Targeted deletion of the gamma-adducin gene (Add3) in mice reveals differences in alpha-adducin interactions in erythroid and nonerythroid cells.

ABSTRACT: In red blood cells (RBCs) adducin heterotetramers localize to the spectrin-actin junction of the peripheral membrane skeleton. We previously reported that deletion of beta-adducin results in osmotically fragile, microcytic RBCs and a phenotype of hereditary spherocytosis (HS). Notably, alpha-adducin was significantly reduced, while gamma-adducin, normally present in limited amounts, was increased approximately 5-fold, suggesting that alpha-adducin requires a heterologous binding partner for stability and function, and that gamma-adducin can partially substitute for the absence of beta-adducin. To test these assumptions we generated gamma-adducin null mice. gamma-adducin null RBCs appear normal on Wright's stained peripheral blood smears and by scanning electron microscopy. All membrane ske

SUBMITTER: Sahr KE 

PROVIDER: S-EPMC2827150 | biostudies-literature | 2009 Jun

REPOSITORIES: biostudies-literature