| First Author | Kim HM | Year | 1993 |
| Journal | J Mol Neurosci | Volume | 4 |
| Issue | 4 | Pages | 245-53 |
| PubMed ID | 7522503 | Mgi Jnum | J:22008 |
| Mgi Id | MGI:69902 | Doi | 10.1007/BF02821556 |
| Citation | Kim HM, et al. (1993) PKC gamma gene expression is delayed in postnatal central nervous system of mi/mi mice. J Mol Neurosci 4(4):245-53 |
| abstractText | In the central nervous system (CNS), the expression of protein kinase C (PKC) genes is strictly controlled by the developmental stage. We have examined the expression of PKC genes (cPKC alpha, beta, gamma, and nPKC delta, epsilon) in the process of the postnatal development in normal (+/+) C57BL/6 and microphthalmic (mi/mi) C57BL/6 mouse brains by Northern blotting and in situ hybridization. By Northern blotting, the expression level of cPKC gamma mRNA in mi/mi mice was significantly lower than that in +/+ littermates at d 9, 13, and 17. By in situ hybridization analysis, cPKC gamma mRNA-positive cells were detected in hippocampal and Purkinje cells in +/+ and mi/mi mice, but the magnitude of the signals in mi/mi mice was lower than that of +/+ mice, and the number of positive cells was smaller, whereas other isozymes (cPKC alpha, beta, and nPKC delta, epsilon) showed no significant difference between normal and mi/mi mice. The neuronal morphometric analysis by anti-P400 antibody revealed the same number and expression level of P400 protein in cerebellar Purkinje cells compared with +/+ mice. These results indicate that the deficiency of mi gene product causes the delayed expression of the cPKC gamma gene. |
