This work was supported by P42ES013660 Superfund Basic Research Program (NIEHS).
The Sycp1-Cre Transgenic Mouse and Male Germ Cell Inhibition of NF-κB
Article first published online: 2 JAN 2013
2006 American Society of Andrology
Journal of Andrology
Volume 27, Issue 6, pages 729–733, November-December 2006
How to Cite
Rasoulpour, R. J. and Boekelheide, K. (2006), The Sycp1-Cre Transgenic Mouse and Male Germ Cell Inhibition of NF-κB. Journal of Andrology, 27: 729–733. doi: 10.2164/jandrol.106.000950
- Issue published online: 2 JAN 2013
- Article first published online: 2 JAN 2013
- Received for Publication January 2, 2006; accepted for Publication June 12, 2006
ABSTRACT: Successful spermatogenesis requires autocrine, paracrine, and endocrine signaling throughout the testes. The seminiferous tubules contain somatic Sertoli cells in tight association with numerous germ cell populations. To address the in vivo biologic roles of genes during spermatogenesis, spatial and temporal restriction of gene inhibition is a useful approach. To this end, Cre-LoxP technology can produce cell-specific knockdowns of genes, allowing dissection of the underlying processes that manifest as functional deficits in whole animals. Here we report the use of the synaptonemal complex protein 1-Cre (Sycp1-Cre) to create germ cell—specific nuclear factor κB knockdown mice through floxed IκB kinaseβ. We observed a LoxP gene recombination rate of approximately 43% using Sycp1-Cre, as determined by offspring genotype. In addition, we confirm that, with multiple generations, the LoxP sites fail to recombine due to epigenetic modification. This detailed examination of the meiotic Sycp1-Cre recombinase activity highlights the obstacles to germ cell—specific gene inhibition through Cre/LoxP technology in the testis. Taken together, these data demonstrate a need for early spermatogonial expression of Cre recombinase, as an alternative to meiotic Cre expression, for the creation of germ cell—specific knockout mice.