Peter Meister

The paper shows that loss of MRG-1 activates a mitochondrial stress response, which contributes to nuclear changes and adaptation to mitochondrial stress rather than just heterochromatin organization.

This study identifies VRK-1 as a regulator of chromatin-nuclear lamina interactions in C. elegans, showing its role in stress-induced chromatin reorganization and survival.

The paper identifies SDC-3 as an adaptor for condensin IDC recruitment to X chromosomes in C. elegans and shows its role in dosage compensation through loop-extrusion activity.

The paper identifies cohesin-dependent 3D chromatin structures called fountains around active enhancers in C. elegans, showing their role in repressing enhancer activity and linking genome architecture to behavior.

This study shows that HP1 dimerization drives H3K9me chromatin condensation and segregation, while LLPS stabilizes foci, and reveals a decoupling between heterochromatin and transcriptional regulation.

This study identifies LET-418 as a regulator of intracellular pathogen response in C. elegans intestine by analyzing its target genes and functional effects on immune response genes.

This study shows that Bicaudal-D is essential for female meiosis II and pronuclear fusion in Drosophila, by localizing key proteins to the meiosis II spindles.

This study shows that condensin I/IDC, not cohesin, is the major genome loop extruder in C. elegans, leading to genome decompaction and loss of TAD structures.

The paper quantifies how enhancer-promoter interactions influence transcription through nonlinear relationships and reveals mechanisms of transcriptional control via chromosome structure.

The paper introduces RAPID, a method to determine tissue-specific transcriptional footprints in C. elegans without cell sorting, and validates it by identifying novel transcriptional profiles in rare cell types.