Fig. 7
From: Distinct adaptive mechanisms drive recovery from aneuploidy caused by loss of the Ulp2 SUMO protease
Short-term and long-term adaptive mechanisms caused by loss of Ulp2. Proposed model showing that yeast have short-term and long-term adaptive mechanisms that allow survival of a dysregulated SUMO system caused by loss of Ulp2. Loss of Ulp2 leads to accumulation of polySUMO-conjugated substrates, enhanced expression of genes encoding ribosomal proteins and reduced cell fitness (irregular cell outline). Duplication of ChrI and ChrXII provides a transient adaptive solution to amplify three protein-coding genes, CCR4, CLN3, and CCW12, and several snoRNA genes, SNR61, SNR55, and SNR57. Following evolution over many cell generations, disomies of both ChrI and XII are eliminated, concomitant with mutations in UBC9, UBA2, or AOS1. These SUMO-ligating enzyme mutations reduce SUMO conjugation and suppress the growth defects of ulp2Δ cells. Upregulation of numerous snoRNA genes appears to promote ribosome biogenesis, which is normally tightly regulated by the SUMO system
