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A nonsense mutation was introduced at the last codon of exon 9 via site directed mutagenesis and subsequent homologous recombination, precluding the translation of 5 carboxy terminal residues (407 through 411). Due to its position at the 3' end of exon 9, the mutation does not affect residues involved in transglutaminase crosslinking and is insensitive to the known splice variation involving exon 10. Northern blot analysis of total hepatic RNA showed that the mutation did not effect expression of any of the three fibrinogen polypeptides (alpha, beta, and gamma). Levels of circulating the fibrinogen complex were determined to be unaffected in mutant mice by Western blot analysis and quantitative capture ELISA of plasma. (J:36873)