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Functional consequences of I56ii Dlx enhancer deletion in the developing mouse forebrain
S Fazel Darbandi1, L Poitras2, S Monis2
1Department of Biology, University of Ottawa, 20 Marie Curie, Ottawa, ON Canada K1N 6N5; Department of Psychiatry, School of Medicine, Rock Hall, University of California, San Francisco (UCSF), San Francisco, CA 94158-2324, USA.
Developmental Biology
|December 17, 2016
Summary
Deleting the I56ii cis-regulatory element impairs Dlx gene expression and disrupts forebrain development. This highlights I56ii's crucial role in regulating gene expression and patterning during brain development.
Area of Science:
- Neuroscience
- Developmental Biology
- Genetics
Background:
- Dlx homeobox genes are critical transcription factors for GABAergic interneuron development.
- Dlx1/2 and Dlx5/6 genes form bigene clusters in the forebrain with associated cis-regulatory elements (CREs).
- I56ii is a CRE located in the Dlx5/Dlx6 intergenic region, implicated in forebrain development.
Purpose of the Study:
- To investigate the phenotypic effects of deleting the I56ii CRE on forebrain development.
- To understand the role of I56ii in the spatial patterning of corridor cells involved in thalamocortical projections.
- To elucidate the regulatory mechanism by which I56ii influences Dlx gene expression.
Main Methods:
- Characterization of phenotypic consequences following I56ii deletion in mice.
- Analysis of Dlx gene expression and expression of downstream targets (Gad2, Islet1, Meis2, Ebf1).
- Assessment of DLX2 binding and H3K9Ac levels at the Dlx5/Dlx6 locus.
- Evaluation of cell populations (parvalbumin, calretinin) in the adult somatosensory cortex.
Main Results:
- I56ii deletion significantly impairs Dlx gene expression and that of downstream targets like Gad2 and striatal markers.
- Reduced DLX2 binding and H3K9Ac at the Dlx5/Dlx6 locus were observed post-I56ii deletion.
- Deletion of I56ii led to decreased ISLET1 and CTIP2 expression in the striatum and altered parvalbumin/calretinin cell numbers in the cortex.
Conclusions:
- The I56ii CRE plays a vital regulatory role in developing forebrain.
- I56ii influences Dlx gene expression, particularly Dlx6, and the spatial patterning of the ventral telencephalon.
- These findings suggest I56ii is essential for normal forebrain development and potentially corridor cell patterning.
