Data from: Sex-specific developmental alterations in DYRK1A expression in the brain of a Down syndrome mouse model

Aberrant neurodevelopment in Down syndrome (DS)-caused by triplication of
human chromosome 21-is commonly attributed to gene dosage imbalance,
linking overexpression of trisomic genes with disrupted developmental
processes, with DYRK1A particularly implicated. We hypothesized that
regional brain DYRK1A protein overexpression in trisomic mice varies over
development in sex-specific patterns that may be distinct from Dyrk1a
transcription, and reduction of Dyrk1a copy number from 3 to 2 in
otherwise trisomic mice reduces DYRK1A, independent of other trisomic
genes. DYRK1A overexpression varied with age, sex, and brain region, with
peak overexpression on postnatal day (P) 6 in both sexes. Sex-dependent
differences were also evident from P15-P24. Reducing Dyrk1a copy number
confirmed that these differences depended on Dyrk1a gene dosage and not
other trisomic genes. Trisomic Dyrk1a mRNA and protein expression were not
highly correlated. Sex-specific patterns of DYRK1A overexpression during
trisomic neurodevelopment may provide mechanistic targets for therapeutic
intervention in DS.