RGD Reference Report - mu1A-adaptin-deficient mice: lethality, loss of AP-1 binding and rerouting of mannose 6-phosphate receptors. - Rat Genome Database

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mu1A-adaptin-deficient mice: lethality, loss of AP-1 binding and rerouting of mannose 6-phosphate receptors.

Authors: Meyer, C  Zizioli, D  Lausmann, S  Eskelinen, EL  Hamann, J  Saftig, P  Von Figura, K  Schu, P 
Citation: Meyer C, etal., EMBO J. 2000 May 15;19(10):2193-203.
RGD ID: 1578385
Pubmed: PMID:10811610   (View Abstract at PubMed)
PMCID: PMC384363   (View Article at PubMed Central)
DOI: DOI:10.1093/emboj/19.10.2193   (Journal Full-text)

The heterotetrameric AP-1 complex is involved in the formation of clathrin-coated vesicles at the trans-Golgi network (TGN) and interacts with sorting signals in the cytoplasmic tails of cargo molecules. Targeted disruption of the mouse mu1A-adaptin gene causes embryonic lethality at day 13.5. In cells deficient in micro1A-adaptin the remaining AP-1 adaptins do not bind to the TGN. Polarized epithelial cells are the only cells of micro1A-adaptin-deficient embryos that show gamma-adaptin binding to membranes, indicating the formation of an epithelial specific AP-1B complex and demonstrating the absence of additional mu1A homologs. Mannose 6-phosphate receptors are cargo molecules that exit the TGN via AP-1-clathrin-coated vesicles. The steady-state distribution of the mannose 6-phosphate receptors MPR46 and MPR300 in mu1A-deficient cells is shifted to endosomes at the expense of the TGN. MPR46 fails to recycle back from the endosome to the TGN, indicating that AP-1 is required for retrograde endosome to TGN transport of the receptor.

Objects referenced in this article
Gene Ap1m1 adaptor related protein complex 1 subunit mu 1 Rattus norvegicus

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