| Literature DB >> 22302994 |
Shuoshuo Wang1, Heiko Meyer, Amanda Ochoa-Espinosa, Ulf Buchwald, Susanne Onel, Benjamin Altenhein, Jürgen J Heinisch, Markus Affolter, Achim Paululat.
Abstract
Here we report on the generation and in vivo analysis of a series of loss-of-function mutants for the Drosophila ArfGEF, Gartenzwerg. The Drosophila gene gartenzwerg (garz) encodes the orthologue of mammalian GBF1. garz is expressed ubiquitously in embryos with substantially higher abundance in cells forming diverse tubular structures such as salivary glands, trachea, proventriculus or hindgut. In the absence of functional Garz protein, the integrity of the Golgi complex is impaired. As a result, both vesicle transport of cargo proteins and directed apical membrane delivery are severely disrupted. Dysfunction of the Arf1-COPI machinery caused by a loss of Garz leads to perturbations in establishing a polarized epithelial architecture of tubular organs. Furthermore, insufficient apical transport of proteins and other membrane components causes incomplete luminal diameter expansion and deficiencies in extracellular matrix assembly. The fact that homologues of Garz are present in every annotated metazoan genome indicates that secretion processes mediated by the GBF-type ArfGEFs play a universal role in animal development.Entities:
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Year: 2012 PMID: 22302994 DOI: 10.1242/jcs.092551
Source DB: PubMed Journal: J Cell Sci ISSN: 0021-9533 Impact factor: 5.285