Fig. 3: C-terminal Nur1 phosphorylation disrupts the rDNA tethering complex.

a Co-immunoprecipitation of Nur1^6HA with ^GFPLrs4 in WT or cdc14-3 mutant cells. Cells were grown at the permissive temperature and shifted to 37 °C for 1 h. Dpm1 served as loading control. b Co-immunoprecipitation of Heh1^GFP with Csm1^TAP in nur1∆ cells. The strains were transformed with empty vector or plasmids bearing NUR1 or its phosphomimetic mutant (nur1Pmim) expressed from the endogenous promoter. Dpm1 served as loading control. c Quantification of rDNA recombination rates in WT or nur1∆ cells as measured by marker loss of an ADE2 marker inserted into rDNA. Cells have been transformed with empty vector or plasmids bearing NUR1 or nur1Pmim expressed from the endogenous promoter. The rate of marker loss is calculated as the ratio of half-sectored colonies (as indicated by the arrows) to the total number of colonies, excluding completely red colonies. Data are mean ± SEM of n independent biological replicates (n = 4 for WT and nur1∆; n = 3 for NUR1 and nur1Pmim), shown in log₂ scale relative to WT. Statistical analysis was performed using ANOVA, and letters denote significant differences with a Tukey’s post hoc test at P ≤ 0.05. Source data are provided as a Source Data file.