| First Author | Filson AJ | Year | 1993 |
| Journal | Development | Volume | 118 |
| Issue | 3 | Pages | 731-6 |
| PubMed ID | 8076514 | Mgi Jnum | J:13165 |
| Mgi Id | MGI:61373 | Doi | 10.1242/dev.118.3.731 |
| Citation | Filson AJ, et al. (1993) Rescue of the T-associated maternal effect in mice carrying null mutations in Igf-2 and Igf2r, two reciprocally imprinted genes. Development 118(3):731-6 |
| abstractText | In mice, only the paternal allele of the Igf2 gene, encoding insulin-like growth factor II (IGF-II) is expressed due to parental imprinting. Interestingly, the Igf2r gene, which encodes one of the two known receptors (IGF2R) to which IGF-II binds with high affinity is also subject to imprinting, but in a reciprocal fashion. This observation raises the possibility that imprinting of these loci serves to regulate the ratios of the gene products, since IGF2R provides a mechanism for IGF-II turnover. To test this hypothesis, we crossed mice mutant for Igf-2 with animals carrying the Thp chromosomal deletion, which encompasses the Igf2r locus. Inheritance of the Thp chromosome through the maternal germline results in a dominant lethal maternal effect (Tme). However, as we show here, Thp/+ embryos that inherit the Thp maternally are variably rescued to birth if they also lack IGF-II. Based on these data, the Tme phenotype can be viewed as a dominant effect resulting from an overabundance of IGF-II. |
