The clathrin adaptor AP-1A mediates basolateral polarity.

The clathrin adaptor AP-1A mediates basolateral polarity.
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DOI:
10.1016/j.devcel.2012.02.004
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发表时间:
2012-04-17
期刊:
影响因子:
11.8
通讯作者:
Rodriguez-Boulan, Enrique
Rodriguez-Boulan, Enrique
中科院分区:
生物学1区
文献类型:
--
作者:
Gravotta, Diego;Carvajal-Gonzalez, Jose Maria;Mattera, Rafael;Deborde, Sylvie;Banfelder, Jason R.;Bonifacino, Juan S.;Rodriguez-Boulan, Enrique

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Clathrin and the epithelial-specific clathrin adaptor AP-1B mediate basolateral trafficking in epithelia. However, several epithelia lack AP-1B and mice knocked-out for AP-1B are viable, suggesting the existence of additional mechanisms that control basolateral polarity. Here, we demonstrate a distinct role of the ubiquitous clathrin adaptor AP-1A in basolateral protein sorting. Knock-down of AP-1A causes missorting of basolateral proteins in MDCK cells but only after knock-down of AP-1B, suggesting that AP-1B can compensate for lack of AP-1A. AP-1A localizes predominantly to the TGN and its knock-down promotes spillover of basolateral proteins into common recycling endosomes, the site of function of AP-1B, suggesting complementary roles of both adaptors in basolateral sorting. Yeast two-hybrid assays detect interactions between the basolateral signal of TfR and the medium subunits of both AP-1A and AP-1B. The basolateral sorting function of AP-1A reported here establishes AP-1 as a major regulator of epithelial polarity.
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