AbstractTaurine is the most abundant free amino acid in heart muscle and protects against heart failure. In the present study, the consequences of hereditary taurine deficiency on cardiac gene expression were examined in 2- and 15–16-month-old taurine transporter knockout (taut-/-) mice using a mouse-specific DNA microarray. This oligonucleotide-based microarray contains probes for 251 genes with relevance for heart function. Of these, 163 probes exhibited a reproducible hybridization signal and were analyzed. α-Actin type 1 mRNA levels were 70% lower in the heart of young and oldertaut-/-mice compared to wild-type controls. Interestingly, the hearts oftaut-/-mice showed a switch from α-actin 1 to α-actin 2 expression, as confirmed by real-time PCR and Western blot analysis. In addition, mRNA levels of biomarkers for pressure overload and hypertension were upregulated intaut-/-hearts, i.e., atrial natriuretic factor (+848%), brain natriuretic peptide (+90%), cardiac ankyrin repeat protein (+118%), and procollagen 1a1, 1a2 and 3a1 (+40% at least). These results point to a stress situation in the heart oftaut-/-mice under laboratory conditions, and it can be speculated thattaut-/-hearts may be even more susceptible to failure in the wild when under exogenous stress.