Supplementary Materials

The PDF file includes:

  • Fig. S1. Genetic knockdown of NLN reduces the growth of leukemic cells.
  • Fig. S2. Genetic knockdown of NLN disrupts cristae but does not alter mitochondrial mass, membrane potential, or ROS.
  • Fig. S3. NLN knockdown impairs RCS formation independently of OPA1.
  • Fig. S4. ClpXP degrades respiratory chain complex subunits and impairs supercomplex formation.
  • Fig. S5. NLN expression and RCS formation are down-regulated under hypoxic conditions.
  • Fig. S6. RCS assembly in patients with AML is not correlated with respiratory chain complex subunit expression.
  • Fig. S7. LETM1 complex assembly is impaired under hypoxic conditions.
  • Fig. S8. Genetic knockdown of NLN reduces LETM1 complex formation.
  • Fig. S9. A small-molecule inhibitor of NLN does not affect individual complex subunits.
  • Fig. S10. A small-molecule inhibitor of NLN reduces LETM1 complex formation.
  • Fig. S11. A small-molecule inhibitor of NLN reduces the growth of leukemic cells.
  • Fig. S12. A small-molecule inhibitor of NLN shows no evidence of toxicity in xenograft models of AML.
  • Table S1. Correlation of NLN with mutations.
  • Table S2. Cell lines.
  • Table S3. Clinical data of primary AML samples.

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Other Supplementary Material for this manuscript includes the following:

  • Data file S1 (Microsoft Excel format). Original data.
  • Data file S2 (Microsoft Excel format). Complete list of NLN’s interactors identified by BioID-MS.