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Assaying Circuit Specific Regulation of Adult Hippocampal Neural Precursor Cells

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Neurog2 regulates Isl1 to modulate horizontal cell number.

Patrick W Keeley¹, Pooja S Patel¹, Matthew S Ryu¹

¹Neuroscience Research Institute, University of California at Santa Barbara, Santa Barbara, CA 93106-5060, USA.

Development (Cambridge, England)

|December 20, 2022

Summary

Geneticists discovered an epistatic interaction between two genes controlling mouse retinal horizontal cell numbers. Neurog2 represses Isl1, with variations impacting cell populations and validated in knockout mice.

Keywords:

Conditional knockout E-box Epistasis QTL Recombinant inbred strain SNP Variant

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Area of Science:

Genetics
Neuroscience
Developmental Biology

Background:

Mouse strain variations influence retinal cell population sizes.
Gene interactions, including epistasis, contribute to these variations.
Quantitative trait loci (QTL) mapping helps identify genes controlling complex traits.

Purpose of the Study:

To identify and characterize an epistatic interaction between genes regulating retinal horizontal cell numbers.
To elucidate the genetic basis of variation in retinal horizontal cell populations.

Main Methods:

Mapping quantitative trait loci (QTL) in a panel of recombinant inbred mouse strains.
Utilizing single and double conditional knockout mice to validate gene functions.
In vitro validation of single nucleotide polymorphisms (SNPs) in gene regulatory regions.

Main Results:

Identified epistatic interaction between QTL on chromosomes 3 and 13 affecting horizontal cell numbers.
Demonstrated that Neurog2 (chromosome 3) represses Isl1 (chromosome 13).
Confirmed the roles of Neurog2 and Isl1 in controlling horizontal cell populations using knockout models and identified specific SNPs mediating repression.

Conclusions:

An epistatic interaction between Neurog2 and Isl1 underlies variation in mouse retinal horizontal cell populations.
Specific SNPs within the Isl1 5'UTR mediate Neurog2's repressive effect.
This study provides a detailed genetic mechanism for cell type population control in the retina.