New modelling, statistics, and experiments show that cellular populations of mitochondrial DNA (mtDNA) evolve during development according to solvable stochastic dynamics involving binomial partitioning and random turnover, facilitating a predictive and quantitative theory of the mtDNA bottleneck.
An insulin-Myc feed-forward loop triggered by transient JNK boosts transcription of genes essential for mitochondrial respiration and biogenesis during early oogenesis to support massive mtDNA replication and inheritance in Drosophila.
Building on previous work (Reznik et al., 2016), independent measurements of mitochondrial genome copy number and expression indicate that several solid tumor types suppress respiratory metabolism compared to normal tissue.
Common nuclear genetic variants are associated with fundamental biological processes occurring in human mitochondria and potentially point to novel roles for nuclear genes in transcriptional regulation of the mitochondrial genome.
Impaired lysosomal acidification results in retention of iron inside lysosomes, triggering functional iron deficiency, dysfunctional mitochondria (especially mtDNA loss), and inflammation in vivo in a mouse model of lysosomal disease.
A genetic approach documents that mitochondrial DNA moves from donor cells to recipient mtDNA-depleted cells in whole mitochondria and that this restores mitochondrial respiration and the capacity of the cells to form tumours.