Biology subjects

Ostersetzer-Biran, O.

Publications and source records attributed to Ostersetzer-Biran, O..

3 recordsLinked to original sources

bioRxiv2025

The mitochondrial splicing factor PPR9 encoded by the AT1G03560 gene-locus is essential for the maturation of several nad transcripts in Arabidopsis plants

The biogenesis of plant mitochondria and their respiratory machinery relies on the transcription and proper processing of primary transcripts into functional, mature organellar RNAs. This includes the removal of introns that reside within many essential organellar genes, an essential step in mitochondria gene-expression that relies on the coordinated action of nuclear-encoded RNA-binding cofactors, such as members of the pentatricopeptide repeat (PPR) protein family. Here, we report the analysis of PPR9 (At1g03560), a mitochondrial P-type PPR protein originally identified in genetic screens for essential protein cofactors. Loss of PPR9 function results in embryonic arrest at early stages of seed development. Nevertheless, homozygous ppr9 mutants can be maintained using a modified embryo-rescue method. The rescued ppr9 mutants display delayed germination and growth retardation associated with mitochondrial dysfunctions. Molecular analyses of ppr9 plantlets reveal that PPR9 is required for the splicing of several mitochondrial transcripts encoding respiratory subunits, including nad2 intron 3 and nad7 introns 1 and 2. Accordingly, defects in the processing of nad2 and nad7 pre-RNAs in ppr9 mutant plantlets impair the biogenesis of respiratory complex I (CI), disrupt OXPHOS activity, and consequently affect plants growth and development. Together, these findings identify PPR9 as a key regulator of mt-RNA maturation in Arabidopsis, enabling CI biogenesis and cellular energy metabolism, and further highlight the roles of nuclear-encoded RNA-processing factors in coordinating mitochondria functions and (early) plant growth and development. Significance statementOur study identifies PPR9 as a key mitochondrial RNA-processing factor required for the splicing of multiple group II introns that reside within genes encoding subunits essential for respiratory complex I biogenesis in Arabidopsis. By linking nuclear control of RNA maturation to mitochondrial function and plant development, this work emphasizes a critical layer of coordination between organellar gene expression, energy metabolism, and developmental regulation in land plants.

plant biology↗

bioRxiv2020

nMAT3 is an essential maturase splicing factor required for holo-complex I biogenesis and embryo-development in Arabidopsis thaliana plants

Group II introns are large catalytic RNAs that are particularly prevalent in the organelles of terrestrial plants. In angiosperm mitochondria, group II introns reside in the coding-regions of many critical genes, and their excision is essential for respiratory-mediated functions. Canonical group II introns are self-splicing and mobile genetic elements, consisting of the catalytic intron-RNA and its cognate intron-encoded endonuclease factor (i.e. maturase, Pfam-PF01348). Plant organellar introns are extremely degenerate, and lack many regions that are critical for splicing, including their related maturase-ORFs. The high degeneracy of plant mitochondrial introns was accompanied during evolution by the acquisition of host-acting protein cofactors. These include several nuclear encoded maturases (nMATs) and various other splicing-cofactors that belong to a diverse set of RNA-binding families, e.g. RNA helicases (Pfam-PF00910), Mitochondrial Transcription Termination Factors (mTERF, Pfam-PF02536), Plant Organelle RNA Recognition (PORR, Pfam-PF11955), and Pentatricopeptide repeat (PPR, Pfam-PF13812) proteins. Previously, we established the roles of MatR and three nuclear-maturases, nMAT1, nMAT2, and nMAT4, in the splicing of different subsets of mitochondrial introns in Arabidopsis. The function of nMAT3 (AT5G04050) was found to be essential during early embryogenesis. Using a modified embryo-rescue method, we show that nMAT3-knockout plants are strongly affected in the splicing of nad1 introns i1, i3 and i4 in Arabidopsis mitochondria. The embryo-defect phenotype is tightly associated with complex I biogenesis defects. Functional complementation of nMAT3 restored the splicing defects and altered embryogenesis phenotypes associated with the nmat3 mutant-line.

plant biology↗

bioRxiv2019

Astaxanthin extends lifespan via altered biogenesis of the mitochondrial respiratory chain complex III

Astaxanthin is a keto-carotenoid produced in some bacteria and algae, which has very important industrial applications (i.e., in cosmetics, coloring additive in aquaculture and as a dietary supplement for human). Here, we analyzed the molecular basis of Astaxanthin-mediated prolongevity in the model organism, Caenorhabditis elegans. The increased lifespan effects of Astaxanthin are restricted in C. elegans to the adult phase and are uninfluenced by various other carotenoids tested. Genetic analyses indicated that the Astaxanthin-mediated life-extension relies on mitochondria activity, via the Rieske iron-sulfur polypeptide-1 (ISP-1), but is not influenced by the functions of other known longevity-related gene-loci, including CLK-1, DAF-2, DAT-16, EAT-2, GAS-1 GLP-1 or MEV-1. Biochemical analyses of native respiratory complexes showed that Astaxanthin affects the biogenesis of holo-complex III (and likely supercomplex I+III, as well). Effects on holo-CIII assembly and activity were also indicated by in-vitro assays, with mitochondria isolated from worms, rodents, human and plants, which were treated with Astaxanthin. These data indicated a cross-species effect on the oxidative phosphorylation (OXPHOS) machinery by the carotenoid, and provide with further insights into the molecular mechanism of animals longevity extension by Astaxanthin.\n\nSignificance StatementAstaxanthin is a widely consumed pigment by animals and human. In this study we find that Astaxanthin, but not other tested carotenoids, significantly extends the lifespan of animals by affecting respiratory complex III (CIII) biogenesis of the mitochondria, in plants, C. elegans, rodents and human. We further propose a model to try explaining this effect of astaxanthin on animals longevity.

developmental biology↗