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Imaging Exocytosis in Retinal Bipolar Cells with TIRF Microscopy
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Xkr8 Modulates Bipolar Cell Number in the Mouse Retina
Amanda G Kautzman1,2, Patrick W Keeley1,3, Caroline R Ackley1,3
1Neuroscience Research Institute, University of California, Santa Barbara, Santa Barbara, CA, United States.
Frontiers in Neuroscience
|December 19, 2018
Summary
Researchers identified X Kell blood group precursor related family member 8 homolog (Xkr8) as a gene influencing bipolar cell numbers in the mouse retina. Genetic variants in Xkr8 affect cell populations, suggesting a role in cell death and retinal development.
Area of Science:
- Neuroscience
- Genetics
- Developmental Biology
Background:
- Bipolar cells are crucial for retinal signal processing.
- Genetic factors influencing retinal cell populations are not fully understood.
Purpose of the Study:
- To identify genes controlling the population sizes of rod bipolar cells and Type 2 cone bipolar cells in the mouse retina.
- To investigate the role of the X Kell blood group precursor related family member 8 homolog (Xkr8) gene in retinal development.
Main Methods:
- Quantitative trait locus (QTL) mapping in recombinant inbred (RI) mouse strains.
- In situ hybridization, immunolabeling, and qPCR to assess Xkr8 expression.
- Microarray analysis to correlate gene expression with cell numbers.
- Plasmid electroporation and sequence analysis to study Xkr8 function and genetic variants.
Main Results:
- A quantitative trait locus on Chr 4 associated with bipolar cell numbers was identified.
- Xkr8 was identified as a candidate gene with robust retinal expression.
- Xkr8 expression negatively correlated with bipolar cell numbers and mapped to a cis-eQTL.
- Genetic variants in Xkr8's 3' UTR and promoter were found in parental strains.
Conclusions:
- Xkr8 plays a role in regulating the number of specific bipolar cell types in the retina.
- Xkr8 may mediate cell death to influence retinal cell specification.
- Genetic variations in Xkr8 contribute to differences in retinal cell populations.
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