Altered pathways in Cockayne syndrome: Involvement of MAPK, PI3K-Akt, extracellular matrix, inflammation, and neuronal signaling
Cockayne syndrome (CS), a disorder characterized by neurodegeneration and a segmental progeroid phenotype, is caused by mutations in CSA or CSB genes, which codify proteins necessary for the DNA repair pathway known as transcription-coupled nucleotide excision repair (TC-NER). To further elucidate the biological pathways associated with this aging-related neurodegenerative phenotype, we analyzed CS transcriptome datasets. We performed RNA-seq on the brains of one Csa-/- mouse model and a respecitive wild-type mouse (C57-Black6J background) in three different age timepoints (45 days, 12 months, 24 months). RNA-seq was performed in 5 lanes using AB SOLiD system. Overall design: RNA-seq profiling of Csa-/- mice and their respective wild-type counterparts in different timepoints (45 days, 12 months and 24 months) during their lifespan.