Autophagy, the highly conserved catabolic mechanism, employs the lysosome system to break down and recycle aged and damaged cellular components, such as macromolecules and organelles. It is a physiological adaptation strategy in response to stress and starvation, as well as an immune mechanism during infection. The processed isoform encoded by Map1lc3a (also called LC3) binds to autophagosomal membranes.
These mCherry-LC3 transgenic mice express mCherry-Map1lc3a (Red Fluorescent protein- microtubule-associated protein 1 light chain 3 alpha) fusion gene, under the control of the mouse Myh6 (myosin, heavy polypeptide 6, cardiac muscle, alpha) promoter. Transgene expression is detected in autophagosomes of myocardiocytes. Rapamycin administration to transgenic mice increases the number of fluorescently labeled autophagosomes in the myocardium. Coadministration of chloroquine with rapamycin further increases the number of autophagosomes. Monodansylcadaverine labeling co-localizes with mCherry fluorescence. The Donating Investigator reports that transgene expression level has been stable since the line was established. Mice that are homozygous for the targeted mutation are viable but express high levels of the transgene fusion protein, which may form protein aggregates and/or dysregulate autophagy. Hemizygotes are viable and fertile.

This mCherry-LC3 transgenic line expresses a mCherry-Map1lc3a, Red Fluorescent protein- microtubule-associated protein 1 light chain 3 alpha fusion gene under the direction of a mouse Myh6, myosin, heavy polypeptide 6, cardiac muscle, alpha, promoter. Applications exist in studies related to cardiac autophagy.

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