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. 2006 Sep 27;103(41):15044–15049. doi: 10.1073/pnas.0607129103

Table 1.

Effect of NLS and PKA mutations on Maf1 function

Mutations Pol III repression* Glycerol 37°C Growth SGal-His ade2-1 color§ Location
−rap +rap
WT 28 ++++ N + C N
maf1Δ 112 ++ +++
6SA 26 ++++ N > C N
6SE 28 ++++ C > N N
6SAΔCtNLS 42 ++++ (+) + N > C N
6SEΔCtNLS 91 +++ +++ ++ C C > N
ΔNtNLS 35 ++++ C C > N
ΔNtCtNLS 101 +++ +++ ++ C C
ΔCtNLS 64 +++ +++ ++ C N

*Residual transcription after 90 min of rapamycin treatment expressed as a percentage of the untreated WT level (from Fig. 4). Data is representative of multiple experiments that generate an SD of 3–8%. An examination of unstressed transcription for many Maf1 mutants found no significant changes compared with WT or the maf1Δ strain.

Glycerol phenotype: + represents each 10-fold dilution at which cells grew on SGly-Trp at 37°C.

tgm-silencing phenotype: + represents each 10-fold dilution at which cells grew on SGal-Ura-Trp-His at 30°C.

§Antisuppression: −, cream color; +, light pink; ++, pink; +++, red on SGal-Ura-Trp media.

Localization: Cytoplasmic (C) and nuclear signal (N) after 60 mins with (+) or without (−) rapamycin treatment. Qualitative changes in distribution are expressed relative to WT.