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Updated: Jul 3, 2026

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4-Dimensional Imaging of Zebrafish Optic Cup Morphogenesis
Published on: May 26, 2021
Bone morphogenetic proteins, eye patterning, and retinocollicular map formation in the mouse
Daniel T Plas1, Onkar S Dhande, Joshua E Lopez
1Department of Neuroscience, University of Texas, M. D. Anderson Cancer Center, Houston, Texas 77030, USA.
Summary
Bone morphogenetic proteins (BMPs) guide retinal ganglion cell (RGC) axon development and targeting in the brain. Disrupting BMP signaling causes RGC axon missorting, impacting retinotopic map formation.
Area of Science:
- Neuroscience
- Developmental Biology
- Ophthalmology
Background:
- Early eye formation involves patterning events that determine retinal cell fate and guide retinal ganglion cell (RGC) axon navigation.
- Bone morphogenetic proteins (BMPs) and their receptors are crucial for initiating gene expression cascades that differentiate retinal regions, particularly along the dorsoventral axis.
Purpose of the Study:
- To investigate the roles of BMP signaling and its downstream effector, EphB, in retinotopic map formation in the lateral geniculate nucleus (LGN) and superior colliculus (SC).
- To compare RGC axon behaviors in wild-type mice with those in mice engineered with defects in BMP and EphB signaling.
Main Methods:
- Comparative analysis of RGC axon sorting and targeting in wild-type mice versus mice with genetically modified BMP and EphB signaling.
- Examination of axon order in the optic tract and map formation in the LGN and SC.
Main Results:
- Disruption of BMP signaling led to significant missorting of RGC axons at the optic chiasm, independent of EphB.
- Genetic modification of BMP signaling in the developing eye resulted in disrupted RGC order in the optic tract and aberrant targeting in the LGN and SC.
Conclusions:
- BMP signaling is essential for regulating dorsoventral RGC cell fate and RGC axon behavior in the optic tract.
- BMP signaling influences retinotopic map formation in the LGN and SC through mechanisms partially distinct from EphB signaling.

