Astrocyte circadian regulation in neurodegeneration: in vivo BMAL1 occupancy mapping using MACS-Calling Cards
This project generated raw high-throughput sequencing data to study how early neurodegenerative pathology reshapes circadian transcription factor binding and regulation in astrocytes. Using a CLN3deltaex7/8 mouse model of neurodegeneration and wild-type controls, we profiled the core circadian transcription factor BMAL1 at the level of genomic occupancy, local chromatin organization, and astrocyte transcriptomes. Because BMAL1 expression changes can be inconsistent in disease, this dataset emphasizes binding and regulatory output as a functional readout of BMAL1 activity in astrocytes.To enable astrocyte-specific, in vivo mapping of transcription factor occupancy, we used MACS-Calling Cards (MACS-CC): astrocytes were enriched from brain dissociates using immunomagnetic selection (MACS), and BMAL1 genomic occupancy was recorded via Calling Cards transposon insertions that mark BMAL1-DNA interactions. In parallel, we generated MNase-seq libraries to measure chromatin architecture (nucleosome positioning/protection patterns) and RNA-seq libraries from sorted/enriched astrocytes to quantify gene expression programs associated with disease status. The uploaded FASTQ files comprise the raw reads for Calling Card insertion profiling, MNase-seq, and RNA-seq across wild-type and CLN3deltaex7/8 samples, enabling full reprocessing and reproduction of downstream analyses such as insertion mapping/peak discovery, chromatin profiling, and differential expression.Data types included (FASTQ):BMAL1 MACS-Calling Cards (MACS-CC): sequencing of transposon insertion junctions to infer BMAL1 genomic occupancy in astrocytes in vivo.MNase-seq: sequencing of MNase-protected DNA fragments to profile nucleosome organization/chromatin structure in the same experimental context.RNA-seq: astrocyte transcriptome sequencing to quantify gene expression changes associated with CLN3deltaex7/8 pathology.