| First Author | Papathanasiou P | Year | 2003 |
| Journal | Immunity | Volume | 19 |
| Issue | 1 | Pages | 131-44 |
| PubMed ID | 12871645 | Mgi Jnum | J:84569 |
| Mgi Id | MGI:2668296 | Doi | 10.1016/s1074-7613(03)00168-7 |
| Citation | Papathanasiou P, et al. (2003) Widespread failure of hematolymphoid differentiation caused by a recessive niche-filling allele of the Ikaros transcription factor. Immunity 19(1):131-44 |
| abstractText | A central issue in understanding the hematolymphoid system is the generation of appropriate mutant alleles in mice to reveal the function of regulatory genes. Here we describe a mouse strain, Plastic, with a point mutation in a zinc finger of Ikaros that disrupts DNA binding but preserves efficient assembly of the full-length protein into higher order complexes. Ikaros(Plastic) homozygosity is embryonically lethal with severe defects in terminal erythrocyte and granulocyte differentiation, excessive macrophage formation, and blocked lymphopoiesis, while heterozygotes display a partial block in lymphocyte differentiation. The contrast with more circumscribed effects of Ikaros alleles that ablate the full-length protein highlights the importance in mammals of generating recessive niche-filling alleles that inactivate function without creating a void in multimolecular assemblies. |
