Figure 1.

HDAC3 Regulates Myelin Gene Transcription and Is Expressed in Adult Myelinating Schwann Cells

(A) Relative luciferase activity of the regulatory elements of the P0 gene (promoter plus enhancer; see STAR Methods for further details) in the absence (control) or presence (dbcAMP) of dbcAMP for 24 hr following the transfection of scrambled (Scr) or two independent siRNAs (siRNA1 and siRNA2) (n = 3, mean ± SEM).

(B) ChIP analysis to detect HDAC3 binding to the P0 promoter. SCs expressing a tamoxifen (TMX)-inducible Raf kinase construct (NSΔRafER cells) were cultured in the absence of presence of dbcAMP for 72 hr and then for a further 24 hr in the absence or presence (−/+) of TMX to induce the dedifferentiation of the cells (n = 3, mean ± SEM).

(C) Relative endogeneous P0 mRNA levels following transfection of scrambled (Scr) or two independent siRNAs (siRNA1 and siRNA2) in the absence (control) or presence (dbcAMP) of dbcAMP (n = 3, mean ± SEM).

(D) Representative confocal images of mouse sciatic nerve of postnatal P5, 6-week-old animals, and 6-week-old animals, 5 days following transection stained for HDAC3 or HDAC2 (green) as indicated with SCs labeled for S100 (red). Note that whereas HDAC2 expression in adulthood is at low levels in myelinating Schwann cells (mSCs) (arrowheads), it is re-induced upon injury (arrowheads). Conversely, nuclear HDAC3 expression is maintained in adult mSCs (arrowheads), whereas it decreases upon injury in myelinating-derived SCs (arrowheads). Other cell types express high levels of HDAC3 after injury (arrows).

^∗p < 0.05, ^∗∗p < 0.01, ^∗∗∗p < 0.001. See also Figure S1.