This work has been years in the making and provides a mechanism by which mammalian neural crest specification is restricted to the neural plate border.
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This analysis showed EtOH exposed embryos had reduced pallium volumes (independent of genotype) and EtOH exposed Zic2^Ku/+ embryos had reduced TLVs compared to exposed wild-type counterparts. This suggests that the Zic2 Ku allele may exacerbate EtOH teratogenesis.
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The pallium and TLVs were then identified in further scans by warping the created labels to each scan using a modified AntsRegistration software package. Organ volumes were then calculated and normalised by whole embryo volume (via custom code from MRC Harwell).
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To analyse if this interaction recapsulates HPE phenotypes, the pallium (red) and third lateral ventricles (TLVs; green) of the forebrain were manually labelled within in a single 碌CT scan of an embryo 12.5 days post coitum (dpc) (bottom right) within MNI-Display.
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As such, we combined a HPE-linked variant that doesn't cause HPE in its heterozygous form (the Zic2 kumba [Ku] allele) with low levels of prenatal ethanol (EtOH) exposure to study (via analysis of 碌CT scans) if this interaction leads to HPE phenotypes (see below).
ALT Study to determine if the Zic2 Ku allele interacts with EtOH exposure at 12 days post coitum (dpc)
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Holoprosencephaly (HPE) is a birth defect in which the developing forebrain fails to separate into left and right hemispheres. ~75% of HPE cases with normal chromosomes remain unsolved. Some unsolved cases may be caused by gene-environment interactions (see below).
