Rhodopsin targeted transcriptional silencing by DNA-binding.
Salvatore BottaElena MarroccoNicola de PriscoFabiola CurionMario RendaMartina SofiaMariangela LupoAnnamaria CarissimoMaria Laura BacciCarlo GesualdoSettimio RossiFrancesca SimonelliEnrico Maria SuracePublished in: eLife (2016)
Transcription factors (TFs) operate by the combined activity of their DNA-binding domains (DBDs) and effector domains (EDs) enabling the coordination of gene expression on a genomic scale. Here we show that in vivo delivery of an engineered DNA-binding protein uncoupled from the repressor domain can produce efficient and gene-specific transcriptional silencing. To interfere with RHODOPSIN (RHO) gain-of-function mutations we engineered the ZF6-DNA-binding protein (ZF6-DB) that targets 20 base pairs (bp) of a RHOcis-regulatory element (CRE) and demonstrate Rho specific transcriptional silencing upon adeno-associated viral (AAV) vector-mediated expression in photoreceptors. The data show that the 20 bp-long genomic DNA sequence is necessary for RHO expression and that photoreceptor delivery of the corresponding cognate synthetic trans-acting factor ZF6-DB without the intrinsic transcriptional repression properties of the canonical ED blocks Rho expression with negligible genome-wide transcript perturbations. The data support DNA-binding-mediated silencing as a novel mode to treat gain-of-function mutations.
Keyphrases
- dna binding
- transcription factor
- binding protein
- gene expression
- poor prognosis
- genome wide
- circulating tumor
- genome wide identification
- dna methylation
- copy number
- protein kinase
- single molecule
- cell free
- emergency department
- smooth muscle
- heat shock
- electronic health record
- sars cov
- big data
- gene therapy
- oxidative stress
- dendritic cells
- drug delivery
- circulating tumor cells
- heat stress