Kelly R. Monk

The paper introduces a CRISPR-Cas13d-based system for cell-specific mRNA knockdown in zebrafish, validated across CNS glia types, showing efficient target mRNA depletion and reproducible phenotypes.

This study shows that PIEZO1 and PIEZO2 channels in oligodendrocytes regulate sheath formation, expansion, and myelination by detecting mechanical cues.

This study identifies ADGRG1 as a key regulator of pre-myelinating oligodendrocyte development and axon ensheathment, showing its role in CNS myelin formation through RhoA activation.

This study investigates the role of P/Q-type voltage-gated calcium channels in oligodendrocyte lineage cells during myelination in zebrafish, finding that these channels are essential for normal myelination and calcium signaling.

This study shows that activating CB1 receptors in zebrafish leads to increased non-axonal ensheathment without affecting OL differentiation or normal myelin formation.

This study identifies TMEM63A as a critical regulator of myelination in the CNS, showing its role in oligodendrocyte function and linking its dysfunction to hypomyelinating leukodystrophies.

This study shows that CNS axon diameter growth does not require oligodendrocyte ensheathment or myelination, contrasting with PNS findings.

This study identifies FBXW7 as a regulator of myelin capacity and homeostasis in the adult CNS by controlling MYRF levels through ubiquitination.

The paper identifies Tre1 and S1pr1 as evolutionarily conserved regulators of astrocyte morphology through lipid signaling and competition for growth-promoting phospholipids.

This study shows Dock1 is essential for Schwann cell function in peripheral myelin development, maintenance, and repair across species.

The paper shows SARM1 is present in oligodendrocytes but not Schwann cells, and its deletion does not affect myelination in zebrafish or mice.

The paper identifies postsynaptic molecules in OPCs and shows their role in predicting myelin sheath formation through Ca2+ activity.

This study identifies mutations affecting spine development in zebrafish, revealing new candidate genes for human spine disorders like scoliosis.

This study shows that Fbxw7 loss enhances Schwann cell myelinating potential by altering mTOR signaling and enabling multiple axon myelination, challenging previous distinctions between myelinating and non-myelinating Schwann cells.