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Decreased viability of nitric oxide synthase double knockout mice
Author(s) -
Tranguch Susanne,
HuetHudson Yvette
Publication year - 2003
Publication title -
molecular reproduction and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 105
eISSN - 1098-2795
pISSN - 1040-452X
DOI - 10.1002/mrd.10274
Subject(s) - nos1 , biology , nitric oxide , nitric oxide synthase , embryo , knockout mouse , gene isoform , embryogenesis , medicine , endocrinology , microbiology and biotechnology , genetics , gene
Nitric oxide acts as an important intracellular messenger in a variety of systems, including reproduction. Previous studies have shown the importance of nitric oxide in embryo development. NO is produced from l ‐arginine by the enzyme, nitric oxide synthase (NOS), which has three isoforms: endothelial (NOS3), neural (NOS1), and inducible (NOS2). We hypothesize that, because of the importance of NOS in development, at least two NOS isoforms are required in order for normal embryo development to occur. Through the generation of NOS3/NOS2, NOS3/NOS1, and NOS2/NOS1 double knockout mice, we found that while litter size remains unchanged, the expected number of generated double knockout mice varies significantly from what would be predicted by Mendelian genetics. Estrous cycles were similar for both DKO and the wild‐type mice, and both groups were deemed fertile by their ability to mate with wild‐type (CD‐1) mice. Together, these results lead us to conclude that the lack of two NOS isoforms leads to a decreased viability in mice because of a developmental problem in the double knockout embryo. Mol. Reprod. Dev. 65: 175–179, 2003. © 2003 Wiley‐Liss, Inc.