Joseph M. Bateman

This study performs phosphoproteomic analysis of TSC brain lesions, finding strong mTORC1 activation and widespread mRNA splicing changes in SEGAs but not tubers.

The paper shows that mitochondrial metabolic activity determines ER stress signaling activation in neurons, conserved across Drosophila and human brains.

This study uses a Drosophila model to show that varying levels of NDUFS1 knockdown lead to distinct phenotypic and metabolic outcomes in complex I deficiency.

The paper identifies a multivalent RBP-effector interface that enables RNA recognition accuracy and functional repurposing of effector proteins.

This study identifies Unkempt as a novel mTORC1 substrate whose phosphorylation regulates cellular morphology by inhibiting its ability to induce bipolar morphology.

The paper shows that yeast NDI1 restores metabolite levels, ER-mitochondria contacts, and rescues behavioral and lifespan defects in Drosophila with neuronal complex I deficiency.