| First Author | Turunen HT | Year | 2012 |
| Journal | Reproduction | Volume | 144 |
| Issue | 4 | Pages | 495-503 |
| PubMed ID | 22869780 | Mgi Jnum | J:191587 |
| Mgi Id | MGI:5462138 | Doi | 10.1530/REP-11-0444 |
| Citation | Turunen HT, et al. (2012) Loss of Bmyc results in increased apoptosis associated with upregulation of Myc expression in juvenile murine testis. Reproduction 144(4):495-503 |
| abstractText | Bmyc is a member of the Myc family of transcriptional regulators in the mouse and the rat. It is predominantly expressed in hormonally controlled tissues, with highest level of expression in the epididymis. The BMYC protein has been shown to function as a transcription factor in vitro and to inhibit MYC. To study the significance of BMYC in vivo, a Bmyc knockout (KO) mouse model was generated by homologous recombination. The KO mice were viable and fertile and did not display gross morphological or histological changes compared to the WT mice. However, the testes and the epididymides of the KO mice were smaller than those of the WT mice. Correspondingly, a tendency for a lower sperm concentration in the cauda epididymides of the KO mice was detected. The testosterone produced/testis was significantly reduced, and accordingly, the LH levels were increased in the KO mice. Also, the expression levels of Myc and several of its target genes were elevated in the testes of prepubertal KO mice, whereas no differences in gene expression levels were detected in adult mice. Associated with the increased Myc expression, more apoptotic spermatogenic cells were detected in the seminiferous tubules of the KO mice. In conclusion, our data suggest that Bmyc is a regulator of Myc in vivo and that overexpression of Myc in the developing testis leads to increased apoptosis of spermatogenic cells. |
