Loss of rapid transferrin receptor recycling due to a mutation in Sec15l1 in hbd mice

Biochim Biophys Acta. 2007 Feb;1773(2):105-8. doi: 10.1016/j.bbamcr.2006.09.032. Epub 2006 Oct 4.


The hbd (hemoglobin deficit) mutation affects iron trafficking in murine reticulocytes. It is due to a deletion that eliminates exon 8 of Sec15l1, 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 pSec15l1 has mutated.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Endocytosis*
  • Exocytosis
  • Hemoglobins / deficiency*
  • Iodine Radioisotopes
  • Iron / metabolism
  • Membrane Proteins / genetics*
  • Mice
  • Mice, Mutant Strains
  • Mutation / genetics*
  • Receptors, Transferrin / metabolism*
  • Reticulocytes / metabolism
  • Time Factors


  • Hemoglobins
  • Iodine Radioisotopes
  • Membrane Proteins
  • Receptors, Transferrin
  • Sec15 protein, mouse
  • Iron