SUV39H1 CRISPR Activation Plasmid (m): sc-423224-ACT

Mouse Suv39h1 encodes SUV39H1, a SET domain histone methyltransferase that catalyzes H3K9 trimethylation to promote heterochromatin formation and transcriptional repression. SUV39H1 cooperates with HP1 proteins and DNA methylation machinery to stabilize epigenetic silencing at pericentromeric repeats, regulate genome integrity, and ensure proper chromosome segregation. Through control of chromatin compaction, SUV39H1 influences cell cycle progression, DNA damage responses, and lineage-specific gene programs. Dysregulated SUV39H1 activity and altered H3K9me3 landscapes have been linked to aberrant transcriptional states observed in cancer biology, senescence, and neurological disease models, making Suv39h1 a common target for epigenetic and chromatin research.

SUV39H1 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Suv39h1 expression without altering the underlying DNA sequence.

SUV39H1 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Suv39h1 locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.

Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the Suv39h1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SUV39H1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Suv39h1 locus and enabling the study of SUV39H1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SUV39H1 pathway restoration in tumor cells with silenced or reduced Suv39h1 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.