| First Author | Chen Y | Year | 2011 |
| Journal | Nat Neurosci | Volume | 14 |
| Issue | 4 | Pages | 437-41 |
| PubMed ID | 21423191 | Mgi Jnum | J:172297 |
| Mgi Id | MGI:5006889 | Doi | 10.1038/nn.2780 |
| Citation | Chen Y, et al. (2011) HDAC-mediated deacetylation of NF-kappaB is critical for Schwann cell myelination. Nat Neurosci 14(4):437-41 |
| abstractText | Schwann cell myelination is tightly regulated by timely expression of key transcriptional regulators that respond to specific environmental cues, but the molecular mechanisms underlying such a process are poorly understood. We found that the acetylation state of NF-kappaB, which is regulated by histone deacetylases (HDACs) 1 and 2, is critical for orchestrating the myelination program. Mice lacking both HDACs 1 and 2 (HDAC1/2) exhibited severe myelin deficiency with Schwann cell development arrested at the immature stage. NF-kappaB p65 became heavily acetylated in HDAC1/2 mutants, inhibiting the expression of positive regulators of myelination and inducing the expression of differentiation inhibitors. We observed that the NF-kappaB protein complex switched from associating with p300 to associating with HDAC1/2 as Schwann cells differentiated. NF-kappaB and HDAC1/2 acted in a coordinated fashion to regulate the transcriptionally linked chromatin state for Schwann cell myelination. Thus, our results reveal an HDAC-mediated developmental switch for controlling myelination in the peripheral nervous system. |
