APOL1 harbors C–terminal sequence variants (G1 and G2), which account for much of the
increased risk for kidney disease in sub–Saharan African ancestry populations. Expression
of the risk variants has also been shown to cause injury to podocytes and other cell types,
but the underlying mechanisms are not understood. We used Drosophila melanogaster and
Saccharomyces cerevisiae to help clarify these mechanisms. Ubiquitous expression of the
human APOL1 G1 and G2 disease risk alleles caused near-complete lethality in D …