The erythrocyte skeletons of beta-adducin deficient mice have altered levels of tropomyosin, tropomodulin and EcapZ |
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Authors: | Porro Fabiola Costessi Luisa Marro Martín L Baralle Francisco E Muro Andrés F |
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Affiliation: | International Centre for Genetic Engineering and Biotechnology, Padriciano 99, I 34012, Trieste, Italy. |
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Abstract: | The erythrocyte membrane cytoskeleton is organized as a polygonal spectrin network linked to short actin filaments that are capped by adducin at the barbed ends. We have constructed a mouse strain deficient in beta-adducin having abnormal erythrocytes. We show here that the levels of several skeletal proteins from beta-adducin mutant erythrocytes are altered. In fact, CapZ, the main muscle actin-capping protein of the barbed ends that in the erythrocytes is cytoplasmic, is 9-fold upregulated in mutant skeletons of erythrocytes suggesting a compensatory mechanism. We also detected upregulation of tropomodulin and downregulation of alpha-tropomyosin and actin. In addition, purified adducin can be re-incorporated into adducin-deficient ghosts. |
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