Partial copy loss of spliceosome genes are common non-driver gene dependencies in cancer.

The loss of genes that encode RNA splicing factors weakens cancer cells in a way that could be exploited by new approaches to treatment.

A subset of the zebrafish Nodal receptor complex is regulated by positive feedback and controls the diffusion and distribution of Nodal signals during germ layer formation.

Ectopic expression of Symbiosis Receptor-like Kinase (SYMRK) in roots of the legume Lotus japonicus resulted in spontaneous activation of nodule organogenesis and mycorrhiza-related gene expression in the absence of microbial symbionts or signalling molecules.

Ligand capture by cell surface receptor complexes sets the shape of the Nodal signaling pattern in zebrafish.

Lefty-mediated feedback inhibition of Nodal signaling mitigates signaling perturbations, but is dispensable for development.

Specific evolutionary gene loss signatures indicated an eye-related function for the uncharacterized SERPINE3 gene, which was experimentally confirmed by zebrafish gene knockouts, showing how comparative genomics can provide insights into the function of uncharacterized genes.

A mutant allele encoding a deregulated subunit of an ion channel tetramer revealed a mechanistic connection between protein heteromerization and quantitative genetic behavior.

A kinetic model of morphogen interpretation is more suitable than classic threshold or ratchet models to understand how a signal gradient generates different target gene expression patterns.

The Apelin receptor acts as a rheostat to ensure that the proper levels of Nodal signaling are achieved for proper cell fate specification at the onset of gastrulation, in particular for cardiac progenitor development.