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Blood, Vol. 93 No. 7 (April 1), 1999:
pp. 2404-2410
Stomatocytosis Is Absent in "Stomatin"-Deficient Murine Red
Blood Cells
Yiwen Zhu,
Chris Paszty,
Tikva Turetsky,
Susan Tsai,
Frans A. Kuypers,
Gloria Lee,
Philip Cooper,
Patrick G. Gallagher,
Mary E. Stevens,
Edward Rubin,
Narla Mohandas, and
William C. Mentzer
From the Department of Pediatrics, University of California San
Francisco, San Francisco, CA; the Department of Pediatrics, Yale
University School of Medicine, New Haven, CT; the Lawrence Berkeley
National Laboratory, Berkeley, CA; and the Childrens Hospital Oakland
Research Institute, Oakland, CA.
To examine the relationship between erythrocyte membrane protein
7.2b deficiency and the hemolytic anemia of human hereditary stomatocytosis, we created 7.2b knock-out mice by standard gene targeting approaches. Immunoblots showed that homozygous knock-out mice
completely lacked erythrocyte protein 7.2b. Despite the absence of
protein 7.2b, there was no hemolytic anemia and mouse red blood cells
(RBCs) were normal in morphology, cell indices, hydration status,
monovalent cation content, and ability to translocate lipids. The
absence of the phenotype of hereditary stomatocytosis implies that
protein 7.2b deficiency plays no direct role in the etiology of this
disorder and casts doubt on the previously proposed role of this
protein as a mediator of cation transport in RBC.
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