Rolf Bodmer

This study shows that Chchd3 deficiency in Drosophila hearts impairs function through mitophagy, ROS, and ER stress, with partial rescue by antioxidant and ER stress interventions.

The paper identifies ribosomal protein genes as contributors to hypoplastic left heart syndrome through functional analysis across multiple model systems.

The paper shows that reduced nucleosome stability impairs cell identity, stress resilience, and healthy aging across species.

This study shows that increasing SLP-2 levels reduces alpha-synuclein-induced mitochondrial damage and neurodegeneration in Parkinson's disease models.

This study identifies the PI(4,5)P2 pathway's role in T-tubule formation and muscle function using Drosophila models.

The paper identifies mitochondrial MICOS complex genes, CHCHD3 and CHCHD6, as contributors to hypoplastic left heart syndrome through functional studies in Drosophila and genetic analysis of patient cohorts.

The paper shows that a single DPE core promoter motif mutation in Drosophila affects cardiac function by disrupting Tinman's regulatory network.

The paper identifies genetic networks and regulatory elements associated with cardiac performance variation in Drosophila and finds conserved genetic architecture between flies and humans.

The paper creates a single-cell transcriptomic atlas of the adult fruit fly, identifying over 250 cell types and analyzing gene signatures and sexual dimorphism across tissues.

This study identifies NAC and SRP as novel regulators of cardiac development and remodeling in Drosophila and human cardiac progenitors, showing their spatial and temporal regulation in heart formation.

The paper investigates the role of KCa1.1 in sinus node function and arrhythmia risk across species, finding conserved effects of its loss of function.

The paper creates a single-cell atlas of the Drosophila embryonic heart and identifies Tinman's cell-type-specific roles in cardiac development.

The paper identifies MYOM2 as a candidate gene for hypertrophic cardiomyopathy and Tetralogy of Fallot and shows its functional role in heart development through Drosophila models.

The paper identifies LRP2 as a novel genetic driver of hypoplastic left heart syndrome using whole genome sequencing and multi-model systems.

This study shows activin signaling negatively regulates cardiac autophagy and health during aging in Drosophila, with mTORC2 playing a key role.