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GFAP? expression in glia of the developmental and adolescent mouse brain.

ABSTRACT: Glial fibrillary acidic protein (GFAP) is the major intermediate filament (IF) protein in astrocytes. In the human brain, GFAP isoforms have unique expression patterns, which indicate that they play distinct functional roles. One isoform, GFAP?, is expressed by proliferative radial glia in the developing human brain. In the adult human, GFAP? is a marker for neural stem cells. However, it is unknown whether GFAP? marks the same population of radial glia and astrocytes in the developing mouse brain as it does in the developing human brain. This study characterizes the expression pattern of GFAP? throughout mouse embryogenesis and into adolescence. Gfap? transcripts are expressed from E12, but immunohistochemistry shows GFAP? staining only from E18. This finding suggests a translational uncoupling. GFAP? expression increases from E18 to P5 and then decreases until its expression plateaus around P25. During development, GFAP? is expressed by radial glia, as denoted by the co-expression of markers like vimentin and nestin. GFAP? is also expressed in other astrocytic populations during development. A similar pattern is observed in the adolescent mouse, where GFAP? marks both neural stem cells and mature astrocytes. Interestingly, the Gfap?/Gfap? transcript ratio remains stable throughout development as well as in primary astrocyte and neurosphere cultures. These data suggest that all astroglia cells in the developing and adolescent mouse brain express GFAP?, regardless of their neurogenic capabilities. GFAP? may be an integral component of all mouse astrocytes, but it is not a specific neural stem cell marker in mice as it is in humans.

SUBMITTER: Mamber C

PROVIDER: S-EPMC3528700 | biostudies-literature | 2012

REPOSITORIES: biostudies-literature

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GFAPδ expression in glia of the developmental and adolescent mouse brain.

Mamber Carlyn C Kamphuis Willem W Haring Nina L NL Peprah Nuzrat N Middeldorp Jinte J Hol Elly M EM

PloS one 20121221 12

Glial fibrillary acidic protein (GFAP) is the major intermediate filament (IF) protein in astrocytes. In the human brain, GFAP isoforms have unique expression patterns, which indicate that they play distinct functional roles. One isoform, GFAPδ, is expressed by proliferative radial glia in the developing human brain. In the adult human, GFAPδ is a marker for neural stem cells. However, it is unknown whether GFAPδ marks the same population of radial glia and astrocytes in the developing mouse bra ...[more]

PMID: 23285135

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Project description:BackgroundGenetic variants in the voltage-gated sodium channels SCN1A, SCN2A, SCN3A, and SCN8A are leading causes of epilepsy, developmental delay, and autism spectrum disorder. The mRNA splicing patterns of all four genes vary across development in the rodent brain, including mutually exclusive copies of the fifth protein-coding exon detected in the neonate (5N) and adult (5A). A second pair of mutually exclusive exons is reported in SCN8A only (18N and 18A). We aimed to quantify the expression of individual exons in the developing human brain.MethodsRNA-seq data from 783 human brain samples across development were analyzed to estimate exon-level expression. Developmental changes in exon utilization were validated by assessing intron splicing. Exon expression was also estimated in RNA-seq data from 58 developing mouse neocortical samples.ResultsIn the mature human neocortex, exon 5A is consistently expressed at least 4-fold higher than exon 5N in all four genes. For SCN2A, SCN3A, and SCN8A, a brain-wide synchronized 5N to 5A transition occurs between 24 post-conceptual weeks (2nd trimester) and 6 years of age. In mice, the equivalent 5N to 5A transition begins at or before embryonic day 15.5. In SCN8A, over 90% of transcripts in the mature human cortex include exon 18A. Early in fetal development, most transcripts include 18N or skip both 18N and 18A, with a transition to 18A inclusion occurring from 13 post-conceptual weeks to 6 months of age. No other protein-coding exons showed comparably dynamic developmental trajectories.ConclusionsExon usage in SCN1A, SCN2A, SCN3A, and SCN8A changes dramatically during human brain development. These splice isoforms, which alter the biophysical properties of the encoded channels, may account for some of the observed phenotypic differences across development and between specific variants. Manipulation of the proportion of splicing isoforms at appropriate stages of development may act as a therapeutic strategy for specific mutations or even epilepsy in general.

Dataset Information

GFAP? expression in glia of the developmental and adolescent mouse brain.

Publications

GFAPδ expression in glia of the developmental and adolescent mouse brain.

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