Identifying 1,907 mitochondrial somatic mutations from 1,675 tumor tissues provides new insights into the causes and effects of the mitochondrial genome mutations found in human cancers.

Epigenome and Mitochondrial Barcode of Lineage from Endogenous Mutations (EMBLEM) enable tracking cell lineage in combination with chromatin profile in ATAC-seq data.

Many tumors are depleted of mitochondrial DNA; this depletion is associated with changes in gene expression and with the incidence of critical somatic mutations and alterations.

RNA Polymerase II transcriptional termination of a nuclear long non-coding RNA is required to maintain the mitochondrial genome and hence promotes budding yeast growth.

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.

Genetics of a canine transmissible tumour show how the world’s oldest cancer “metastasised” through the global dog population – and captured, maintained and rearranged its mitochondrial DNA along the way.

Recombinant mitochondrial genomes can be selected, traits can be genetically mapped and new genetic combinations can be made.

Mitochondrial anti-viral signaling proteins form three-stranded helical filaments in launching innate immune responses against RNA viruses.

Mitochondrial genomes harbor male-fertility-reducing mutations that can be harnessed to control population viability as a novel approach to control economic and environmental pests.

Genome-wide RNA-seq analysis of single cells of the developing mouse endolymphatic sac reveals its molecular-cellular architecture and a model for salt and fluid absorption required for acquisition of normal inner ear structure and function.