Generation of transgenic zebrafish with liver-specific expression of EGFP-Lc3: A new in vivo model for investigation of liver autophagy
- Authors
- Cui, J., Sim, T.H., Gong, Z., and Shen, H.M.
- ID
- ZDB-PUB-120516-7
- Date
- 2012
- Source
- Biochemical and Biophysical Research Communications 422(2): 268-273 (Journal)
- Registered Authors
- Gong, Zhiyuan
- Keywords
- zebrafish, autophagy, liver, Lc3, Torin1, mTOR
- MeSH Terms
-
- Naphthyridines/pharmacology
- Chloroquine/pharmacology
- Microtubule-Associated Proteins/biosynthesis
- Microtubule-Associated Proteins/genetics
- Molecular Sequence Data
- Mice
- Up-Regulation
- Green Fluorescent Proteins/biosynthesis
- Green Fluorescent Proteins/genetics
- Animals
- Amino Acid Sequence
- Liver/cytology*
- Liver/metabolism
- Liver/physiology
- Animals, Genetically Modified*
- Zebrafish/genetics*
- Models, Animal
- Autophagy/drug effects
- Autophagy/genetics*
- PubMed
- 22580284 Full text @ Biochem. Biophys. Res. Commun.
Transgenic expression of GFP-Lc3 is a useful tool for an in vivo model to monitor the formation of autophagosomes during the autophagy process. So far, two transgenic animals (mice and zebrafish) with expression of GFP-Lc3 have been reported. Liver is one of the most important organs for autophagy research. Here, we generated a transgenic zebrafish line with liver-specific EGFP-Lc3 expression. By exposing transgenic larvae to the autophagy inducer, Torin1, we observed a substantial increase in the number of EGFP-Lc3 puncta in the liver as well as the increase of Lc3-II protein. Notably, addition of a chloroquine (CQ) led to further increase of EGFP-Lc3 puncta in liver cells due to the blockage of lysosomal function and degradation stage of autophagy. Thus, the newly established transgenic line will be a useful in vivo model to investigate liver autophagy, and, in particular, the involvement of autophagy in basic biology and diseases in the liver.