Muenke syndrome, also known as FGFR3-associated coronal synostosis, is defined 
molecularly by the presence of a heterozygous nucleotide transversion, c.749C>G, 
encoding the amino acid substitution Pro250Arg, in the fibroblast growth factor 
receptor type 3 gene (FGFR3). This frequently occurs as a new mutation, 
manifesting one of the highest documented rates for any transversion in the 
human genome. To understand the biology of this mutation, we have investigated 
its parental origin, and the ages of the parents, in 19 families with de novo 
c.749C>G mutations. All ten informative cases originated from the paternal 
allele (95% confidence interval 74-100% paternal); the average paternal age at 
birth overall was 34.7 years. An exclusive paternal origin of mutations, and 
increased paternal age, were previously described for a different mutation 
(c.1138G>A) of the FGFR3 gene causing achondroplasia, as well as for mutations 
of the related FGFR2 gene causing Apert, Crouzon and Pfeiffer syndromes. We 
conclude that similar biological processes are likely to shape the occurrence of 
this c.749C>G mutation as for other mutations of FGFR3 as well as FGFR2.