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. 2017 May 3;206(2):811–828. doi: 10.1534/genetics.116.197590

Table 3. ER stress, sphingolipid, and chromatin anchoring mutations in rad9∆ background.

Genotype Unstable Chr. (×10−5) Allelic rec. (×10−5) Chr. loss (×10−4)
Median (Q1, Q3) Fold stabil. Median (Q1, Q3) Fold stabil. Median (Q1, Q3) Fold stabil.
rad9 57 (40, 71) 1 6.0 (2.8, 8.2) 1 22 (16, 39) 1
rad9erv25 26 (23, 37) 2.3* 4.2 (3.1, 5.4) 1.5 12 (7.5, 23) 1.8*
rad9scj1 28 (22, 36) 2.0* 3.7 (2.9, 5.3) 1.6* 8.5 (7.1, 11) 2.6*
rad9isc1 34 (24, 39) 1.7* 4.0 (2.0, 5.0) 1.5* 14 (11, 27) 1.6*
rad9scs7 77 (51, 154) 0.74 8.6 (5.9, 11) 0.70 66 (33, 120) 0.33*
rad9sur2 45 (39, 53) 1.3 4.5 (3.0, 6.2) 1.3 15 (11, 27) 1.5
rad9esc1 96 (78, 120) 0.59* 5.3 (2.9, 7.7) 1.1 34 (24, 46) 0.65
rad9esc1yku80 75 (61, 100) 0.76* 4.1 (3.1, 5.7) 1.5 29 (15, 63) 0.76

Instability frequencies and genome fold stabilization in mutant protein folding/transport, sphingolipid, and chromatin anchoring in rad9Δ background normalized to rad9Δ. Cells with a light gray background indicate genome fold stabilization increase; cells with a white background indicate decreased fold stabilization (<1.0 = increased instability) or no change in stabilization (=1.0). Statistically significant appears in boldface type. Kruskal–Wallis test, * P < 0.01.