RETRACTION: Visualization of lipid metabolism in the zebrafish intestine reveals a relationship between NPC1L1-mediated cholesterol uptake and dietary fatty acid
- Authors
- Walters, J.W., Anderson, J.L., Bittman, R., Pack, M., and Farber, S.A.
- ID
- ZDB-PUB-170301-13
- Date
- 2012
- Source
- Chemistry & Biology 19: 913-925 (Other)
- Registered Authors
- Anderson, Jennifer, Farber, Steven, Pack, Michael, Walters, James
- Keywords
- none
- MeSH Terms
- none
- PubMed
- 26640839 Full text @ Chem. Biol.
In our original Resource, we reported a regulatory link between NPC1L1-mediated cholesterol uptake and dietary fatty acid in zebrafish larvae. In the absence of dietary long-chain fatty acids (LCFA), larval enterocytes failed to internalize luminal BODIPY-cholesterol. We attributed this LCFA dependence to the cholesterol transport protein NPC1L1, as dietary LCFAs were shown to induce the translocation of transgenic human NPC1L1 from a perinuclear compartment to the intestinal brush border (supported by the data shown in Figure 5 of the Resource). When overexpressed, human NPC1L1 localized to the brush border, where it was able to mediate the internalization of BODIPY-cholesterol even in the absence of dietary LCFAs (Figure 5). We also reported that NPC1L1 directly mediates cholesterol uptake by larval enterocytes (shown in Figure 6 of the Resource). However, we recently discovered that the larval expression of the human NPC1L1 transgenic construct hsp70:HsNPC1L1-mCherry we reported was in fact that of hsp70:mCherryCAAX, which encodes an mCherry fluorophore modified with a prenylation motif. When employing a recloned hsp70:HsNPC1L1-mCherry vector, our experiments failed to replicate the LCFA-induced translocation of NPC1L1 to the intestinal brush border, indicating that the findings reported in Figures 5 and 6 are no longer valid.