E-MTAB-7398
RNA-seq from cortex and hippocampus of mice harboring heterozygous and homozygous deletion of Kctd13, as well as wild-type controls.
Modeling haploinsufficiency and complete knockout of Kctd13--a candidate contributory gene within the syntenic 16p11.2 copy number variation region--in mice. Transcriptome analyses from cortex and hippocampus highlighted the dysregulation of pathways important in neurodevelopment, the most significant of which was synaptic formation. Differential expression (DE) analyses of genes was performed by comparing heterozygous deletion mice samples to wild-type control littermates, and homozygous deletion samples to their wild-type control littermates, separately for both Hippocampus and Cortex tissues. DE analyses were performed using DESeq2 with surrogate variable analysis package in R/Bioconductor, sva (72, version 3.26.0).
Modeling haploinsufficiency and complete knockout of Kctd13--a candidate contributory gene within the syntenic 16p11.2 copy number variation region--in mice. Transcriptome analyses from cortex and hippocampus highlighted the dysregulation of pathways important in neurodevelopment, the most significant of which was synaptic formation. Differential expression (DE) analyses of genes was performed by comparing heterozygous deletion mice samples to wild-type control littermates, and homozygous deletion samples to their wild-type control littermates, separately for both Hippocampus and Cortex tissues. DE analyses were performed using DESeq2 with surrogate variable analysis package in R/Bioconductor, sva (72, version 3.26.0).