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← Theoretical 2

Q59 — Mitochondrial Innate Immunity — Yme1L, SLC25A33 and mtDNA Release

Theoretical 2 Real exam question — full text reproduced under IBO's CC BY-NC-SA 4.0 license
Mitochondria & Chloroplasts: Structure & Endosymbiotic Origin Immune Physiology

Mitochondria are a convergence point of cellular signals and are closely related to signalling pathways of innate immunity. The immune response enhances antiviral immunity and protects nuclear DNA from damage.

Figure. mtDNA-dependent innate immunity is coupled to cellular nucleotide metabolism. Yme1L = an ATP-dependent proteolytic complex of the internal mitochondrial membrane responsible for maintaining mitochondrial morphology (and normally degrading SLC25A33); STING = an adaptive protein responsible for stimulating interferons; SLC25A33 = pyrimidine transporter; TREX1 = exonuclease; cGAS = cGMP-AMP-synthase. Yme1L knockout causes SLC25A33 accumulation and impaired pyrimidine synthesis, leading to imbalanced nucleotide pools, mtDNA release, cGAS-STING activation, innate immunity and autophagy; TREX1 degrades released mtDNA, replenishing nucleotide pools. Figure. mtDNA-dependent innate immunity coupled to cellular nucleotide metabolism.

Determine whether the following statements are true or false:

A. The knockout of Yme1L in cells supports pyrimidine metabolism by maintaining de novo synthesis of nucleotides and proteolysis of SLC25A33.
B. The information presented in this figure indicates that the accumulation of SLC25A33 can cause an immune response.
C. TREX1-mediated lysis of DNA can restore the imbalance of nucleotides in the cell.
D. The inhibition of the mitochondrial protease Yme1L downregulates the expression of genes needed for interferon production.
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Question reproduced from IBO 2022, Theoretical Paper 2, licensed under CC BY-NC-SA 4.0 — attributed to the International Biology Olympiad. Open the full exam PDF · Community solutions (unofficial)