6533b873fe1ef96bd12d4472
RESEARCH PRODUCT
Creating a conditional mutation of Wnt-1 by antisense transgenesis provides evidence that Wnt-1 is not essential for spermatogenesis.
Judy GrimesRobert P. EricksonLi Wen Laisubject
MaleTransgeneRecombinant Fusion ProteinsMolecular Sequence DataMice Inbred StrainsMice TransgenicWnt1 ProteinBiologyMiceProto-Oncogene ProteinsGene expressionTestisGeneticsAnimalsRNA AntisenseRNA MessengerPromoter Regions GeneticSpermatogenesisRegulation of gene expressionMice KnockoutMessenger RNABase SequenceWnt signaling pathwayRNACell BiologyZebrafish ProteinsMolecular biologyAntisense RNATransgenesisMice Inbred C57BLWnt ProteinsPhosphoglycerate KinaseFertilityGene Expression RegulationOrgan SpecificityDevelopmental Biologydescription
We have used mice transgenic for an antisense construct for Wnt-1 to study the role of this gene in post-meiotic sperm development. The human PGK-2 promoter provided levels of Wnt-1 antisense mRNA in testes in 5 transgenic lines greatly in excess of Wnt-1 mRNA concentrations, and Wnt-1 mRNA levels were greatly decreased in the lines, by 98% in three of them. There was a general correlation between copy number of the insert, levels of antisense RNA, and decreases in mRNA. There was little effect of the antisense transgene on fertility or testicular histology suggesting that normal levels of Wnt-1 transcript are not essential for spermatogenesis.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 1993-01-01 | Developmental genetics |