecting the neural tube to the general ectoderm, teleosts do not possess a clear morphological neural crest. Initially, the dorsal surface of the keel is broadly attached to the ectoderm as described by Shepard (1961). As the neural primordia become larger and more discrete, the region of attachment narrows, and cells become loose (the ‘loose crest stage’). These cells represent the neural crest. Subsequently they begin to migrate and to differentiate into the various derivatives of neural crest. Both sensory and sympathetic neurons arise from neural crest. At the time of their migration the cells are not morphologically distinguishable.


Development ◽  
1981 ◽  
Vol 62 (1) ◽  
pp. 309-323
Author(s):  
C. H. J. Lamers ◽  
J. W. H. M. Rombout ◽  
L. P. M. Timmermans

A neural crest transplantation technique is described for fish. As in other classes ofvertebrates, two pathways of neural crest migration can be distinguished: a lateroventral pathway between somites and ectoderm, and a medioventral pathway between somites and neural tube/notochord. In this paper evidence is presented for a neural crest origin of spinal ganglion cells and pigment cells, and indication for such an origin is obtained for sympathetic and enteric ganglion cells and for cells that are probably homologues to adrenomedullary and paraganglion cells in the future kidney area. The destiny of neural crest cells near the developing lateral-line sense organs is discussed. When grafted into the yolk, neural crest cells or neural tube cells appear to differentiate into ‘periblast cells’; this suggests a highly activating influence of the yolk. Many neural crest cells are found around the urinary ducts and, when grafted below the notochord, even within the urinary duct epithelium. These neural crest cells do not invade the gut epithelium, even when grafted adjacent to the developing gut. Consequently enteroendocrine cells in fish are not likely to have a trunkor rhombencephalic neural crest origin. Another possible origin of these cells will be proposed.


Development ◽  
1986 ◽  
Vol 98 (1) ◽  
pp. 251-268
Author(s):  
J. Sternberg ◽  
S. J. Kimber

The earliest stage of neural crest cell (NCC) migration is characterized by an epitheliomesenchymal transformation, as the cells leave the neural tube. There is evidence that in a number of cell systems this transformation is accompanied by alteration or depletion of associated basement membranes. This study examines the ultrastructural relationship between mouse NCCs and adjacent basement membranes during the earliest stages of migration from the neural tube. Basement membranes were identified by transmission electron microscopy (TEM) and immunofluorescence using antibodies to type-IV collagen. The ultrastructural features of NCCs and their relationship with surrounding tissues were also examined using TEM. In the dorsal region of the neural tube, from which NCCs originate, the basement membrane was depleted or absent, and with the immunofluorescence technique it was shown that this pattern was reflected in a deficit of type-IV collagen. TEM observations indicated that ultrastructurally NCCs differ from their neuroepithelial neighbours only in overall cell shape and their relationship to other cells and the extracellular matrix.


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