title: PKC gamma gene expression is delayed in postnatal central nervous system of mi/mi mice.
abstract: 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.
authors.affiliation: Department of Pathology, Osaka University Medical School, Japan.
authors.forename: H M
authors.initials: HM
authors.lastname: Kim
authors.forename: S
authors.initials: S
authors.lastname: Hirota
authors.forename: H T
authors.initials: HT
authors.lastname: Chung
authors.forename: H
authors.initials: H
authors.lastname: Onoue
authors.forename: A
authors.initials: A
authors.lastname: Ito
authors.forename: E
authors.initials: E
authors.lastname: Morii
authors.forename: T
authors.initials: T
authors.lastname: Hirata
authors.forename: S
authors.initials: S
authors.lastname: Ohno
authors.forename: S
authors.initials: S
authors.lastname: Osada
authors.forename: Y
authors.initials: Y
authors.lastname: Kitamura
mesh_terms: D000818:Animals; D015152:Blotting, Northern; D001921:Brain / Q000201:enzymology* / Q000254:growth & development; D004268:DNA-Binding Proteins / Q000235:genetics / Q000502:physiology*; D004790:Enzyme Induction; D005260:Female; D005786:Gene Expression Regulation; D006624:Hippocampus / Q000201:enzymology / Q000473:pathology; D017403:In Situ Hybridization; D007527:Isoenzymes / Q000096:biosynthesis* / Q000235:genetics; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains / Q000235:genetics* / Q000254:growth & development / Q000378:metabolism; D051739:Microphthalmia-Associated Transcription Factor; D008850:Microphthalmos / Q000235:genetics; D009419:Nerve Tissue Proteins / Q000096:biosynthesis* / Q000235:genetics; D010022:Osteopetrosis / Q000235:genetics; D010859:Pigmentation Disorders / Q000235:genetics; D011493:Protein Kinase C / Q000096:biosynthesis* / Q000235:genetics; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis / Q000235:genetics; D019009:Proto-Oncogene Proteins c-kit; D011689:Purkinje Cells / Q000201:enzymology / Q000473:pathology; D020794:Receptor Protein-Tyrosine Kinases / Q000096:biosynthesis / Q000235:genetics; D016184:Receptors, Colony-Stimulating Factor / Q000096:biosynthesis / Q000235:genetics; D015398:Signal Transduction / Q000235:genetics; D013577:Syndrome; D014157:Transcription Factors
chemical_list: D004268:DNA-Binding Proteins; D007527:Isoenzymes; D051739:Microphthalmia-Associated Transcription Factor; C497235:Mitf protein, mouse; D009419:Nerve Tissue Proteins; D011518:Proto-Oncogene Proteins; D016184:Receptors, Colony-Stimulating Factor; D014157:Transcription Factors; C087857:protein kinase C gamma; D019009:Proto-Oncogene Proteins c-kit; D020794:Receptor Protein-Tyrosine Kinases; D011493:Protein Kinase C