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High Expression of the γ 5 Isoform of G Protein in Neuroepithelial Cells and Its Replacement of the γ 2 Isoform During Neuronal Differentiation in the Rat Brain
Author(s) -
Morishita Rika,
Shinohara Haruo,
Ueda Hiroshi,
Kato Kanefusa,
Asano Tomiko
Publication year - 1999
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1999.0732369.x
Subject(s) - gene isoform , biology , retinoic acid , neuroepithelial cell , embryogenesis , embryonal carcinoma , embryonic stem cell , cellular differentiation , immunohistochemistry , microbiology and biotechnology , p19 cell , endocrinology , embryo , medicine , biochemistry , gene , immunology , adult stem cell
: High concentrations of G proteins, which include multiple isoforms of each subunit, α, β, and γ, are expressed in the adult brain. In this study, we concentrated attention on changes of these isoforms during embryonic development in the rat brain. Concentrations of γ 2 as well as G o Aα, G o Bα, and β 2 were low in early embryogenesis and then increased, whereas expression of γ 5 , in contrast, was initially high followed by a drop, with only very low levels observed throughout postnatal development. Among the other isoforms, G i1 α, G s α‐short, G 12 α, G 13 α, β 4 , γ 3 , γ 7 , and γ 12 were present in the embryonic brain at low levels, but their levels markedly increased after birth. In contrast, the levels of G i2 α, G s α‐long, G q/11 α, and β 1 were essentially constant throughout. Immunohistochemical staining of the brain vesicles in the embryos showed γ 5 to be specifically expressed in the proliferative region of the ventricular zone, whereas γ 2 was mainly present in differentiated neuronal cells of the marginal zone. Furthermore, differentiation of P19 mouse embryonal carcinoma cells to neuronal cells with retinoic acid induced the expression of γ 2 and a decrease of γ 5 , the major isoform in the undifferentiated state. These results suggest that neuronal differentiation is responsible for the on/off switch of the expression of γ 2 and γ 5 subunits.