Lindsey Barske

Abstract Heterozygous variants in the gene encoding the SOX10 transcription factor cause congenital syndromes affecting pigmentation, digestion, hearing, and neural function. Most of these symptoms are attributable to failed differentiation and loss of neural crest cells. Extensive research on mouse and zebrafish models has confirmed that Sox10 is essential for most non-skeletal crest derivatives, but seemingly dispensable for skeletal development.

1 Introduction The craniofacial skeletal framework constitutes a pivotal element in vertebrate morphogenesis, serving indispensable functions in the encapsulation and protection of the brain, as well as facilitating vital processes such as respiration, alimentary intake, and communicative functions.

• None Scleraxis genes are required for normal musculoskeletal development and for rib growth and mineralization in zebrafish. : • None FGF10 and Sox9 are essential for the establishment of distal progenitor cells during mouse salivary gland development. : • None Mutations in the gene encoding fibroblast growth factor 10 are associated with aplasia of lacrimal and salivary glands. : • None Generation of transgenic tendon reporters, ScxGFP and ScxAP, using regulatory elements of the scleraxis gene.