Highly quantitative measurement of differential protein-genome binding with PerCell chromatin sequencing.

We report a universal strategy for 2D chromatin sequencing, to increase uniform data analyses and sharing across labs, and to facilitate highly quantitative comparisons across experimental conditions. Within our system, we provide wetlab and drylab tools for researchers to establish and analyze protein-genome binding data with PerCell ChIP-seq. Our methodology is virtually no cost and flexible, enabling rapid, quantitative, internally normalized chromatin sequencing to catalyze project development in a variety of systems, including in vivo zebrafish epigenomics and cancer cell epigenomics.

Rhabdomyosarcoma fusion oncoprotein initially pioneers a neural signature in vivo.

Fusion-positive rhabdomyosarcoma is an aggressive pediatric cancer molecularly characterized by arrested myogenesis. The defining genetic driver, PAX3::FOXO1, functions as a chimeric gain-of-function transcription factor. An incomplete understanding of PAX3::FOXO1's in vivo epigenetic mechanisms has hindered therapeutic development.

Inducible Protein Degradation to Understand Genome Architecture.

We review exciting recent advances in protein degradation, with a focus on chromatin structure. In our analysis of the literature, we highlight studies of kinetic control of protein stability for cohesin, condensin, ATP-dependent chromatin remodeling, and pioneer transcription factors. With new connections emerging between chromatin remodeling and genome structure, we anticipate exciting developments at the intersection of these topics to be revealed in the coming years.

Virus spread in the liver: mechanisms, commonalities, and unanswered questions.

The liver is home to five known human hepatitis viruses (hepatitis A virus-hepatitis E virus). Despite being phylogenetically unrelated, these viruses replicate and spread in the liver without causing apparent cytopathic effects, and all have evolved strategies to counteract antibody-mediated inhibition of virus spread. In this review, we discuss the current understanding regarding the spread mechanisms for these viruses with an attempt to extract common principles and identify key questions for future studies.

A Novel, Modified Human Butyrylcholinesterase Catalytically Degrades the Chemical Warfare Nerve Agent, Sarin.

Chemical warfare nerve agents (CWNAs) present a global threat to both military and civilian populations. The acute toxicity of CWNAs stems from their ability to effectively inhibit acetylcholinesterase (AChE). This inhibition can lead to uncontrolled cholinergic cellular signaling, resulting in cholinergic crisis and, ultimately, death.