An autoradiographic study of neuronal development, vascularization and glial cell migration from hippocampal transplants labelled in intermediate explant culture

Neuroscience ◽  
1984 ◽  
Vol 12 (2) ◽  
pp. 513-530 ◽  
Author(s):  
R.M. Lindsay ◽  
G. Raisman
1958 ◽  
Vol 41 (5) ◽  
pp. 1027-1034 ◽  
Author(s):  
T. D. C. Grace

1. The ovarian tissues from diapausing pupae of the promethea moth (Callosamia promethea) have survived and grown for 186 days under in vitro conditions. There was continual cell migration and multiplication for a period of 53 days, followed by a period of 47 days during which no cells migrated from the tissues. Between the 100th and 105th days after setting up the cultures, cell migration was resumed, and by the 111th day 250 cells were present in the medium. A few cell divisions were observed between the 126th and 136th days. After the tissues were subcultured on the 140th day, the explant culture continued to survive, but the cell culture died 3 days later. 2. The tissues were subcultured a total of 6 times during the 186 days. By the introduction of a piece of live tissue into the cell cultures, the growth and survival of the cells were increased from 8 days to about 20 days. 3. It is possible that the tissues had become adapted to the medium during their long survival, as the cells which migrated from them after 100 days showed considerably longer survival than those in earlier cultures.


2013 ◽  
Vol 453 (2) ◽  
pp. 201-208 ◽  
Author(s):  
Chang-Chun Wang ◽  
Hsiao-Fan Lo ◽  
Shu-Yu Lin ◽  
Hungwen Chen

GCM1 (glial cell missing 1) is a short-lived transcription factor essential for placental development. The F-box protein, FBW2 (F-box and WD-repeat domain-containing 2), which contains five WD (tryptophan–aspartate) repeats, recognizes GCM1 and mediates its ubiquitination via the SCFFBW2 E3 ligase complex. Although the interaction between GCM1 and FBW2 is facilitated by GCM1 phosphorylation, it is possible that this interaction might be regulated by additional cellular factors. In the present study, we perform tandem-affinity purification coupled with MS analysis identifying RACK1 (receptor for activated C-kinase 1) as an FBW2-interacting protein. RACK1 is a multifaceted scaffold protein containing seven WD repeats. We demonstrate that the WD repeats in both RACK1 and FBW2 are required for the interaction of RACK1 and FBW2. Furthermore, RACK1 competes with GCM1 for FBW2 and thereby prevents GCM1 ubiquitination, which is also supported by the observation that GCM1 is destabilized in RACK1-knockdown BeWo placental cells. Importantly, RACK1 knockdown leads to decreased expression of the GCM1 target gene HTRA4 (high-temperature requirement protein A4), which encodes a serine protease crucial for cell migration and invasion. As a result, migration and invasion activities are down-regulated in RACK1-knockdown BeWo cells. The present study reveals a novel function for RACK1 to regulate GCM1 activity and placental cell migration and invasion.


Author(s):  
Patrick Cafferty ◽  
Xiaojun Xie ◽  
Kristen Browne ◽  
Vanessa J. Auld

Hypertension ◽  
2004 ◽  
Vol 43 (2) ◽  
pp. 452-459 ◽  
Author(s):  
Chun-Fang Xia ◽  
Hang Yin ◽  
Cesar V. Borlongan ◽  
Lee Chao ◽  
Julie Chao

2007 ◽  
Vol 27 (19) ◽  
pp. 6659-6668 ◽  
Author(s):  
Kiyohiko Angata ◽  
Valerie Huckaby ◽  
Barbara Ranscht ◽  
Alexey Terskikh ◽  
Jamey D. Marth ◽  
...  

ABSTRACT Polysialic acid, which is synthesized by two polysialyltransferases, ST8SiaII and ST8SiaIV, plays an essential role in brain development by modifying the neural cell adhesion molecule (NCAM). It is currently unclear how polysialic acid functions in different processes of neural development. Here we generated mice doubly mutant in both ST8SiaII and ST8SiaIV to determine the effects of loss of polysialic acid on brain development. In contrast to NCAM-deficient, ST8SiaII-deficient, or ST8SiaIV-deficient single mutant mice, ST8SiaII and ST8SiaIV double mutants displayed severe defects in anatomical organization of the forebrain associated with apoptotic cell death. Loss of polysialic acid affected both tangential and radial migration of neural precursors during cortical development, resulting in aberrant positioning of neuronal and glial cells. Glial cell differentiation was aberrantly increased in vivo and in vitro in the absence of polysialic acid. Consistent with these findings, polysialic acid-deficient mice exhibited increased expression of the glial cell marker glial fibrillary acidic protein and a decrease in expression of Pax6, a transcription factor regulating neural cell migration. These results indicate that polysialic acid regulates cell migration and differentiation of neural precursors crucial for brain development.


Development ◽  
1996 ◽  
Vol 122 (1) ◽  
pp. 131-139 ◽  
Author(s):  
S. Vincent ◽  
J.L. Vonesch ◽  
A. Giangrande

Glial cells constitute the second component of the nervous system and are important during neuronal development. In this paper we describe a gene, glial cell deficient, (glide), that is necessary for glial cell fate commitment in Drosophila melanogaster. Mutations at the glide locus prevent glial cell determination in the embryonic central and peripheral nervous system. Moreover, we show that the absence of glial cells is the consequence of a cell fate switch from glia to neurones. This suggests the existence of a multipotent precursor cells in the nervous system. glide mutants also display defects in axonal navigation, which confirms and extends previous results indicating a role for glial cells in these processes.


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