Acute knock down of Sgce that is mutated in Myoclonus Dystonia (DYT11), in the cerebellum of mice, leads to dystonia and myoclonus-like motor signs that like patients improve with alcohol.

Structural and functional striatal synaptic plasticity abnormalities occur early in a sensitive developmental period, representing a potential unique endophenotypic traits that increase the risk of manifesting clinical symptoms in DYT1 mutation carriers.

Patients with DYT1 dystonia show aberrant risk-aversion in a simple decision-making task, in accordance with predictions of a reinforcement learning model of corticostriatal trial-and-error learning.

The most common inherited dystonia, DYT1, is likely caused primarily by the dysfunction of the cerebellum rather than the basal ganglia.

First comprehensive genetic analysis of a Myt1 family protein reveals that neurogenesis requires direct repression of non-neuronal identities by the Myt1 family protein through MuvB co-repressor complex.

Enhancing levels of the torsinA paralog torsinB prevents essentially all torsinA loss-of-function neuropathological and behavioral phenotypes, identifying torsinB as a novel therapeutic target for DYT1 dystonia.

Light signaling components interact with a histone H2B deubiquitination module, adjusting chromatin states at global level during Arabidopsis seedling development.

The interrogation of histone modifications on DNA barcodes enables efficient and direct screening for epigenetic regulators in thousands of mutants in parallel.

A recently discovered contagious cancer in the Tasmanian devil has the potential to become widespread in the population due to the loss of histocompatibility antigens that are allogeneic to its hosts.

A Syt1-tdTomato transgenic mice with normal synaptic transmission is established to label synapse in situ and screen synaptogenic adhesion molecules.