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. 2006 Nov 13;27(2):768–776. doi: 10.1128/MCB.01034-06

TABLE 1.

Hsc82 mutants used in this work

Mutation Location of mutation Growth phenotype of hsc82 hsp82 straina
Reference(s) (protein)
30°C 37°C
None ++++ ++++ 2
T22I ATPase 23 (Hsp82-T22I)
E33A ATPase 24, 25 (Hsp82-E33A)
D79N ATPase 24, 25 (Hsp82-D79N)
T101I ATPase 23 (Hsp82-T101I)
A107N ATPase ++++ +++ 29 (Hsp82-A107N)
W296A Middle ++ 20 (Hsp82-W300A)
G309S Middle ++++ 23 (Hsp82-G313S)
F325A Middle ++++ +++ This study
F345A Middle ++++ 20 (Hsp82-F349A)
N373A Middle ++++ ++ 20 (Hsp82-N377A)
R376A Middle 20 (Hsp82-R380A)
E377K Middle 23 (Hsp82-E381K)
Q380A Middle ++++ 20 (Hsp82-Q384A)
S481Y Middle ++++ 15 (Hsp82-S485Y)
L487S Middle ++++ 10; this study
T521I Middle ++++ 15 (Hsp82-T525I)
A583T C terminus ++++ 23 (Hsp82-A587T)
I588A M589A C terminus ++++ This study
L647S L648S C terminus ++ 40; this study
F660A C terminus ++++ ++++ This study
ΔMEEVD C terminus ++++ ++++ 16 (Hsp82-ΔMEEVD)
a

WT growth. Growth defects correspond to an approximate 10-fold (+++) and 100-fold (++) reduction in colony numbers observed upon serial dilation growth assays.