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. Author manuscript; available in PMC: 2022 May 4.
Published in final edited form as: Cell Metab. 2021 Feb 19;33(5):1013–1026.e6. doi: 10.1016/j.cmet.2021.02.001

Figure 1. Asparagine restores proliferation during ETC inhibition.

Figure 1.

(A) Schematic diagramming asparagine synthesis from TCA cycle-derived aspartate.

(B) Relative levels of intracellular aspartate 6 hours post-treatment with rotenone (Rot) or vehicle (DMSO) in asparagine-free medium.

(C) Relative levels of intracellular asparagine 6 hours post-treatment with rotenone or DMSO in asparagine-free medium.

(D) Relative proliferation rate of indicated cell lines with rotenone or DMSO treatment in the presence or absence of 0.1 mM exogenous asparagine (N).

(E) Relative proliferation rate of indicated cell lines with metformin (Met) or vehicle control (PBS) treatment in the presence or absence of 0.1 mM exogenous asparagine (N).

(F) Relative proliferation rate of indicated cell lines with IACS-010759 (IACS) or vehicle control (DMSO) treatment in the presence or absence of 0.1 mM exogenous asparagine (N).

(G) Proliferation rate of indicated cell lines with metformin treatment in the presence or absence of 0.1 mM exogenous asparagine (N) or 20 mM aspartate, relative to respective PBS control proliferation in unsupplemented DMEM.

(H) Relative HeLa cell proliferation rate with the indicated ETC inhibitor in the presence or absence of 0.1 mM exogenous asparagine (N) or 20 mM aspartate. Proliferation with antimycin A is in medium lacking uridine. Data are mean +/− s.d. (n = 3 independent experiments). P value determined by unpaired two-tailed t-test: *p<0.05; **p<0.01; ***p<0.001; ns, not significant. See also Figure S1.