Journal
INTERNATIONAL JOURNAL OF DEVELOPMENTAL BIOLOGY
Volume 54, Issue 1, Pages 215-220Publisher
UNIV BASQUE COUNTRY UPV-EHU PRESS
DOI: 10.1387/ijdb.072356rb
Keywords
DDAH; nitric oxide; embryonic development; mouse; transgenic
Categories
Funding
- Biotechnology and Biological Sciences Research Council [BB/E527098/1] Funding Source: Medline
- Medical Research Council [MC_U120097118, MC_U117562103] Funding Source: Medline
- BBSRC [BB/E527098/1] Funding Source: UKRI
- MRC [MC_U120097118, MC_U117562103] Funding Source: UKRI
Ask authors/readers for more resources
Nitric oxide has been linked to a number of embryonic processes, yet the role of nitric oxide signalling in development remains largely unknown. Dimethylarginine Dimethylaminohydrolase 1 and 2 (DDAH1/2) catalyse the breakdown of asymmetric dimethylarginine, an endogenous inhibitor of nitric oxide production, and may also have nitric oxide-independent functions. We have generated transgenic mice targeting the DDAH1 and DDAH2 loci. Here we report that homozygous DDAH1 null embryos are generated at low frequency, and do not progress through embryonic development. During normal development DDAH1 RNA is expressed in the left ventricle, cardiac outflow tract and developing vasculature. In contrast, DDAH2 homozygous null mice are viable and fertile, with a normal lifespan. DDAH2 expression is seen in the developing left ventricle and cardiac outflow tract, and additionally in the peripheral nervous system. Both DDAH1 and 2 are expressed in the developing limb buds in patterns overlapping areas with high nitric oxide synthase activity. These expression patterns implicate DDAH1 and DDAH2 in embryonic development, possibly through specific effects on nitric oxide pathways.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available