<jats:sec><jats:label /><jats:p>Pentatricopeptide repeat (<jats:styled-content style="fixed-case">PPR</jats:styled-content>) proteins characterized by tandem arrays of a degenerate 35‐amino‐acid repeat belong to a large family of <jats:styled-content style="fixed-case">RNA</jats:styled-content>‐binding proteins that are involved in post‐transcriptional control of organelle gene expression. <jats:styled-content style="fixed-case">PPR</jats:styled-content> proteins are ubiquitous in eukaryotes, and particularly prevalent in higher plants. <jats:italic>Schizosaccharomyces pombe</jats:italic> has 10 <jats:styled-content style="fixed-case">PPR</jats:styled-content> proteins. Among them, <jats:italic>ppr3</jats:italic>,<jats:italic> ppr4</jats:italic>,<jats:italic> ppr6</jats:italic>, and <jats:italic>ppr10</jats:italic> participate in mitochondrial post‐transcriptional processes and are required for mitochondrial electron transport chain (<jats:styled-content style="fixed-case">ETC</jats:styled-content>) function. In the present work, we showed that deletion of <jats:italic>ppr3</jats:italic>,<jats:italic> ppr4</jats:italic>,<jats:italic> ppr6</jats:italic>, or <jats:italic>ppr10</jats:italic> led to apoptotic cell death, as revealed by <jats:styled-content style="fixed-case">DAPI</jats:styled-content> and Annexin V‐<jats:styled-content style="fixed-case">FITC</jats:styled-content> staining. These mutants also exhibited elevated levels of reactive oxygen species (<jats:styled-content style="fixed-case">ROS</jats:styled-content>). <jats:styled-content style="fixed-case">RNA</jats:styled-content> sequencing (<jats:styled-content style="fixed-case">RNA</jats:styled-content>‐seq) and quantitative <jats:styled-content style="fixed-case">RT</jats:styled-content>‐<jats:styled-content style="fixed-case">PCR</jats:styled-content> analyses revealed that deletion of <jats:italic>ppr10</jats:italic> affected critical biological processes. In particular, a core set of genes involved in iron uptake and/or iron homeostasis was elevated in the Δ<jats:italic>ppr10</jats:italic> mutant, suggesting an elevated level of intracellular iron in the mutant. Consistent with this notion, Δ<jats:italic>ppr3</jats:italic>, Δ<jats:italic>ppr4</jats:italic>, Δ<jats:italic>ppr6</jats:italic>, and Δ<jats:italic>ppr10</jats:italic> mutants exhibited increased sensitivity to iron. Furthermore, the iron chelator, bathophenanthroline disulfonic acid, but not the calcium chelator <jats:styled-content style="fixed-case">EGTA</jats:styled-content>, nearly restored the viabilities of Δ<jats:italic>ppr3</jats:italic>, Δ<jats:italic>ppr4</jats:italic>, Δ<jats:italic>ppr6</jats:italic>, and Δ<jats:italic>ppr10</jats:italic> mutants, and reduced <jats:styled-content style="fixed-case">ROS</jats:styled-content> levels in the mutants. These results show for the first time that deletion of a <jats:italic>ppr</jats:italic> gene leads to perturbation of iron homeostasis. Our results also suggest that disrupted iron homeostasis in Δ<jats:italic>ppr3</jats:italic>, Δ<jats:italic>ppr4</jats:italic>, Δ<jats:italic>ppr6</jats:italic>, and Δ<jats:italic>ppr10</jats:italic> mutants may lead to an increase in the level of <jats:styled-content style="fixed-case">ROS</jats:styled-content> and induction of apoptotic cell death in <jats:italic>S. pombe</jats:italic>.</jats:p></jats:sec><jats:sec><jats:title>Database</jats:title><jats:p>The <jats:styled-content style="fixed-case">RNA</jats:styled-content>‐seq data have been deposited in the National Center for Biotechnology Information (<jats:styled-content style="fixed-case">NCBI</jats:styled-content>) BioProject database (accession number SRP091623) and Gene Expression Omnibus (<jats:styled-content style="fixed-case">GEO</jats:styled-content>) database (accession number <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE90144">GSE90144</jats:ext-link>).</jats:p></jats:sec>