Michael A. Q. Martinez

This study shows that cell cycle perturbation allows post-mitotic cells to maintain invasive behavior without exiting the cell cycle.

The paper investigates how NHR-67 and Groucho regulate the switch between proliferative and invasive states in C. elegans uterine cells.

This paper introduces a FLP-ON::TIR1 system for precise spatiotemporal protein degradation in C. elegans, showing it can drive efficient target protein degradation in specific cell types.

The paper reevaluates the relationship between EGL-43 and LIN-12 in C. elegans anchor cell invasion using a novel co-expression system and finds that LIN-12 is not required for AC proliferation after EGL-43 loss.

The paper shows that BAF and PBAF SWI/SNF complexes differentially regulate cell cycle arrest and invasion in C. elegans anchor cells.

The paper introduces an engineered auxin analog and AtTIR1(F79G) pair to improve the specificity and efficacy of the auxin degradation system in C. elegans.

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 introduces a CDK sensor to distinguish cycling cells from terminally differentiated cells in C. elegans and zebrafish, revealing commitment points and stochasticity in cell cycle control.

This paper improves the AID system in C. elegans for single-cell protein degradation using NAA and demonstrates its application in developmental studies.

This study shows that dynein forces on ruptured nuclei counteract lamin-mediated nuclear envelope repair in C. elegans embryos, affecting NE rupture duration and recovery.

This study uses an AAV-mediated CRISPR screen in mice to identify functional suppressors of glioblastoma, revealing novel and canonical tumor suppressors and their interactions.