High expression of the gamma(5) isoform of G protein in neuroepithelial cells and its replacement of the gamma(2) isoform during neuronal differentiation in the rat brain

Citation
R. Morishita et al., High expression of the gamma(5) isoform of G protein in neuroepithelial cells and its replacement of the gamma(2) isoform during neuronal differentiation in the rat brain, J NEUROCHEM, 73(6), 1999, pp. 2369-2374
Citations number
29
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROCHEMISTRY
ISSN journal
00223042 → ACNP
Volume
73
Issue
6
Year of publication
1999
Pages
2369 - 2374
Database
ISI
SICI code
0022-3042(199912)73:6<2369:HEOTGI>2.0.ZU;2-C
Abstract
High concentrations of G proteins, which include multiple isoforms of each subunit, alpha, beta, and gamma, are expressed in the adult brain. In this study, we concentrated attention on changes of these isoforms during embryo nic development in the rat brain. Concentrations of gamma(2) as well as G(o )A alpha, G(o)B alpha, and beta(2) were low in early embryogenesis and then increased, whereas expression of gamma(5), in contrast, was initially high followed by a drop, with only very low levels observed throughout postnata l development. Among the other isoforms, G(i1)alpha, G(s)alpha-short, G(12) alpha, G(13)alpha, beta(4), gamma(3), gamma(7), and gamma(12) were present in the embryonic brain at low levels, but their levels markedly increased a fter birth. In contrast, the levels of G(i2)alpha, G(s)alpha-long, G(q/11)a lpha, and beta(1) were essentially constant throughout. Immunohistochemical staining of the brain vesicles in the embryos showed gamma(5) to be specif ically expressed in the proliferative region of the ventricular zone, where as gamma(2) was mainly present in differentiated neuronal cells of the marg inal zone. Furthermore, differentiation of P19 mouse embryonal carcinoma ce lls to neuronal cells with retinoic acid induced the expression of gamma(2) and a decrease of gamma(5), the major isoform in the undifferentiated stat e. These results suggest that neuronal differentiation is responsible for t he on/off switch of the expression of gamma(2) and gamma(5) subunits.