Science Advances

Supplementary Materials

This PDF file includes:

  • Supplementary Methods
  • Table S1. Antibodies used throughout the study.
  • Table S2. Sampling used for quantifications in the enteric nervous system.
  • Table S3. Sampling used for quantifications in the sciatic nerves.
  • Fig. S1. Conditional ablation of Lkb1 in NCCs causes hypopigmentation, hind limb paralysis, and intestinal pseudo-obstruction.
  • Fig. S2. Lkb1 inactivation impairs melanocyte formation.
  • Fig. S3. Lkb1 inactivation in neural crest–derived enteric cells triggers neurodegeneration.
  • Fig. S4. Defective myelination of sciatic nerves in Lkb1 cKO mice correlates with defects in maturation of Schwann cells.
  • Fig. S5. Lkb1 loss triggers a lack of progenitor differentiation.
  • Fig. S6. Validation of the neural crest stem cell line JoMa1.3.
  • Fig. S7. Lkb1 loss rewires glial cell metabolism but does not affect glycolysis.
  • Fig. S8. Alanine biosynthesis and mTORC1 activity are connected in glial cells.
  • Fig. S9. AICAR rescues glial differentiation independently of alanine levels, mitochondrial respiration, or glycolysis.
  • Fig. S10. Schematic model depicting the antagonistic regulation of alanine production by LKB1/AMPK and the postulated mechanistic integration of the signal on mTOR and the tricarboxylic acid.
  • References (78–81)

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