To execute the complex choreography of embryogenesis, cells require energy. Mitochondria are essential for cellular energy generation, but the details of mitochondrial function during development remain surprisingly poorly understood. Now, Jesse Mager and colleagues provide an in vivo analysis of mitochondrial ribosomal proteins (MRPs), nuclear-encoded proteins that are crucial for translation of the mitochondrial genome and thus oxidative phosphorylation. Null alleles of five Mrp genes cause similar embryonic arrest in mice – development stalls just before the onset of gastrulation, at the egg cylinder stage (which is reached normally). The expression of the pluripotency marker Oct4 is retained in epiblasts of E7.5 mutant embryos, and mutants also fail to initiate expression of brachury (T), a marker of the primitive streak. While mutant embryos do not show widespread apoptosis, transmission electron microscopy reveals dramatic morphological changes in mitochondria (although the mitochondrial:nuclear DNA ratio was unaffected). Mutant embryos have a higher ADP to ATP ratio, display defective mitochondrial translation (inferred by the absence of the subunit II of the cytochrome c oxidase protein) and exhibit high levels of Cdc25c phosphorylation (indicative of cell cycle arrest at the G2/M checkpoint). Finally, novel knockouts of 16 other nuclear-encoded mitochondrial genes show similar embryonic phenotypes. MRPs are thus indispensable for development, and the initiation of gastrulation depends critically on oxidative phosphorylation.