Relationship between genital ridge formation and settlement site of primordial germ cells in chick embryos

1987 ◽  
Vol 219 (3) ◽  
pp. 311-314 ◽  
Author(s):  
Atsumi Ukeshima ◽  
Masayuki Kudo ◽  
Toyoaki Fujimoto
1992 ◽  
Vol 16 (9) ◽  
pp. 853-857 ◽  
Author(s):  
I CHANG ◽  
A TAJIMA ◽  
Y YASUDA ◽  
T CHIKAMUNE ◽  
T OHNO

Biology Open ◽  
2021 ◽  
Vol 10 (4) ◽  
Author(s):  
Yoshikazu Haramoto ◽  
Mino Sakata ◽  
Shin Kobayashi

ABSTRACT X chromosome inactivation (XCI), determined during development, remains stable after embryonic cell divisions. However, primordial germ cells (PGCs) are exceptions in that XCI is reprogrammed and inactivated X chromosomes are reactivated. Although interactions between PGCs and somatic cells are thought to be important for PGC development, little is known about them. Here, we performed imaging of X chromosome reactivation (XCR) using the ‘Momiji’ mouse system, which can monitor the X chromosome's inactive and active states using two color fluorescence reporter genes, and investigated whether interactions would affect XCR in PGCs. Based on their expression levels, we found that XCR of the Pgk1 locus began at embryonic day (E)10.5 and was almost complete by E13.5. During this period, PGCs became distributed uniformly in the genital ridge, proliferated, and formed clusters; XCR progressed accordingly. In addition, XCR of the Pgk1 locus preceded that of the Hprt locus, indicating that the timing of epigenetic memory erasure varied according to the locus of each of these X-linked genes. Our results indicate that XCR proceeds along with the proliferation of PGCs clustered within the genital ridge. This article has an associated First Person interview with the first author of the paper.


2003 ◽  
Vol 40 (2) ◽  
pp. 101-113 ◽  
Author(s):  
Dong-Feng Zhao ◽  
Hiroaki Yamashita ◽  
Masaharu Matsuzaki ◽  
Toshinori Takano ◽  
Shin-Ichi Abe ◽  
...  

Development ◽  
1978 ◽  
Vol 46 (1) ◽  
pp. 5-20
Author(s):  
H. Lee ◽  
N. Karasanyi ◽  
R. G. Nagele

Effects of concanavalin A (Con A) on the morphology and migration of primordial germ cells (PGCs) in stage-6 to -12 chick embryos were investigated. Con A, at a sublethal dose (10µg/ml), inhibited migration of PGCs from the germinal crescent area to other parts of the embryo. Affected PGCs were more rounded without the usual cytoplasmic extensions, but the integrity of other structures was unaffected. Nearly identical results were obtained with another lectin, wheat germ agglutinin (10µg/ml). Histochemistry using Con A-horseradish peroxidase revealed that PGCs in control embryos had a thin, rather uniform layer of extracellular coat material (ECM). Con A appeared to alter the distribution of ECM on PGCs, i.e. some parts of the cell surface were devoid of any detectable ECM, while others had small, scattered patches of ECM. Con A effects were alleviated by α-methyl-d-mannoside. Overall results of the present study indicated that the observed inhibition of PGC migration in early chick embryos is a consequence of Con A-induced alterations of cell surface properties.


Development ◽  
2002 ◽  
Vol 129 (5) ◽  
pp. 1155-1164 ◽  
Author(s):  
Ian R. Adams ◽  
Anne McLaren

During embryogenesis, primordial germ cells (PGCs) have the potential to enter either spermatogenesis or oogenesis. In a female genital ridge, or in a non-gonadal environment, PGCs develop as meiotic oocytes. However, male gonadal somatic cells inhibit PGCs from entering meiosis and direct them to a spermatogenic fate. We have examined the ability of PGCs from male and female embryos to respond to the masculinising environment of the male genital ridge, defining a temporal window during which PGCs retain a bipotential fate. To help understand how PGCs respond to the male gonadal environment, we have identified molecular differences between male PGCs that are committed to spermatogenesis and bipotential female PGCs. Our results suggest that one way in which PGCs respond to this masculinising environment is to synthesise prostaglandin D2. We show that this signalling molecule can partially masculinise female embryonic gonads in culture, probably by inducing female supporting cells to differentiate into Sertoli cells. In the developing testis, prostaglandin D2 may act as a paracrine factor to induce Sertoli cell differentiation. Thus part of the response of PGCs to the male gonadal environment is to generate a masculinising feedback loop to ensure male differentiation of the surrounding gonadal somatic cells.


PLoS Genetics ◽  
2015 ◽  
Vol 11 (3) ◽  
pp. e1005019 ◽  
Author(s):  
Yueh-Chiang Hu ◽  
Peter K. Nicholls ◽  
Y. Q. Shirleen Soh ◽  
Joseph R. Daniele ◽  
Jan Philipp Junker ◽  
...  

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