adaptor protein complexes, AP-1, clathrin, trans-Golgi network, membrane traffic, zebrafish, gut
Adaptor Protein Complex 1/genetics; Adaptor Protein Complex 1/metabolism*; Adaptor Protein Complex mu Subunits/classification; Adaptor Protein Complex mu Subunits/genetics; Adaptor Protein Complex mu Subunits/metabolism*
Adaptor Protein Complex 1/genetics; Adaptor Protein Complex 1/metabolism*; Adaptor Protein Complex mu Subunits/classification; Adaptor Protein Complex mu Subunits/genetics; Adaptor Protein Complex mu Subunits/metabolism*; Amino Acid Sequence; Animals; Gene Expression Regulation, Developmental; Gene Knockdown Techniques; Genome; Humans; Mice; Molecular Sequence Data; Morphogenesis/physiology*; Phenotype; Phylogeny; Protein Isoforms/classification; Protein Isoforms/genetics; Protein Isoforms/metabolism*; Sequence Alignment; Tissue Distribution; Zebrafish/anatomy & histology; Zebrafish/embryology*; Zebrafish/genetics; Zebrafish/growth & development*; Zebrafish Proteins/classification; Zebrafish Proteins/genetics; Zebrafish Proteins/metabolism*
Zizioli, D., Forlanelli, E., Guarienti, M., Nicoli, S., Fanzani, A., Bresciani, R., Borsani, G., Preti, A., Cotelli, F., and Schu, P. (2010) Characterization of the AP-1 mu1A and mu1B adaptins in zebrafish (Danio rerio). Developmental dynamics : an official publication of the American Association of Anatomists. 239(9):2404-2412.
Protein transport between the trans-Golgi network and endosomes is mediated by transport vesicles formed by the adaptor-protein complex AP-1, consisting of the adaptins gamma1, beta1, mu1, sigma1. Mammalia express mu1A ubiquitously and isoform mu1B in polarized epithelia. Mouse gamma1 or mu1A 'knock out's revealed that AP-1 is indispensable for embryonic development. We isolated mu1A and mu1B from Danio rerio. Analysis of mu1A and mu1B expression revealed tissue-specific expression for either one during embryogenesis and in adult tissues in contrast to their expression in mammalia. mu1B transcript was detected in organs of endodermal derivation and "knock-down" experiments gave rise to embryos defective in formation of intestine, liver, and pronephric ducts. Development ceased at 7-8 dpf. mu1B is not expressed in murine liver, indicating loss of mu1B expression and establishment of alternative sorting mechanisms during mammalian development.