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Gene Review:

Trex1 - three prime repair exonuclease 1

Mus musculus

Synonyms: 1661, 3'-5' exonuclease TREX1, AU041952, DNase III, Three-prime repair exonuclease 1

Nguyen, Q.G. et al., Morita, M. et al., Mazur, D.J. et al., Mann, M. et al., Crow, Y.J. et al.

Crow, Hayward, Parmar, Robins, Leitch, Ali, Black, van Bokhoven, Brunner, Hamel, Corry, Cowan, Frints, Klepper, Livingston, Lynch, Massey, Meritet, Michaud, Ponsot, Voit, Lebon, Bonthron, Jackson, Barnes, Lindahl,

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Disease relevance of Trex1

Gene-targeted mice lacking the Trex1 (DNase III) 3'-->5' DNA exonuclease develop inflammatory myocarditis [1].
Unexpectedly, Trex1(-/-) mice exhibit a dramatically reduced survival and develop inflammatory myocarditis leading to progressive, often dilated, cardiomyopathy and circulatory failure [1].
To study the activities of these exonucleases we have developed strategies to express and purify the recombinant mouse Trex1 and human TREX2 proteins in Escherichia coli in quantities sufficient for biochemical characterization [2].

High impact information on Trex1

Similar loss of function in the Trex1(-/-) mouse leads to an inflammatory phenotype [3].
The null mice are viable and do not show the increase in spontaneous mutation frequency or cancer incidence that would be predicted if Trex1 served an obligatory role of editing mismatched 3' termini generated during DNA repair or DNA replication in vivo [1].
In addition, two novel genes expressed in trophoblast were identified, 1661 and RA81 [4].
Upon mutation of the Trex site, median transgene expression levels decreased 3- to 120-fold in the muscles examined, with statistically significant differences in all muscles except the EDL [5].
Transfections into neonatal rat myocardiocytes confirmed the importance of the Trex site for MCK enhancer activity in heart muscle, but the effect is larger in transgenic mice than in cultured cells [5].

Biological context of Trex1

Transgenic and tissue culture analyses of the muscle creatine kinase enhancer Trex control element in skeletal and cardiac muscle indicate differences in gene expression between muscle types [5].

References

Gene-targeted mice lacking the Trex1 (DNase III) 3'-->5' DNA exonuclease develop inflammatory myocarditis. Morita, M., Stamp, G., Robins, P., Dulic, A., Rosewell, I., Hrivnak, G., Daly, G., Lindahl, T., Barnes, D.E. Mol. Cell. Biol. (2004) [Pubmed]
Excision of 3' termini by the Trex1 and TREX2 3'-->5' exonucleases. Characterization of the recombinant proteins. Mazur, D.J., Perrino, F.W. J. Biol. Chem. (2001) [Pubmed]
Mutations in the gene encoding the 3'-5' DNA exonuclease TREX1 cause Aicardi-Goutières syndrome at the AGS1 locus. Crow, Y.J., Hayward, B.E., Parmar, R., Robins, P., Leitch, A., Ali, M., Black, D.N., van Bokhoven, H., Brunner, H.G., Hamel, B.C., Corry, P.C., Cowan, F.M., Frints, S.G., Klepper, J., Livingston, J.H., Lynch, S.A., Massey, R.F., Meritet, J.F., Michaud, J.L., Ponsot, G., Voit, T., Lebon, P., Bonthron, D.T., Jackson, A.P., Barnes, D.E., Lindahl, T. Nat. Genet. (2006) [Pubmed]
Identification of genes showing altered expression in preimplantation and early postimplantation parthenogenetic embryos. Mann, M., Latham, K.E., Varmuza, S. Dev. Genet. (1995) [Pubmed]
Transgenic and tissue culture analyses of the muscle creatine kinase enhancer Trex control element in skeletal and cardiac muscle indicate differences in gene expression between muscle types. Nguyen, Q.G., Buskin, J.N., Himeda, C.L., Fabre-Suver, C., Hauschka, S.D. Transgenic Res. (2003) [Pubmed]

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