Disease relevance of Tme

• These data show that the biological function of imprinting Igf2r is to increase birth weight and they also establish Igf2r as the Tme gene [1].

High impact information on Tme

• The apparent nonequivalence of the Igf2r gene and Tme results in occurrence of viable mice lacking an active Igf2r gene [2].
• Genetic analysis of genomic imprinting: an Imprintor-1 gene controls inactivation of the paternal copy of the mouse Tme locus [2].
• The Thp deletion on mouse chromosome 17 is lethal when inherited from the mother, because it deletes the T-associated maternal effect (Tme) locus, the paternal copy of which is inactivated by genomic imprinting [2].
• Igf2/Mpr has been mapped to the mouse Tme locus and shown to be an imprinted gene, which further suggests a role in embryonic growth regulation [3].
• The mouse insulin-like growth factor type-2 receptor is imprinted and closely linked to the Tme locus [4].

Biological context of Tme

• The defect is nuclear-encoded and embryos that inherit a deletion of the Tme locus from their mother die at day 15 of gestation [4].
• The Tme locus is absent in two chromosome-17 deletion mutants, Thp and the tLub2, and its position has been localized using these deletions to a 1-cM region [4].
• Based on these data, the Tme phenotype can be viewed as a dominant effect resulting from an overabundance of IGF-II [5].
• Documentation of inheritance patterns suggests that Tme is an imprinted gene which is required for viability; maternal deletion is lethal while paternal deletion is viable [6].
• Thp is a large deletion on chromosome 17 which includes the maternal lethal gene Tme [6].

Anatomical context of Tme

• We demonstrate that the presence of an additional copy of the region with the Tme gene in the female gamete entirely compensates maternal Thp lethality [7].

Other interactions of Tme

• Therefore Igf2r is imprinted and closely linked or identical to Tme [4].
• The results presented here allow a mapping of the Tme locus between the quaking and tufted loci which are 3 cM apart within the proximal region of chromosome 17 [8].
• Mice with duplications and deletions at the Tme locus have altered MnSOD activity [9].
• These results indicate that Tcp-1 is not responsible for the maternal lethality effect, and therefore is not located at the Tme locus [10].

References