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Fig. 1. The Sox10 mutations. (A) Schematic of the aa1 and 
K2
mutations. (B) Subcellular localization of wild-type Sox10 and the
K2 mutant in transiently transfected Neuro2a cells was determined by
immunocytochemistry with a Sox10-specific antibody. Nuclei were counterstained
by DAPI. (C) Stability of wild-type Sox10 (blue circle) and the
K2 mutant (red square) were compared in transiently transfected Neuro2a
cells cultured for various times in the presence of cycloheximide as
indicated. Extracts were prepared and Sox10 proteins detected by western blot.
Relative amounts were quantified from band intensities with the amount in
untreated cells set to 100%. (D) The transactivation capacity of the
K2 mutant was analyzed in luciferase reporter gene assays. Transient
transfections were performed in Neuro2a cells with luciferase reporters under
the control of the Mpz promoter (positions -915 to +48), the
Dct promoter (positions -3240 to +443) and the Mbp promoter
(positions -656 to +31). Luciferase reporters were transfected either alone or
in combination with wild-type Sox10, the K2 or the Q377X mutant. Data
from three independent experiments each performed in duplicate are presented
as fold inductions±s.d., with the activity for each luciferase reporter
in the absence of co-transfected Sox10 set to 1.
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