Transcriptional programs mediating neuronal toxicity and altered glial-neuronal signaling in a knock-in tauopathy model.

Missense mutations in the gene encoding the microtubule-associated protein TAU (current and approved symbol is MAPT) cause autosomal dominant forms of frontotemporal dementia. Multiple models of frontotemporal dementia based on transgenic expression of human in experimental model organisms, including , have been described. These models replicate key features of the human disease but do not faithfully recreate the genetic context of the human disorder.

Transcriptional programs mediating neuronal toxicity and altered glial-neuronal signaling in a knock-in tauopathy model.

Missense mutations in the gene encoding the microtubule-associated protein tau cause autosomal dominant forms of frontotemporal dementia. Multiple models of frontotemporal dementia based on transgenic expression of human tau in experimental model organisms, including , have been described. These models replicate key features of the human disease, but do not faithfully recreate the genetic context of the human disorder.

Deciphering multi-way interactions in the human genome.

Chromatin architecture, a key regulator of gene expression, can be inferred using chromatin contact data from chromosome conformation capture, or Hi-C. However, classical Hi-C does not preserve multi-way contacts. Here we use long sequencing reads to map genome-wide multi-way contacts and investigate higher order chromatin organization in the human genome.