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- Title
Cell-specific mitotic defect and dyserythropoiesis associated with erythroid band 3 deficiency.
- Authors
Paw, Barry H; Davidson, Alan J; Zhou, Yi; Li, Rong; Pratt, Stephen J; Lee, Charles; Trede, Nikolaus S; Brownlie, Alison; Donovan, Adriana; Liao, Eric C; Ziai, James M; Drejer, Anna H; Guo, Wen; Kim, Carol H; Gwynn, Babette; Peters, Luanne L; Chernova, Marina N; Alper, Seth L; Zapata, Agustin; Wickramasinghe, Sunitha N; Lee, Matthew J; Lux, Samuel E; Fritz, Andreas; Postlethwait, John H; Zon, Leonard I
- Abstract
Most eukaryotic cell types use a common program to regulate the process of cell division. During mitosis, successful partitioning of the genetic material depends on spatially coordinated chromosome movement and cell cleavage. Here we characterize a zebrafish mutant, retsina (ret), that exhibits an erythroid-specific defect in cell division with marked dyserythropoiesis similar to human congenital dyserythropoietic anemia. Erythroblasts from ret fish show binuclearity and undergo apoptosis due to a failure in the completion of chromosome segregation and cytokinesis. Through positional cloning, we show that the ret mutation is in a gene (slc4a1) encoding the anion exchanger 1 (also called band 3 and AE1), an erythroid-specific cytoskeletal protein. We further show an association between deficiency in Slc4a1 and mitotic defects in the mouse. Rescue experiments in ret zebrafish embryos expressing transgenic slc4a1 with a variety of mutations show that the requirement for band 3 in normal erythroid mitosis is mediated through its protein 4.1R-binding domains. Our report establishes an evolutionarily conserved role for band 3 in erythroid-specific cell division and illustrates the concept of cell-specific adaptation for mitosis.
- Publication
Nature genetics, 2003, Vol 34, Issue 1, p59
- ISSN
1061-4036
- Publication type
Journal Article
- DOI
10.1038/ng1137