Would the mice’s memory of mitochondrial stress pass on to mice offspring

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This study investigates whether the offspring of genetically modified mice with AD-induced UPRmt have genetic memory, which makes the offspring more likely to produce UPRmt or even with a more obvious effect. We first conducted biochemical studies using double transgenic mice of different ages to explore the expression levels of UPRmt-related proteins in hippocampal lysates. The two groups of mice were then mated to produce offspring, then the expression levels of UPRmt-related proteins in the offspring were explored. The offspring were tested for UPRmt characterization and physiological changes. Our analysis shows with inherited mtDNA and the consequent UPRmt, UPRmt can also communicate across tissues via intracellular signals; the cell-autonomous induction of UPRmt enables individuals to engage in global stress responses, whereby individuals exhibit greater resistance to adverse mitochondrial stresses, bacterial infections, and toxins, resulting in longer life. Due to the limitations of experimental materials, we propose more theories without a large amount of experimental data as support. We conclude that stress resistance can also develop in mammalian offspring due to mitochondrial stress-induced mitochondrial nuclear imbalance and the consequent increase in lifespan, thus increasing the survival advantage of the mammalian species.