Faculty Research 1990 - 1999
Protein 4.1R-deficient mice are viable but have erythroid membrane skeleton abnormalities.
Document Type
Article
Publication Date
1999
Keywords
Animal, Blood Proteins/deficiency/*genetics, Erythrocyte Membrane/*pathology, Erythrocytes/*metabolism/ultrastructure, Gene Expression, Human, Mice, Mice, Knockout/genetics/metabolism, Proteins/*genetics/metabolism
First Page
331
Last Page
340
JAX Source
J Clin Invest 1999 Feb;103(3):331-40
Grant
DK32094/DK/NIDDK, HL55321/HL/NHLBI
Abstract
A diverse family of protein 4.1R isoforms is encoded by a complex gene on human chromosome 1. Although the prototypical 80-kDa 4.1R in mature erythrocytes is a key component of the erythroid membrane skeleton that regulates erythrocyte morphology and mechanical stability, little is known about 4.1R function in nucleated cells. Using gene knockout technology, we have generated mice with complete deficiency of all 4.1R protein isoforms. These 4.1R-null mice were viable, with moderate hemolytic anemia but no gross abnormalities. Erythrocytes from these mice exhibited abnormal morphology, lowered membrane stability, and reduced expression of other skeletal proteins including spectrin and ankyrin, suggesting that loss of 4. 1R compromises membrane skeleton assembly in erythroid progenitors. Platelet morphology and function were essentially normal, indicating that 4.1R deficiency may have less impact on other hematopoietic lineages. Nonerythroid 4.1R expression patterns, viewed using histochemical staining for lacZ reporter activity incorporated into the targeted gene, revealed focal expression in specific neurons in the brain and in select cells of other major organs, challenging the view that 4.1R expression is widespread among nonerythroid cells. The 4.1R knockout mice represent a valuable animal model for exploring 4.1R function in nonerythroid cells and for determining pathophysiological sequelae to 4.1R deficiency.
Recommended Citation
Shi ZT,
Afzal V,
Coller B,
Patel D,
Chasis JA,
Parra M,
Lee G,
Paszty C,
Stevens M,
Walensky L,
Peters LL,
Mohandas N,
Rubin E,
Conboy JG.
Protein 4.1R-deficient mice are viable but have erythroid membrane skeleton abnormalities. J Clin Invest 1999 Feb;103(3):331-40