The University of Tokyo · Biochemistry, Genetics and Molecular Biology
Professor Sota Fujii's research lab focuses on the molecular mechanisms underlying mitochondrial-nuclear interactions in flowering plants, with a central emphasis on cytoplasmic male sterility (CMS) and fertility restoration. The lab investigates the role of pentatricopeptide repeat (PPR) proteins in regulating mitochondrial RNA metabolism, particularly in controlling the expression and degradation of CMS-associated mitochondrial genes. Using integrative approaches combining genomics, molecular genetics, and reverse genetics, the lab uncovers evolutionary and functional dynamics of mitochondrial genome rearrangements and their impact on plant fertility and development. Their work provides fundamental insights into organelle-nucleus co-evolution and has significant implications for plant breeding and biotechnology.
Figures are computed from collected data and may differ slightly.
The pentatricopeptide repeat (PPR) is a degenerate 35-amino-acid structural motif identified from analysis of the sequenced genome of the model plant Arabidopsis thaliana. From the wealth of sequence information now available from plant genomes, the PPR protein family is now known to be one of the largest families in angiosperm species, as most genomes encode 400-600 members. As the number of PPR genes is generally only c. 10-20 in other eukaryotic organisms, including green algae, the family ha
Eukaryotic cells have harbored mitochondria for at least 1.5 billion years in an apparently mutually beneficial symbiosis. Studies on the agronomically important crop trait cytoplasmic male sterility (CMS) have suggested the semblance of a host-parasite relationship between the nuclear and mitochondrial genomes, but molecular evidence for this is lacking. Key players in CMS systems are the fertility restorer (Rf) genes required for the development of a functional male gametophyte in plants carry
Conflict/reconciliation between mitochondria and nuclei in plants is manifested by the fate of pollen (viable or nonviable) in the cytoplasmic male sterility (CMS)/fertility restoration (Rf) system. Through positional cloning, we identified a nuclear candidate gene, RETROGRADE-REGULATED MALE STERILITY (RMS) for Rf17, a fertility restorer gene for Chinese wild rice (CW)-type CMS in rice (Oryza sativa L.). RNA interference-mediated gene silencing of RMS restored fertility to a CMS plant, whereas i
Our results demonstrate novel mitochondrial genomic rearrangements that are unique in CMS cytoplasm, and one of the genes that is unique in the CW mitochondrial genome, CW-orf307, appeared to be the candidate most likely responsible for the CW-CMS event. Genomic rearrangements were dynamic in the CMS lines in comparison with those of rice cultivars, suggesting that 'death' and possible 'birth' processes of the CMS genes occurred during the breeding history of rice.
Cytoplasmic male sterility (CMS) is one of the most ideal phenomena known in higher plants to describe the incompatibilities between mitochondrial-nuclear genomic interactions. To elucidate the dependency of pollen development on mitochondrial genotypes and cytoplasmic-nuclear genomic barriers, we employed five CMS isogenic lines of rice, CW-, W11-, LD-, BT- and WA-type CMS lines, that exhibit distinct pollen-defective phenotypes, and we characterized the CMS phenotypes and the nuclear gene expr
Eukaryotes harbor mitochondria obtained via ancient symbiosis events. The successful evolution of energy production in mitochondria has been dependent on the control of mitochondrial gene expression by the nucleus. In flowering plants, the nuclear-encoded pentatricopeptide repeat (PPR) superfamily proteins are widely involved in mitochondrial RNA metabolism. Here, we show that an Arabidopsis nuclear-encoded RNA-binding protein, Restorer-of-fertility-like PPR protein 2 (RFL2), is required for RNA
Pentatricopeptide repeat (PPR) proteins bind RNA and act in multiple eukaryotic processes, including RNA editing, RNA stability, and translation. Here, we investigated the mechanism underlying the functional versatility of Arabidopsis thaliana proton gradient regulation3 (PGR3), a chloroplast protein harboring 27 PPR motifs. Previous studies suggested that PGR3 acts in (1) stabilization of photosynthetic electron transport L (petL) operon RNA, (2) translation of petL, and (3) translation of ndhA
Causes of cytoplasmic male sterility (CMS) in plants have been studied for two decades, and mitochondrial chimeric genes have been predicted to induce CMS. However, it is unclear what happens after CMS-associated proteins accumulate in mitochondria. In our previous study of microarray analysis, we found that 140 genes are aberrantly regulated in anthers of CW-type CMS of rice (Oryza sativa L.). In the present study, we investigated DCW11, one of the down-regulated genes in CW-CMS encoding a prot
OsNek3 (Oryza sativa L. NIMA-related kinase) and DCW11 encoding a mitochondrial putative protein phosphatase 2C were found in our previous microarray study as down-regulated genes in the rice CW-CMS line, which lacked pollen germination ability. Further analysis of DCW11 revealed that DCW11 is strongly correlated with CW-CMS occurrence. Here we show the relationship between OsNek3 and DCW11. OsNek3 was preferentially expressed in mature pollen. A knockout mutant with Tos17 inserted into OsNek3 d
The present study indicated the previously unexpected complexity of plant mitochondrial RNA metabolism. Our transcriptomic data (Oryza sativa Mitochondrial rna Expression Server: OsMES) is publicly accessible at [http://bioinf.mind.meiji.ac.jp/cgi-bin/gbrowse/OsMes/#search].
Selfing is a frequent evolutionary trend in angiosperms, and is a suitable model for studying the recurrent patterns underlying adaptive evolution. Many plants avoid self-fertilization by physiological processes referred to as self-incompatibility (SI). In the Brassicaceae, direct and specific interactions between the male ligand SP11/SCR and the female receptor kinase SRK are required for the SI response. Although Arabidopsis thaliana acquired autogamy through loss of these genes, molecular evo
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