Expression of the fras1/frem gene family during zebrafish development and fin morphogenesis

Philippe Gautier, Cecilia Naranjo-Golborne, Martin S. Taylor, Ian J. Jackson, Ian Smyth

Research output: Contribution to journalArticlepeer-review


Mouse studies have highlighted the requirement of the extracellular matrix Fras and Frem proteins for embryonic epidermal adhesion. Mutations of the genes encoding some of these proteins underlie the blebs mouse mutants, whereas mutations in human FRAS1 and FREM2 cause Fraser syndrome, a congenital disorder characterized by embryonic blistering and renal defects. We have cloned the zebrafish homologues of these genes and characterized their evolutionary diversification and expression during development. The fish gene complement includes fras1, frem1a, frem1b, frem2a, frem2b, and frem3, which display complex overlapping and complementary expression patterns in developing tissues including the pharyngeal arches, hypochord, musculature, and otic vesicle. Expression during fin development delineates distinct populations of epidermal cells which have previously only been described at a morphological level. We detect relatively little gene expression in epidermis or pronephros, suggesting that the essential role of these proteins in mediating their development in humans and mice is recently evolved.
Original languageEnglish
Pages (from-to)3295-3304
Number of pages10
JournalDevelopmental Dynamics
Issue number11
Publication statusPublished - Nov 2008


  • Fras
  • Frem
  • Fraser Syndrome
  • caudal fin fold
  • cleft cell
  • ridge cell
  • basement membrane
  • extracellular matrix


Dive into the research topics of 'Expression of the fras1/frem gene family during zebrafish development and fin morphogenesis'. Together they form a unique fingerprint.

Cite this