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These centers instruct the surrounding cells to adopt a positional fate and to form the patterned structures of the phylotypic embryo. Abnormalities in these processes have devastating consequences for the individual, as exemplified by holoprosencephaly in which anterior midline development fails, leading to structural defects of the brain and\/or face. In the 25\u2009years since the first association between human holoprosencephaly and the sonic hedgehog gene, a combination of human and animal genetic studies have enhanced our understanding of the genetic and embryonic causation of this congenital defect. Comparative biology has extended the holoprosencephaly network via the inclusion of gene mutations from multiple signaling pathways known to be required for anterior midline formation. It has also clarified aspects of holoprosencephaly causation, showing that it arises when a deleterious variant is present within a permissive genome, and that environmental factors, as well as embryonic stochasticity, influence the phenotypic outcome of the variant. More than two decades of research can now be distilled into a framework of embryonic and genetic causation. This framework means we are poised to move beyond our current understanding of variants in signaling pathway molecules. The challenges now at the forefront of holoprosencephaly research include deciphering how the mutation of genes involved in basic cell processes can also cause holoprosencephaly, determining the important constituents of the holoprosencephaly permissive genome, and identifying environmental compounds that promote holoprosencephaly.<\/jats:p><jats:p>This article is categorized under:<jats:list list-type=\"simple\">\n<jats:list-item><jats:p>Congenital Diseases &gt; Stem Cells and Development<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Congenital Diseases &gt; Genetics\/Genomics\/Epigenetics<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Congenital Diseases &gt; Molecular and Cellular Physiology<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Congenital Diseases &gt; Environmental Factors<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p>","DOI":"10.1002\/wsbm.1552","type":"journal-article","created":{"date-parts":[[2022,2,9]],"date-time":"2022-02-09T07:38:22Z","timestamp":1644392302000},"source":"Crossref","is-referenced-by-count":9,"title":["Patterning of the antero\u2010ventral mammalian brain: Lessons from holoprosencephaly comparative biology in man and mouse"],"prefix":"10.1002","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0531-5231","authenticated-orcid":false,"given":"Kristen S.","family":"Barratt","sequence":"first","affiliation":[{"name":"John Curtin School of Medical Research The Australian National University  Canberra Australian Capital Territory Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kyle A.","family":"Drover","sequence":"additional","affiliation":[{"name":"John Curtin School of Medical Research The Australian National University  Canberra Australian Capital Territory Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0188-6785","authenticated-orcid":false,"given":"Zoe M.","family":"Thomas","sequence":"additional","affiliation":[{"name":"John Curtin School of Medical Research The Australian National University  Canberra Australian Capital Territory Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6213-7323","authenticated-orcid":false,"given":"Ruth M.","family":"Arkell","sequence":"additional","affiliation":[{"name":"John Curtin School of Medical Research The Australian National University  Canberra Australian Capital Territory Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2022,2,8]]},"reference":[{"key":"e_1_2_11_2_1","unstructured":"Diabetes What is diabetes?\u2014Australian Institute of Health and Welfare. 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