Slc25a3 (solute carrier family 25 (mitochondrial carrier, phosphate carrier), member 3; also called PiC) encodes a protein that is critical for ATP synthesis, serving as the primary means for mitochondrial phosphate import across the inner membrane. 

Exons 1 and 2 of the mouse Slc25a3 gene are flanked by loxP sites in this Slc25afl conditional mutant strain. Homozygous floxed mice are viable, fertile, and without overt phenotype.

When crossed with mice expressing a cardiac-specific, tamoxifen-inducible cre recombinase (see Stock No. <a href="https://www.jax.org/strain/005657"">005657</a>), the resultant pups develop severe cardiomyopathy 10 weeks after tamoxifen administration. Heart weight to body weight ratios are increased by a marked 300% compared to controls, with a corresponding ~80% increase in myocyte cross-sectional area. Extensive sarcomeric disarray with fragmented and disrupted mitochondria, as well as mitochondrial hyperproliferation are also seen in electron micrographs. Cardiac-specific knock-out of Slc25a3 results in desensitization of mitochondrial permeability transition pores, leading to cardiomyopathy.

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Exons 1 and 2 of the mouse Slc25a3 gene are flanked by loxP sites in this Slc25a3fl conditional mutant strain. Cardiac-specific knock-out of Slc25a3 results in decreased mitochondrial phosphate transport, desensitization of mitochondrial permeability transition pore, and cardiomyopathy.

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