Maxwell G. Heiman

The paper shows that cilia in C. elegans form stereotyped interciliary contacts independent of physical proximity, suggesting instructive mechanisms guide these interactions.

The paper identifies a glial attachment mechanism in C. elegans neurons that affects cilia morphology and function.

The paper identifies a multivalent adhesion complex in glia that promotes dendrite extension through interactions involving SAX-7/L1CAM, MAGI-1, HMR-1/Cadherin, and AFD-1/Afadin.

The paper identifies oscillatory gene expression in specific cell types using single-cell RNA sequencing and computational methods, finding that cuticle-producing cells exhibit oscillatory patterns while neurons and muscle do not.

The paper reconstructs and analyzes C. elegans sense organs from a high-resolution EM dataset to infer developmental steps in glial and neuronal morphogenesis.

The paper shows that a sex-specific genetic switch in a single C. elegans glial cell patterns the apical extracellular matrix into a specific pore structure.

This study shows that loss of the ECM protein DIG-1 in C. elegans causes glial fragmentation, dendrite breakage, and dendrite extension defects.

The paper identifies UNC-130 as a lineage-specific repressor that enables convergent differentiation in C. elegans by allowing proper specification of glial cells from distinct lineages.

The paper identifies and compares cell-type-specific promoters for C. elegans glia, highlighting variability and plasticity, and proposes a method to discover novel promoters using single-cell data.

This study shows that long-term neuronal activity in C. elegans URX sensory neurons leads to dendritic branch elaboration, independent of oxygen sensitivity.

The paper identifies SAX-7 and GRDN-1 as essential for dendrite development through retrograde extension in C. elegans neurons.

The paper shows that C. elegans amphid neurons form a multicellular rosette to collectively extend dendrites, using adhesion molecules and mechanical cues from surrounding tissues.

The paper studies how neurons and glia in C. elegans develop epithelial-like structures, showing they share properties and mechanisms with other epithelia.

The paper quantifies dendrite arrangement in C. elegans and shows that cell adhesion molecules regulate their stereotyped order, which can be disrupted by genetic perturbations.

The paper identifies genes that constrain dendrite growth in C. elegans throughout life, revealing a mechanism distinct from developmental growth pathways.