Proteotoxicity caused by perturbed protein complexes underlies hybrid incompatibility in yeast

Lastly, we confirmed that the proteotoxic stress noticed within the alternative line was not on account of an ineffective proteasome system. Proteasomal exercise assays confirmed that the exercise of endogenous 26S proteasomes in 16L cells didn’t differ from that of Sc cells (Supplementary Fig. 8d). Collectively, our outcomes show that destabilized protein complexes in hybrid cells typically enhance the burden of proteasomes, a key regulator of proteostasis. Relying on the quantity and abundance of chimeric complexes, that overburdening leads to differential ranges of hybrid incompatibility.