Allele/Variant

CriptTn(sb-rtTA)2427.SB1Ove

Species
Mus musculus
Symbol
CriptTn(sb-rtTA)2427.SB1Ove
Category
allele
Allele of gene
Cript
Transgenic Constructs
None
Synonyms
  • OVE#2427-SB1
  • OVE2427-SB1
Description
A lentiviral transgenic approach was used to generate these mice. The SB-sa-IRES-rtTA-pA-SB-Tyro-WPRE-FUGW lentiposon transgene (LV2223) was designed with a Sleeping Beauty (SB) transposon (containing a slice-acceptor::IRES::rtTA::polyA gene trap), a mouse tyrosinase minigene (Tyro), and a woodchuck hepatitis virus post-transcriptional regulatory element (WPRE) in the FUGW self-inactivating HIV-based lentiviral vector backbone. The SB transposon and Tyro minigene replaced the ubiquitin-c promoter and EGFP sequences originally found in the FUGW lentiviral vector. The 1200 bp SB transposon used in this transgene has an inverted repeat/direct repeat sequence (IR/DR; the SB transposon recognition site), an adenovirus splice acceptor, a stop sequence (3xSTOP), an internal ribosome entry site (IRES; from human X-chromosome-linked inhibitor of apoptosis (XIAP)), a sequence encoding an optimized form of reverse tetracycline controlled transactivator (rtTA2S; with stop codon), a human growth hormone polyA sequence, and a second IR/DR sequence. The IR/DR sequences are outward-facing (pointed away from the sa-IRES-rtTA-pA). The Tyro minigene is composed of the mouse Tyr enhancer region (623 bp), promoter region (657 bp), and 1566 bp cDNA sequence (including the stop codon); all in sense orientation relative to the FUGW backbone. There is no polyA site between the Tyro minigene and WPRE sequence. The WPRE sequence functions to enhance the mRNA transcript stability. The splice-acceptor::IRES::rtTA::polyA transposon is mobilized by testes-specific expression of the SB transposase. In line OVE2427-SB1, the transposon integrated into intron 3 [NCBI37/mm9; R3-87,432,586(+)] in the sense orientation.
Additional Information
Literature

Transgenic Constructs

No data available

Genomic Variant Information

No data available

Variant Molecular Consequences

Phenotypes

Disease Associations