Effect of the notochord on proliferation and differentiation in the neural tube of the chick embryo

Development ◽  
1989 ◽  
Vol 107 (4) ◽  
pp. 793-803 ◽  
Author(s):  
H.W. van Straaten ◽  
J.W. Hekking ◽  
J.P. Beursgens ◽  
E. Terwindt-Rouwenhorst ◽  
J. Drukker

After implantation of a notochord fragment lateral to the neural tube in a 2-day chick embryo, at 4 days the ipsilateral neural tube half was increased in size and axons left the neural tube in a broad dorsoventral area (van Straaten et al. 1985). This enlargement appears to coincide with an increased area of AChE-positive basal plate neuroblasts, as determined with scan-cytophotometry. The effect was ipsilateral and local: clear effects were seen only when the implant was localized less than 80 microns from the neural tube and over 120 microns from the ventral notochord. In order to investigate the expected enhancement of proliferation, the mitotic density and the number of cells at the site of the implant at 3 days was determined and the mitotic index calculated. All three parameters showed an increase. It was concluded that the cell cycle was shorter in the implant area relative to the control area, at least during the third day. At 4 days the number of cells was still increased, predominantly in the basal plate. It appeared that the numerical increase was for the larger part due to neuroblasts. The synergism of two notochords thus resulted in enhancement of proliferation and differentiation in the neural tube. It is suggested that the notochord merely regulates and arranges the surrounding sclerenchymal cells, which are the effective cells in the regulation of neural tube development.

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Xian Li ◽  
Wenjuan Zhou ◽  
Xinyue Li ◽  
Ming Gao ◽  
Shufang Ji ◽  
...  

Abstract Objective Neural tube defects (NTDs) are the most serious and common birth defects in the clinic. The SRY-related HMG box B1 (SoxB1) gene family has been implicated in different processes of early embryogenesis. Sox19b is a maternally expressed gene in the SoxB1 family that is found in the region of the presumptive central nervous system (CNS), but its role and mechanism in embryonic neural stem cells (NSCs) during neural tube development have not yet been explored. Considering that Sox19b is specific to bony fish, we intended to investigate the role and mechanism of Sox19b in neural tube development in zebrafish embryos. Material and methods Morpholino (MO) antisense oligonucleotides were used to construct a Sox19b loss-of-function zebrafish model. The phenotype and the expression of related genes were analysed by in situ hybridization and immunolabelling. Epigenetic modifications were detected by western blot and chromatin immunoprecipitation. Results In this study, we found that zebrafish embryos exhibited a reduced or even deleted forebrain phenotype after the expression of the Sox19b gene was inhibited. Moreover, we found for the first time that knockdown of Sox19b reduced the proliferation of NSCs; increased the transcription levels of Ngn1, Ascl1, HuC, Islet1, and cyclin-dependent kinase (CDK) inhibitors; and led to premature differentiation of NSCs. Finally, we found that knockdown of Sox19b decreased the levels of EZH2/H3K27me3 and decreased the level of H3K27me3 at the promoters of Ngn1 and ascl1a. Conclusion Together, our data demonstrate that Sox19b plays an essential role in early NSC proliferation and differentiation through EZH2-mediated histone methylation in neural tube development. This study established the role of transcription factor Sox19b and epigenetic factor EZH2 regulatory network on NSC development, which provides new clues and theoretical guidance for the clinical treatment of neural tube defects.


Author(s):  
R. González Santander ◽  
M.V. Toledo Lobo ◽  
F.J. Martínez Alonso ◽  
G. Martínez Cuadrado ◽  
M González-Santander Martínez ◽  
...  

Myoblast fusion results from a sequence of different stages, previously demonstrated “in vitro”. After withdrawal from the cell cycle, myoblasts align forming long chains, in a process termed “recognition-alignment”. This stage is extracellular Ca2+ and N-Cadherin dependent. Alignment is followed by adhesion, defined as the stage prior to membrane fusion when aggegates are resistant to dispersal by EDTA. Adhesion is extracellular Ca2+-independent and N-CAM-dependent. Membrane fusion originates multinucleate myotubes.We have studied these stages of myoblast fusion at the brachial myotome of chick embryo from 51 to 105 h. of incubation. Samples were obtained by embryo microdissection and included the neural tube, the notochord and the brachial somites. These samples were embedded in araldite by conventional methods. Some samples were embedded in Unicryl, a recently formulated GMA derived resin.The first myoblasts clusters were observed in the ventral-lateral region of the brachial myotome in 22-24 Hamburger and Hamilton stages embryos. Clusters of pre-fusion myoblasts are usually surrounded by “electrondense blast cells” within a basal lamina in process of formation.


1972 ◽  
Vol 54 (3) ◽  
pp. 465-471 ◽  
Author(s):  
A. R. MORLEY ◽  
N. A. WRIGHT

SUMMARY Castrated male mice were injected with 250 μg testosterone propionate on 3 consecutive days. With the third injection, 1 μCi tritiated thymidine/g body weight was given intraperitoneally. A pulse-chase analysis in the seminal vesicle and coagulating gland was performed during the next 50 h and labelling and mitotic indices were obtained. One hour after the injection of tritiated thymidine the labelling index was 19% in the seminal vesicle and 13% in the coagulating gland. The mitotic index was 1·7% in the seminal vesicle and 1·4% in the coagulating gland. The observed cell cycle (Tc) duration in the seminal vesicle was 25 h, and the duration of DNA synthesis (ts) was 9 h. The calculated duration of mitosis (tm) was 0·6 h, the presynthetic duration (tG1) was 14·2 h, and the postsynthetic duration (tG2) 1·2 h. Forty-eight hours after testosterone propionate the growth fraction was 0·62 and a decycling ratio of 0·8 was calculated. In the coagulating gland Tc was 52·0 h, ts 9·0 h, tm 1·0 h, tg1 41·0 h and tG2 1·0 h.


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