Genetic analyses illustrate the novel requirement of Ftz-f1 and Sim in adult Drosophila ovaries for regulating follicle cell differentiation and ovulation that is likely conserved in mammals.

Elevating FUS level by saturating autoregulation loop in mice causes aggressive motor neuron disease via disrupting protein and RNA homeostasis.

DCX negatively regulates dynein-mediated retrograde transport through two critical interactions by regulating dynein binding to microtubules and regulating the composition of dynein/dyactin/JIP3 motor complex.

Single-cell combined spatial transcriptomics provides the molecular foundation for investigating how ligamental cell identities, biochemical functions, and interactions contributed to the ligamental degeneration process.

A single-cell transcriptome atlas reveals meniscal microenvironment variations during degeneration and cellular heterogeneity foundations of the inner–outer zone differences, suggesting novel cell subtypes as potential therapeutic targets.

Quantitative time-resolved crosslinking mass spectrometry is developed to monitor protein interactions and dynamics inside molecular condensates and used to identify misfolding of the RNA-binding domain of FUS as a key driver of condensate-aging.

Bacterial population can coordinate individuals of different phenotypes by spatial modulation of their run-and-tumble behaviors, resulting in collective group migration with an ordered structure of phenotypes.

A novel mechanism of gene regulation is discovered wherein a specific long non-coding RNA abolishes the blocking activity of chromatin insulator in the Drosophila HOX gene cluster.

The crystal structure of Norrie Disease Protein in complex with the extracellular cysteine-rich domain of Frizzled4 receptor and sucrose octasulfate reveals binding sites for Frizzled4, low density lipoprotein receptor related protein 5/6, and proteoglycan.

Building on previous work (Kaneko and Stryker, 2014), we report that the specific population of inhibitory neurons that increases the responses of neurons in the visual cortex during locomotion will also, when activated or blocked artificially, dramatically alter adult cortical plasticity, revealing that the aerobic exercise of locomotion is not necessary.