B6;129-Trdmt1^tm1Bes/J

Stock number: 006240
Product name: Dnmt2 KO
Strain synonyms: B6;129-Dnmt2^tm1Bes/J
Research areas: Cancer Research, Cell Biology Research, Research Tools

Description

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

Detailed description

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 (tRNA^Asp) 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.

Development

A targeting vector was designed to insert a loxP site upstream of exon 7 and a PGK1-neo cassette and second loxP site downstream of exon 10 of the endogenous gene. This construct was microinjected into (129X1/SvJ x 129S1/Sv)F1-derived R1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into blastocysts. Chimeric mice were bred to C57BL/6 to establish heterozygous mice, which were then bred to Hsp70-Cre mice on a B6;129 mixed genetic background. The resulting mutant mice (with exons 7-10 replaced with a single loxP site) were bred together for many generations before arrival at The Jackson Laboratory.

Allele

Symbol: Trdmt1^tm1Bes
Name: targeted mutation 1, Timothy H Bestor
MGI accession ID: MGI:3695409
Generation method: Targeted
Attributes: Null/Knockout
Marker symbol: Trdmt1
Marker name: tRNA aspartic acid methyltransferase 1
Chromosome: 2
Strain of origin: (129X1/SvJ x 129S1/Sv)F1-Kitl⁺
Molecular note: LoxP sites were introduced to flank exons 7-10 of the gene. Cre-mediated recombination resulted in deletion of exons 7-10.