The mitochondrial genome modulates oxidative stress and telomere length in human cells-A transmitochondrial cybrid approach
(2021) CSH meeting on Telomeres & Telomerase — Location: CSH-Virtual meeting (14.December.2021)
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- Abstract
- More than two decades ago, the G-rich sequences of telomeric DNA were proposed to be preferential targets of oxidative damage with potential detrimental impact on telomere length and integrity. If not breathing is not an option (Markkanen, 2017), understanding how cellular respiration impacts on telomere regulation remains a challenging question that has, so far, not been addressed in the context of naturally-induced oxidative stress. ATP production, through oxidative phosphorylation in mitochondria, is the major endogenous source of ROS in cells. Both oxygen consumption and the proton gradient strength across the inner mitochondrial membrane regulate ROS production. Here, using a transmitochondrial cybrid approach with mitochondria isolated from donors with either very long (>P90), average or short telomeres, we evaluated the impact of the mitochondrial genome on oxidative stress and telomere length in Rho0 recipient cells. Our data revealed that specific mtDNA-encoded mitochondrial protein variants regulate oxidative stress and telomere length. We will discuss how these variants may impact on ROS production and offer a maternal inheritance of telomere length.
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Citations
Mahieu, M., Defour, J.-P., Scheers, I., Brichard, B., Levy, G., Arnould, T., Corbet, C., & Decottignies, A. (2021). The mitochondrial genome modulates oxidative stress and telomere length in human cells-A transmitochondrial cybrid approach. CSH meeting on Telomeres & Telomerase, CSH-Virtual meeting.