| First Author | Biellmann F | Year | 2008 |
| Journal | Mol Reprod Dev | Volume | 75 |
| Issue | 5 | Pages | 699-706 |
| PubMed ID | 18008318 | Mgi Jnum | J:135364 |
| Mgi Id | MGI:3793519 | Doi | 10.1002/mrd.20828 |
| Citation | Biellmann F, et al. (2008) Impaired sexual behavior in male mice deficient for the beta1-3 N-acetylglucosaminyltransferase-I gene. Mol Reprod Dev 75(5):699-706 |
| abstractText | The beta1-3 N-acetylglucosaminyltransferase-1 (B3gnt1) gene encodes a poly-N-acetyllactosamine synthase which can initiate and extend poly-N-acetyllactosamine chains [Gal(beta1-4)GlcNAc (beta1-3)(n)]. Previous investigations with heterozygous and homozygous null mice for this gene have revealed the importance of poly-N-acetyllactosamine chains for the formation of olfactory axon connections with the olfactory bulb and the migration of gonadotropin releasing hormone neurons to the hypothalamus. The possible long-term effects of these developmental defects, however, has not yet been studied. Here we have examined a reproductive phenotype observed in B3gnt1-null mice. Whereas the B3gnt1 null females were fertile, the B3gnt1 null males were not able to sire litters at the expected rate when mated to either wildtype or B3gnt1-null females. We assessed male sexual behavior as well as male reproduction parameters such as testes size, spermatogenesis, sperm number, morphology, and the development of early embryos in order to identify the source of a reduced rate of reproduction. Our findings show that the B3gnt1 null male reproductive organs were functional and could not account for the lower rate at which they produced offspring with wildtype conspecifics. Hence, we propose that the phenotype observed resulted from an impaired sexual response to female mating partners. |
