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. Author manuscript; available in PMC: 2010 Apr 5.
Published in final edited form as: DNA Repair (Amst). 2009 Feb 23;8(4):517–524. doi: 10.1016/j.dnarep.2009.01.010

Table 1.

Phenotypic comparisons of SUMO isopeptidases vs. STUbLs

ulp2Δ (Ulp1 mut) STUbLts References
SUMO pathway interaction Accumulation of SUMO chains Y (ulp2Δ) (S.c., S.p.) Y (S.c., S.p.) [11, 14, 15, 25, 92]
Growth defects suppressed by SUMO mutants defective for chain formation Y (ulp2Δ) (S.c.) N (S.c.) [16, 25]
Growth phenotype suppressed by deleting SUMO E3 ligase Y (ulp2Δ) (S.c.) N (S.c.)
Y (S.p.)
[11, 15, 25]
Growth phenotype suppressed by over-expressing SUMO E3 ligase Y (ulp2Δ2) (S.c.) n.d. [93]
UV sensitivity suppressed by ULP2 overexpression n.d./n.a. Y (S.p.) [14]
Synthetic lethal with STUbL Y (ulp1ΔN338) (S.c.) n.a. [27]
High copy suppressor of ulp1ts N (S.c.) Y (S.c.) [17]
DNA damage sensitivity HU Sensitivity Y (ulp2Δ, ulp1ts) (S.c.) Y (S.p., S.c.) [10, 11, 92, 94]
MMS sensitivity Y (ulp2Δ, ulp1ts) (S.c.) N (S.c.)
Y (S.p.)
[11, 28, 92]
UV sensitivity Y (ulp2Δ, ulp1ts) (S.c.) Y (S.c., S.p.) [11, 17, 92, 95]
CPT sensitivity n.d. N (S.c.)
Y (S.p.)
[11, 28]
Genomic instability Elevated DNA repair foci Y (ulp1ts, ulp1ΔN338) (S.c.) Y (S.c., S.p.) [11, 27, 28, 95, 96]
Elevated spontaneous GCR n.d. Y (mainly telomere addition) (S.c.) [28]
Elevated 2μm plasmid number Y (ulp1T490L, ulp1ΔES) (S.c.) Y (S.c.) [27, 97]
Elevated chromosome & centromeric plasmid loss Y (ulp2Δ2, ulp2Δ) (S.c.) n.d. [92, 93]
Hyper-recombination Y (ulp1ΔN338, ulp1I615N) (S.c.) Y (S.c.) [27, 95, 96]
Elevated mutation rate Y (ulp1I615N) (S.c.) Y (S.c.) [28, 95]
Telomeric and rDNA silencing defect Y and n.d. (ulp2Δ) (S.c.) Y (S.c.) [73]
Role in telomere maintenance Y (ulp1Δ160) Y (S.c.) [59, 98]
Meiotic defects Sporulation defect Y (ulp2Δ) (S.c.) Y (S.c.) [10, 92]
Cell cycle progression Growth reduced with G2/M arrest Y (ulp1ts, ulp1I615N, ulp1ΔES) (S.c.) Y (S.c., S.p.) [11, 95, 97, 99]
Checkpoint constitutively activated n.d. Y (S.c.) [28]
Impaired checkpoint recovery/adaptation Y (S.c.) n.d. [92, 94]
Key genetic interactions Suppressor of mot1ts Y (ulp1, ulp2) (S.c.) Y (S.c.) [15]
High-copy suppressor of Smc2-6 Y (ULP2) (S.c.) N (S.c.) [93]
High-copy suppressor of pds5-1 Y N [100]
Synthetic lethal with srs2Δ Y (ulp1I615N) (S.c.) N (S.c.) [95, 101]
Synthetic lethal with sgs1Δ/rqh1Δ N (S.c.) Y (S.c., S.p.) [10, 11]
Synthetic lethal with mus81Δ/eme1Δ N N (S.c.) Y (S.p.) [11, 28]
Synthetic lethal/sick with recombination mutants rad51/52/54/55/50Δ or mre11Δ Y (ulp1I615N) (S.c.) Y (S.p.: rad51/55Δ and n.d.; S.c.1) [11, 48, 95, 101]
Synthetic sick with sir2/4Δ Y (ulp2Δ) (S.c.) Y (S.c.) [73]
Other Microtubule destabilizing agent sensitivity Y (ulp2Δ (S.c.) Y (S.p.) [92] & our unpublished results
Aberrant mitotic spindles Y (ulp2Δ) (S.c.) n.d. [92]
Temperature sensitivity Y(ulp2Δ, ulp1I615N) (S.c.) n.d. [92, 95]
Localization Nuclear Y Nuclear (Ulp2) and Nuclear pores (Ulp1) (S.c.) Y (S.c., S.p.) Slx8 foci formation during S/G2 phase, colocalizing with PCNA and nucleolar protein Not1 (S.c.) [11, 27, 93, 102, 103]
1

Burgess et al. reported suppression of the nibbled growth phenotype in slx8Δ cells by deletion of homologous recombination enzymes Rad50, 52, 59 and Mre11 [27]. (S.c.), S. cerevisiae; (S.p.), S. pombe; n.a., not applicable; n.d., not done; Y, yes; N, no.