A new publication by the Pende team, in collaboration with the Spassky lab (IBENS), uncovers how the metabolic regulator mTORC1 orchestrates the differentiation of ependymal cells, multiciliated glial cells that line the brain’s ventricles.

The study, published in EMBO Reports, shows that mTORC1 activity promotes progression through an alternative cell cycle required for centriole amplification and multiciliogenesis. Inhibiting mTORC1 preserves the progenitor pool in a quiescent state and impairs key steps in differentiation.

The authors further identify a role for GAS2L1,  a centrosomal protein that links actin and microtubule cytoskeletons, as a downstream target of mTORC1. mTORC1-mediated phosphorylation of GAS2L1 contributes to centriole disengagement, linking metabolic signaling to centrosome dynamics.

This work highlights a multilayered control of ependymal development by mTORC1, with potential relevance for conditions such as brain aging and hydrocephalus-prone genetic diseases.

🔗 Read the full article: https://www.embopress.org/doi/full/10.1038/s44319-025-00460-2