Comparison of monkey and pig cells indicates the primate-specific expression of PINK1 and phosphorylation

PINK1 is believed to be a mitochondrial kinase that phosphorylates Parkin and other proteins, playing a crucial role in mitophagy and protecting against neurodegeneration. Mutations in PINK1 and Parkin lead to loss of function and early onset of Parkinson's disease. However, there is a lack of strong in vivo evidence in rodent models to support the theory that loss of PINK1 affects mitophagy and induces neurodegeneration. Additionally, PINK1 knockout pigs have not been reported to exhibit neurodegeneration. Our recent work on non-human primates demonstrates that PINK1 is selectively expressed in primate brains, but not in rodent brains. To extend this finding to other species, such as pigs, we used multiple antibodies to examine the expression of PINK1 in pig tissues. Compared to monkey tissues, we were unable to obtain convincing data showing detectable PINK1 protein expression in pig tissues. Knocking down PINK1 in cultured pig cells did not result in altered phosphorylation of Parkin and BAD, as observed in cultured monkey cells. A comparison of monkey and pig striatum revealed that there were more PINK1-phosphorylated substrates in the monkey brain. Consistently, knocking out PINK1 in pigs did not lead to obvious changes in the phosphorylation of Parkin and BAD. These findings provide new evidence that PINK1 expression is specific to primates and underscores the importance of using non-human primates to investigate the function of PINK1 and the pathology related to PINK1 deficiency.