For anyone interested in SLE (systemic lupus erythematosus), this is a weird finding, maybe a paper worth investigating…..
Symptoms of systemic lupus erythematosus are diagnosed in leptin transgenic pigs
Junchen Chen, Weiqi Zeng, Weirong Pan, Cong Peng, Jianglin Zhang, Juan Su, Weihu Long, Heng Zhao, Xiaoxia Zuo, Xiaoyun Xie, Jing Wu, Ling Nie, Hong-ye Zhao, Hong-jiang Wei, Xiang Chen
Overexpression of leptin in transgenic pigs resulted in a phenotype bearing a remarkable resemblance to human systemic lupus erythromatosus (SLE), sharing multiple aspects of the disease.
Walt ––––– This is an excellent criticism. And it touches on a topic near-and-dear to my heart –– from years ago when my lab was involved in creating transgenic mouse lines. When a gene (derived from mouse, human, or other species) is ligated (i.e. cut from a circular plasmid; opened up; linearized) and then “inserted randomly” into the recipient mouse’s genome, the gene under investigation often forms tandem (head-to-tail) structures (concatamers) –– which can represent two, or five, or ten identical genes.
On the other side, the “insertion point” in the recipient genome depends on a lot of factors (including nearby homologous sequences that might attract the incoming cloned gene construct). Inserted foreign DNA –– into or near a protein-coding gene or a conserved regulatory region –– sometimes will affect the expression of these nearby genes. This is called “the neighborhood effect” and, for any study to be complete, this possibility should be ruled out. Or demonstrated to be the cause for the phenotype (trait), which in this case is “symptoms of systemic lupus erythematosus.” 🙂
COMMENTS: From my quick look at this, I don’t see that they identified where their construct became integrated into the pig genome. So is this an effect of over-producing leptin? Or is this an artifact of untargeted disruption of some other pig gene?