MitoCarta3.0: an updated mitochondrial proteome now with sub-organelle localization and pathway annotations

TLDR

The mammalian mitochondrial proteome is largely nuclear‑encoded (≈99%) with a small mtDNA component, and the original MitoCarta catalog listed over 1,000 genes. This work presents MitoCarta3.0, an updated mitochondrial gene inventory. The authors refined the previous list by manually removing 100 genes and adding 78, yielding 1,136 human genes, and incorporated Bayesian‑integrated sequence and mass‑spectrometry data along with curated sub‑mitochondrial localization and 149 MitoPathway annotations. MitoCarta3.0, featuring sub‑organellar localization and pathway annotations, is freely accessible at the Broad Institute website and is intended as a community resource for mitochondrial biology and medicine.

Abstract

Abstract The mammalian mitochondrial proteome is under dual genomic control, with 99% of proteins encoded by the nuclear genome and 13 originating from the mitochondrial DNA (mtDNA). We previously developed MitoCarta, a catalogue of over 1000 genes encoding the mammalian mitochondrial proteome. This catalogue was compiled using a Bayesian integration of multiple sequence features and experimental datasets, notably protein mass spectrometry of mitochondria isolated from fourteen murine tissues. Here, we introduce MitoCarta3.0. Beginning with the MitoCarta2.0 inventory, we performed manual review to remove 100 genes and introduce 78 additional genes, arriving at an updated inventory of 1136 human genes. We now include manually curated annotations of sub-mitochondrial localization (matrix, inner membrane, intermembrane space, outer membrane) as well as assignment to 149 hierarchical ‘MitoPathways’ spanning seven broad functional categories relevant to mitochondria. MitoCarta3.0, including sub-mitochondrial localization and MitoPathway annotations, is freely available at http://www.broadinstitute.org/mitocarta and should serve as a continued community resource for mitochondrial biology and medicine.