David J. Reiner

This study shows RAL-1 regulates the Exocyst complex in C. elegans, affecting secretion and development through direct interactions and genetic perturbations.

The paper uses structure-guided CRISPR/Cas9 to study PI3K mutations in C. elegans, revealing a novel Ras>PI3K signaling axis that affects growth, dauer formation, and lifespan.

The paper develops a single-component optogenetic toolkit to control microtubule organization and dynamics in living systems, revealing their role in lysosomal trafficking and ER signaling.

This study identifies a conserved Hippo signaling pathway in C. elegans, showing canonical activity in epithelium and non-canonical regulation in intestine.

This study identifies FGF-dependent, polarized SOS activity as a mechanism for directing C. elegans muscle progenitor migration, independent of canonical RTK effectors.

This study identifies a vulva-specific transcriptome in C. elegans using immunoprecipitation of a poly(A) binding protein, revealing gene expression patterns and validating their roles in vulval development.

The paper uses CRISPR to tag ERK-1 in C. elegans and shows nuclear translocation as a marker of activation events during development.

The paper identifies the roles of RalGEF>Ral, Rap1, and Ras signaling in C. elegans nervous system development, showing Ral's permissive role and Ras's instructive role in cell migration.

The paper engineers threshold-based selection systems in C. elegans to identify novel downstream effectors by disrupting embryonic morphogenesis with conditional CED-10/Rac activation.

The paper introduces new tools for the auxin-inducible degron system in C. elegans, enabling conditional protein depletion through CRISPR/Cas9-mediated genome editing.

The paper identifies a Ral-dependent signaling cascade in C. elegans that transduces lower EGF doses to promote 2° vulval precursor cell fate.

This study identifies RGL-1 as a balanced switch that coordinates opposing signals to ensure developmental fidelity in C. elegans vulval precursor cells.

This study investigates the role of RAP-1 in Ras-dependent cell fate decisions in C. elegans, showing it promotes fate induction and functions alongside LET-60/Ras.