A combination of single-cell analysis, genomics, and simulations shows that a glutamine-rich low-complexity sequence in the SWI/SNF chromatin remodeling complex senses transient intracellular acidification as a signal for cells to switch their global transcriptional program.

Discovery of new Snf1/AMPK targets in the TORC1 pathway highlights the complex, multilayered crosstalk between major signaling pathways in the regulation of nutrient deprivation sensing.

The structure of the entire Mot1 Swi2/Snf2 protein uncovers an unexpected auto-inhibited resting state activated by substrate binding, and suggests a DNA pulling mechanism of TBP displacement.

SND1 has m6A-reading ability and is essential for Kaposi's sarcoma-associated lytic replication.

Neurofibromatosis type 1 gene (NF1) signaling is causally linked to the acquisition of a mesenchymal gene expression program in gliomas through the regulation of the AP-1 transcription factor FOSL1.

The emerging importance of interorganellar communication is demonstrated by documentation of a feedback loop wherein peroxisome-generated metabolites affect mitochondrial ATP production and peroxisomal functions via signaling pathways requiring transmission of signals also through the cytosol and the nucleus.

Visualization of BRM remodelers engaging their endogenous genomic targets revealed highly transient and dynamic interactions with chromatin, which are fueled by ATP-hydrolysis.

Inositol polyphosphate multikinase physically binds to the core subunits of SWI/SNF complex and plays an important role in regulating BRG1 occupancy and BRG-mediated chromatin accessibility in mouse embryonic stem cells.

Snf7 crystal structures reveal the mechanisms of ESCRT-III activation and polymerization into membrane-remodeling filaments.

A zebrafish model of neuroblastoma reveals that the tumor suppressor NF1 uses different mechanisms to suppress malignant transformation and to down-modulate normal neural crest cell growth during embryogenesis.