Mitochondrial flashes counteract the imbalance of ATP supply-and-demand and constitute an auto-regulator of ATP homeostasis in the heart.

Mitochondrial flashes have a central role in ensuring that ATP levels remain constant in heart cells.

The primary respiratory defect seen in aged cardiomyocytes is an elevated proton leak mediated by ANT1, and this is prevented by treatment with SS-31 (elamipretide).

An immunofluorescent analysis of 465 protein kinases revealed a substantial role of liquid-liquid phase separation in kinase localization and identified new kinase localizations to mitochondria and other organelles.

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.

The discovery of three distinct and independent trans-regulating genomic loci influencing heart mass using a well-characterized mouse reference population provides evidence in support of the hypothesis that genetic diversity in the mitochondrial proteome plays a critical role in heart pathophysiology.

In neuronal mitophagy, Parkin and OPTN induce efficient sequestration of damaged somal mitochondria into autophagosomes, but slow turnover via lysosomal acidification may be a point of vulnerability for the cell.

The structures of plant CIII2, CIV, and SC III2+IV challenge long-standing assumptions, generate new mechanistic hypotheses and allow for the generation of more selective agricultural inhibitors.

A new mitochondrial protein degradation pathway selectively sorts and destroys a subset of the mitochondrial membrane proteome to protect mitochondria in times of stress.

A university genomics class provides detailed examples of how to design and execute Oxford Nanopore MinION hackathons as part of an academic curriculum.