Pentatricopeptide repeat (PPR) proteins constitute a large protein family in flowering plants and are thought to be mostly involved in organellar RNA metabolism. The subgroup of PLS-type PPR proteins were found to be the main specificity factors of cytidine to uridine RNA editing. Identifying the targets of PLS-type PPR proteins can help in elucidating the molecular function of proteins encoded in the organellar genomes. In this study, plants lacking the SLOW GROWTH 4 PPR protein were characterized. Slo4 mutants were characterized as having restricted root growth, being late flowering and displaying an overall delayed growth phenotype. Protein levels and activity of mitochondrial complex I were decreased and putative complex I assembly intermediates accumulated in the mutant plants. An editing defect, leading to an amino acid change, in the mitochondrial nad4 transcript, encoding for a complex I subunit, was identified. Furthermore, the splicing efficiency of the first intron of nad2, encoding for another complex I subunit, was also decreased. The change in splicing efficiency could however not be linked to any editing defects in the nad2 transcript.