Mice homozygous for this targeted mutation are viable, fertile, and morphologically indistinguishable from wildtype mice. Despite the sequence and motif similarities of the endogenous gene to DNA methyltransferases, homozygous deletion does not lead to detectable alterations in genomic methylation patterns. However, homozygotes exhibit abnormal RNA methylation; specifically, cytosine 38 in the anticodon loop of the aspartic acid transfer RNA (tRNAAsp) remains unmethylated. Mutant mice may be useful in studies of RNA and DNA methylation, transcription and translation, imprinting, X-inactivation, and other nucleic acid research.

Mice homozygous for this Trdmt1 (formerly Dnmt2) knock-out have abnormal RNA methylation while genomic DNA methylation patterns are not detectably altered.

Typically mice are recovered in 12-16 weeks. Contact Customer Service to place an order or for more information.

<a target="_blank" href="https://www.jax.org/jax-mice-and-services/customer-support" rel="noreferrer">Contact Customer Service</a> for more information.