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HIV-1 capsids enter the host cell nucleus, where they are partially disrupted to release the viral genome upon completion of reverse transcription.

A combination of in vitro and in vivo experiments demonstrate a cell-autonomous role of the KIT ligand/KIT signaling pathway in protecting retinal photoreceptor cells from environmentally or genetically caused degeneration.

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

Depletion of vsx genes in zebrafish confirms a conserved role in bipolar cells specification across vertebrates, but do not interfere with the formation of the neural retina domain, which reveal an unexpected robustness of the genetic network sustaining the retina.

Mouse retina manifests homeostatic plasticity and adapts to photoreceptor degeneration to resist visual decline.

Metabolic cues enlist ubiquitin ligase adaptors for the selective control of cellular nutrient acquisition strategies.

NMNAT1, a ubiquitously expressed metabolic enzyme linked to inherited blinding disease, is crucial for the proper differentiation of photoreceptor cells and subsequent survival of multiple cell types in the retina.

Nodal signaling regulates gastrulation cell behaviors largely in parallel with planar cell polarity signaling and is sufficient for ex vivo extension of embryonic explants.

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.

A microphysiological system (retina-on-a-chip) shows the potential to promote drug development and provide new insights into the underlying pathology of retinal diseases.