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Published on: March 12, 2021
DSCAM and DSCAML1 function in self-avoidance in multiple cell types in the developing mouse retina
Peter G Fuerst1, Freyja Bruce, Miao Tian
1The Jackson Laboratory, Bar Harbor, ME 04609, USA.
Abstract:
DSCAM and DSCAM-LIKE1 (DSCAML1) serve diverse neurodevelopmental functions, including axon guidance, synaptic adhesion, and self-avoidance, depending on the species, cell type, and gene family member studied. We examined the function of DSCAM and DSCAML1 in the developing mouse retina. In addition to a subset of amacrine cells, Dscam was expressed in most retinal ganglion cells (RGCs). RGCs had fasciculated dendrites and clumped cell bodies in Dscam(-/-) mice, suggesting a role in self-avoidance. Dscaml1 was expressed in the rod circuit, and mice lacking Dscaml1 had fasciculated rod bipolar cell dendrites and clumped AII amacrine cell bodies, also indicating a role in self-avoidance. Neurons in Dscam or Dscaml1 mutant retinas stratified their processes appropriately in synaptic laminae in the inner plexiform layer, and functional synapses formed in the rod circuit in mice lacking Dscaml1. Therefore, DSCAM and DSCAML1 function similarly in self-avoidance, and are not essential for synaptic specificity in the mouse retina.
Insights
Down syndrome cell adhesion molecule (DSCAM) and DSCAM-LIKE1 (DSCAML1) are crucial for neuronal self-avoidance in the developing mouse retina. These genes ensure proper dendritic and cell body spacing but are not essential for synaptic specificity.
Area of Science:
- Neuroscience
- Developmental Biology
- Retinal Circuitry
Background:
- Down syndrome cell adhesion molecule (DSCAM) and DSCAM-LIKE1 (DSCAML1) are known to play roles in neuronal development, including axon guidance and synaptic adhesion.
- Their specific functions in the developing mammalian retina, particularly concerning neuronal self-avoidance and synaptic specificity, require further elucidation.
Purpose of the Study:
- To investigate the roles of DSCAM and DSCAML1 in the developing mouse retina.
- To determine if DSCAM and DSCAML1 are essential for neuronal self-avoidance and synaptic specificity in retinal ganglion cells (RGCs) and the rod circuit.
Main Methods:
- Utilized knockout mouse models (Dscam(-/-) and Dscaml1(-/-)) to study gene function.
- Examined retinal morphology, including dendritic fasciculation and cell body clustering, using microscopy.
- Assessed neuronal stratification and synapse formation in the inner plexiform layer.
Main Results:
- Dscam deficiency in mice led to fasciculated dendrites and clumped cell bodies in retinal ganglion cells (RGCs), indicating a role in RGC self-avoidance.
- Dscaml1 deficiency resulted in fasciculated rod bipolar cell dendrites and clumped AII amacrine cell bodies, also suggesting a role in self-avoidance within the rod circuit.
- Despite defects in self-avoidance, neuronal processes stratified correctly, and functional synapses formed in the Dscaml1 mutant retina.
Conclusions:
- DSCAM and DSCAML1 function analogously in mediating neuronal self-avoidance in the developing mouse retina.
- Neither DSCAM nor DSCAML1 appears to be essential for establishing synaptic specificity within the studied retinal circuits.
- These findings highlight the conserved role of DSCAM family members in preventing neuronalprocess overlap during development.
