our data raise the possibility that TBC1D15 localized to mitochondria in neurons treated with LLOMe
Is it possible that under these conditions, neurons transfer damaged mitochondria and/or other cellular material to astrocytes? It could be interesting to do neuron-specific labeling prior to co-culturing to track mitochondria.
Thus, the lack of robust ESCRT recruitment is not simply attributed to insufficient protein expression in neurons.
I’m curious if you looked at CHMP2B levels by western blot in addition to immunofluorescence. Is it possible that neurons express alternate mRNA isoforms and/or proteoforms (e.g. truncated CHMP2B) that disrupt canonical ESCRT recruitment?