| First Author | Scandaglia M | Year | 2017 |
| Journal | Cell Rep | Volume | 21 |
| Issue | 1 | Pages | 47-59 |
| PubMed ID | 28978483 | Mgi Jnum | J:255232 |
| Mgi Id | MGI:6104037 | Doi | 10.1016/j.celrep.2017.09.014 |
| Citation | Scandaglia M, et al. (2017) Loss of Kdm5c Causes Spurious Transcription and Prevents the Fine-Tuning of Activity-Regulated Enhancers in Neurons. Cell Rep 21(1):47-59 |
| abstractText | During development, chromatin-modifying enzymes regulate both the timely establishment of cell-type-specific gene programs and the coordinated repression of alternative cell fates. To dissect the role of one such enzyme, the intellectual-disability-linked lysine demethylase 5C (Kdm5c), in the developing and adult brain, we conducted parallel behavioral, transcriptomic, and epigenomic studies in Kdm5c-null and forebrain-restricted inducible knockout mice. Together, genomic analyses and functional assays demonstrate that Kdm5c plays a critical role as a repressor responsible for the developmental silencing of germline genes during cellular differentiation and in fine-tuning activity-regulated enhancers during neuronal maturation. Although the importance of these functions declines after birth, Kdm5c retains an important genome surveillance role preventing the incorrect activation of non-neuronal and cryptic promoters in adult neurons. |
