FOXO3A binds its cognate sequences within the Prx III promoter.
A and B, binding of FOXO3A to Prx III promoter in
vitro. Representative EMSA demonstrating that a 50 bp double-stranded
oligonucleotide encompassing both putative FOXO3A binding sites (sequence
WT-FDBE in panel A) exhibits an electromobility shift when incubated
with nuclear extracts from human cardiac fibroblasts (see under
“Experimental Procedures” for EMSA). C, binding of FOXO3A
to Prx III is specific to –267 and –259 sites. To show specificity
for binding, the FOXO3A binding sites within Prx III promoter were replaced
with random sequences (sequences M01, M02, and M03 as indicated in A)
and used in EMSA performed on HEK-293 cells nuclear extracts. D,
endogenous FOXO3A binds to Prx III promoter. To test whether endogenous FOXO3A
is required, HEK-293 cells were transfected (as described under
“Experimental Procedures”) with siCon or siFOXO3A, and 96 h later
cells were harvested and processed, and the corresponding nuclear extracts (10
and 20 μg, respectively) were employed in mobility shift assay
(D). Each blot is representative of three similar experiments.
E, binding of FOXO3A to the Prx III promoter is impaired by IGF-1
treatment. HEK-293 cells were treated with IGF-1 (40 ng/ml medium) for 8 h and
the corresponding nuclear extracts employed in EMSA as described under
“Experimental Procedures.” Shown are increasing amounts of nuclear
lysates. F, FOXO3A binds in vivo to Prx III promoter.
Chromatin immunoprecipitation assays were performed in HEK-293 cells as
described under “Experimental Procedures.” HEK-293 cells were
transfected with control or FOXO3A plasmids and harvested for ChIP assay after
48 h. FOXO3A was immunoprecipitated either with an antibody against FLAG from
cells transfected with pcDNA3-FLAG-FOXO3 (upper panel) or with FOXO3A
antibody (middle and lower panels). This is representative
of three similar experiments. The lower panel is identical with
middle panel; however the image was inverted to enhance the intensity
of FOXO3A PCR band.