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Loss of ppr3 , ppr4 , ppr6 , or ppr10 perturbs iron homeostasis and leads to apoptotic cell death in Schizosaccharomyces pombe
Author(s) -
Su Yang,
Yang Yanmei,
Huang Ying
Publication year - 2017
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.13978
Subject(s) - pentatricopeptide repeat , schizosaccharomyces pombe , mutant , biology , microbiology and biotechnology , schizosaccharomyces , programmed cell death , mitochondrion , reactive oxygen species , gene , biochemistry , apoptosis , arabidopsis
Pentatricopeptide repeat ( PPR ) proteins characterized by tandem arrays of a degenerate 35‐amino‐acid repeat belong to a large family of RNA ‐binding proteins that are involved in post‐transcriptional control of organelle gene expression. PPR proteins are ubiquitous in eukaryotes, and particularly prevalent in higher plants. Schizosaccharomyces pombe has 10 PPR proteins. Among them, ppr3 , ppr4 , ppr6 , and ppr10 participate in mitochondrial post‐transcriptional processes and are required for mitochondrial electron transport chain ( ETC ) function. In the present work, we showed that deletion of ppr3 , ppr4 , ppr6 , or ppr10 led to apoptotic cell death, as revealed by DAPI and Annexin V‐ FITC staining. These mutants also exhibited elevated levels of reactive oxygen species ( ROS ). RNA sequencing ( RNA ‐seq) and quantitative RT ‐ PCR analyses revealed that deletion of ppr10 affected critical biological processes. In particular, a core set of genes involved in iron uptake and/or iron homeostasis was elevated in the Δ ppr10 mutant, suggesting an elevated level of intracellular iron in the mutant. Consistent with this notion, Δ ppr3 , Δ ppr4 , Δ ppr6 , and Δ ppr10 mutants exhibited increased sensitivity to iron. Furthermore, the iron chelator, bathophenanthroline disulfonic acid, but not the calcium chelator EGTA , nearly restored the viabilities of Δ ppr3 , Δ ppr4 , Δ ppr6 , and Δ ppr10 mutants, and reduced ROS levels in the mutants. These results show for the first time that deletion of a ppr gene leads to perturbation of iron homeostasis. Our results also suggest that disrupted iron homeostasis in Δ ppr3 , Δ ppr4 , Δ ppr6 , and Δ ppr10 mutants may lead to an increase in the level of ROS and induction of apoptotic cell death in S. pombe . Database The RNA ‐seq data have been deposited in the National Center for Biotechnology Information ( NCBI ) BioProject database (accession number SRP091623) and Gene Expression Omnibus ( GEO ) database (accession number GSE90144 ).