An experimental investigation into the possible neural crest origin of pancreatic APUD (islet) cells

Development ◽  
1976 ◽  
Vol 35 (3) ◽  
pp. 577-593
Author(s):  
Ann Andrew

It has recently been contended that pancreatic APUD cells are neural crest derivatives. In an experimental investigation, isotopic grafts of neural tube containing neural crest cells were transplanted from chick and quail embryos labelled with tritiated thymidine, and from unlabelled quail embryos, to host chick embryos at the same stage of development. Transplantations were performed at various levels between so mites 5 and 24 in embryos at 6- to 24-so mite stages. In operated embryos at 3¾ days of incubation, the pancreatic APUD cells were not labelled; nor did their nuclei show quail features. Migration of cells from the graft was evidenced by the presence of quail nuclei and/or radioactive label in autoradiographs, in spinal and sympathetic ganglia in the operated region. It is concluded that the pancreatic APUD cells of the 3¾-day-old chick embryo are not derived from the trunk neural crest up to the level of so mite 24. It is unlikely that more caudal levels contribute, because APUD cells are already concentrated in the dorsal pancreatic bud region at the 24-so mite stage, by which time no migration of crest cells has occurred caudal to so mite 24. This conclusion probably concerns A, B and D pancreatic endocrine cells.

Development ◽  
1991 ◽  
Vol 112 (4) ◽  
pp. 913-920 ◽  
Author(s):  
S.E. Fraser ◽  
M. Bronner-Fraser

Trunk neural crest cells migrate extensively and give rise to diverse cell types, including cells of the sensory and autonomic nervous systems. Previously, we demonstrated that many premigratory trunk neural crest cells give rise to descendants with distinct phenotypes in multiple neural crest derivatives. The results are consistent with the idea that neural crest cells are multipotent prior to their emigration from the neural tube and become restricted in phenotype after leaving the neural tube either during their migration or at their sites of localization. Here, we test the developmental potential of migrating trunk neural crest cells by microinjecting a vital dye, lysinated rhodamine dextran (LRD), into individual cells as they migrate through the somite. By two days after injection, the LRD-labelled clones contained from 2 to 67 cells, which were distributed unilaterally in all embryos. Most clones were confined to a single segment, though a few contributed to sympathetic ganglia over two segments. A majority of the clones gave rise to cells in multiple neural crest derivatives. Individual migrating neural crest cells gave rise to both sensory and sympathetic neurons (neurofilament-positive), as well as cells with the morphological characteristics of Schwann cells, and other non-neuronal cells (both neurofilament-negative). Even those clones contributing to only one neural crest derivative often contained both neurofilament-positive and neurofilament-negative cells. Our data demonstrate that migrating trunk neural crest cells can be multipotent, giving rise to cells in multiple neural crest derivatives, and contributing to both neuronal and non-neuronal elements within a given derivative.(ABSTRACT TRUNCATED AT 250 WORDS)


2020 ◽  
Author(s):  
Sofie Mohlin ◽  
Camilla U. Persson ◽  
Elina Fredlund ◽  
Emanuela Monni ◽  
Jessica M. Lindvall ◽  
...  

AbstractThe neural crest is a stem cell population that gives rise to sympathetic ganglia, the cell type of origin of neuroblastoma. Hypoxia Inducible Factor (HIF)-2α is associated with high risk neuroblastoma, however, little is known about its role in normal neural crest development. To address this important question, here we show that HIF-2α is expressed in trunk neural crest cells of human, murine and avian embryos. Modulating HIF-2α in vivo not only causes developmental delays but also induces proliferation and stemness of neural crest cells while altering the number of cells migrating ventrally to sympathoadrenal sites. Transcriptome changes after loss of HIF-2α reflect the in vivo phenotype. The results suggest that expression levels of HIF-2α must be strictly controlled and abnormal levels increase stemness and may promote metastasis. Our findings help elucidate the role of HIF-2α during normal development with implications also in tumor initiation at the onset of neuroblastoma.


PLoS ONE ◽  
2014 ◽  
Vol 9 (1) ◽  
pp. e84072 ◽  
Author(s):  
Kunie Hagiwara ◽  
Takeshi Obayashi ◽  
Nobuyuki Sakayori ◽  
Emiko Yamanishi ◽  
Ryuhei Hayashi ◽  
...  

2010 ◽  
Vol 344 (1) ◽  
pp. 531
Author(s):  
Judith A. Cebra-Thomas ◽  
James Robinson ◽  
Melinda Yin ◽  
James McCarthy ◽  
Sonal Shah ◽  
...  

2021 ◽  
Vol 480 ◽  
pp. 78-90
Author(s):  
Jennifer C. Kasemeier-Kulesa ◽  
Jennifer A. Spengler ◽  
Connor E. Muolo ◽  
Jason A. Morrison ◽  
Thomas E. Woolley ◽  
...  

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.


Author(s):  
Juan Du ◽  
Sanbing Zhang ◽  
Jiqian Zhao ◽  
Sha Li ◽  
Wenyong Chen ◽  
...  

Development ◽  
1980 ◽  
Vol 57 (1) ◽  
pp. 71-78
Author(s):  
N. B. Levy ◽  
Ann Andrew ◽  
B. B. Rawdon ◽  
Beverley Kramer

Two- to ten-somite chick embryos were studied in order to ascertain whether, as has been proposed, there exists a ‘ventral neural ridge’ which gives rise to the hypophyseal (Rathke's) pouch. Serial sections and stereo-microscopy were used. The neural ridges arch around the rostral end of the embryo onto the ventral surface of the head, but no evidence was found for their extension to form a ‘ventral neural ridge’ reaching the stomodaeum: in fact a considerable expanse of non-thickened surface ectoderm was seen to separate the ventral portions of the neural ridges from the stomodaeum. The thickening of neural ectoderm which does appear on the ventral surface of the head results from apposition and fusion of the opposite neural ridges flanking the neural plate and thus the tip of the anterior neuropore - the classically accepted mode of closure of the neuropore. These findings are in accord with the generally accepted concept of the origin of thehypophyseal pouch rather than with its derivation from a ‘ventral neural ridge’. No sign of neural crest formation was encountered ventrally; this observation excludes the possibility that endocrine cells of the APUD series could originate from neural crest in this region.


2018 ◽  
Vol 11 (12) ◽  
pp. dmm035097 ◽  
Author(s):  
Maria R. Replogle ◽  
Virinchipuram S. Sreevidya ◽  
Vivian M. Lee ◽  
Michael D. Laiosa ◽  
Kurt R. Svoboda ◽  
...  

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