A short linear motif in BNIP3L (NIX) mediates mitochondrial clearance in reticulocytes

Ji Zhang, Melanie R. Loyd, Mindy S. Randall, M. Brett Waddell, Richard W. Kriwacki, Paul A. Ney

Research output: Contribution to journalArticle

39 Scopus citations


Elimination of defective mitochondria is essential for the health of long-lived, postmitotic cells. To gain insight into this process, we examined programmed mitochondrial clearance in reticulocytes. BNIP3L is a mitochondrial outer membrane protein that is required for clearance. It has been suggested that BNIP3L functions by causing mitochondrial depolarization, activating autophagy, or engaging the autophagy machinery. Here we showed in mice that BNIP3L activity localizes to a small region in its cytoplasmic domain, the minimal essential region (MER). The MER is a novel sequence, which comprises three contiguous hydrophobic amino acid residues, and flanking charged residues. Mutation of the central leucine residue causes complete loss of BNIP3L activity, and prevents rescue of mitochondrial clearance. Structural bioinformatics analysis predicts that the BNIP3L cytoplasmic domain lacks stable tertiary structure, but that the MER forms an α-helix upon binding to another protein. These findings support an adaptor model of BNIP3L, centered on the MER.

Original languageEnglish (US)
Pages (from-to)1325-1332
Number of pages8
Issue number9
StatePublished - Sep 2012


  • Autophagy
  • Mitophagy
  • NIX
  • Reticulocyte
  • SLiM

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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    Zhang, J., Loyd, M. R., Randall, M. S., Waddell, M. B., Kriwacki, R. W., & Ney, P. A. (2012). A short linear motif in BNIP3L (NIX) mediates mitochondrial clearance in reticulocytes. Autophagy, 8(9), 1325-1332. https://doi.org/10.4161/auto.20764