Simon Berger

This study uses a C. elegans model to show that SMN-1 deficiency causes developmental and degenerative defects in motor and touch receptor neurons, suggesting conserved SMA pathology.

The paper identifies transcriptional asymmetry in Wnt pathway components during C. elegans seam cell divisions, revealing feedback mechanisms that reinforce cell fate decisions.

This study shows EGFR signaling is essential for efferocytosis in C. elegans and zebrafish, with EGF acting as an engulfment signal.

This study shows that vitamin B12 regulates RAS/MAPK-mediated cell fate decisions in C. elegans through one-carbon metabolism, with conserved effects in mammalian cells.

The paper shows that mitochondria are unevenly segregated during asymmetric cell division in C. elegans, contributing to cell fate divergence.

The paper shows that cell size predicts physiological germ cell death in C. elegans, regulated by actomyosin contractility at apical rachis bridges.

The paper identifies a reciprocal EGFR signaling mechanism in the C. elegans anchor cell that ensures precise alignment and connection between the uterus and vulva during development.

This paper introduces a microfluidic imaging method for long-term, stable, and parallel live-imaging of C. elegans larval development, enabling observation of previously inaccessible processes.