Cui-Ting Wu

YTHDF1 modulates CAP1-mediated actin turnover to regulate synaptic function and anxiodepressive-like behaviors.

Neuroplasticity and synaptic dysfunction are central to the pathophysiology of depression, yet their underlying mechanisms remain not fully understood. Here, we identify the m6A reader protein YTHDF1 as a key regulator of depression pathogenesis. Mice with genetic deletion of Ythdf1 exhibited anterior cingulate cortex...