Loss of rapid transferrin receptor recycling due to a mutation in Sec1511 in hbd mice

摘要

The hbd (hemoglobin deficit) mutation affects iron trafficking in murine reticulocytes. It is due to a deletion that eliminates exon 8 of Sec,1511, the homolog of a gene that encodes an exocyst component in yeast. We tested the hypothesis that the mutation causes defective slow or rapid receptor recycling by measuring endocytosis and exocytosis of transferrin by hbd reticulocytes. Endocytosis and initial iron incorporation were relatively unaffected, but exocytosis was unexpectedly slowed. These data indicate that rapid transferrin recycling is defective after pSec 1511 has mutated. (c) 2006 Elsevier B.V. All rights reserved.