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Dyrk1a is required for craniofacial development in . | LitMetric

AI Article Synopsis

  • * Researchers found that DYRK1A is expressed in the developing head, particularly in the branchial arches, and reduced function caused orofacial malformations like slanted eyes and altered mouth shape.
  • * The study revealed that these malformations are linked to misexpression of crucial craniofacial regulators, which contribute to smaller neural crest domains, ultimately leading to increased cell death and decreased cell proliferation in embryos lacking DYRK1A, offering insights into related human birth defects.

Article Abstract

Loss of function mutations in the dual specificity tyrosine-phosphorylation-regulated kinase 1A (DYRK1A) gene are associated with craniofacial malformations in humans. Here we characterized the effects of deficient DYRK1A in craniofacial development using a developmental model, . mRNA and protein was expressed throughout the developing head and was enriched in the branchial arches which contribute to the face and jaw. Consistently, reduced Dyrk1a function, using morpholinos and pharmacological inhibitors, resulted in orofacial malformations including hypotelorism, altered mouth shape, slanted eyes, and narrower face accompanied by smaller jaw cartilage and muscle. Inhibition of Dyrk1a function resulted in misexpression of key craniofacial regulators including transcription factors and members of the retinoic acid signaling pathway. Two such regulators, and are required for neural crest development and their decreased expression corresponds with smaller neural crest domains within the branchial arches. Finally, we determined that the smaller size of the faces, jaw elements and neural crest domains in embryos deficient in Dyrk1a could be explained by increased cell death and decreased proliferation. This study is the first to provide insight into why craniofacial birth defects might arise in humans with DYRK1A mutations.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10802584PMC
http://dx.doi.org/10.1101/2024.01.13.575394DOI Listing

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