ArticlePlanta2020
The Mitochondrial Iron-Regulated (MIR) gene is Oryza genus specific and evolved before speciation within the Oryza sativa complex.
Article in Planta, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 12 citations in OpenAlex.
- Aluminum Alleviation of Iron Deficiency Chlorosis Is Conserved in Wild Rice RelativePlants (Basel, Switzerland) · 2026Article
- You can't always get as much iron as you want: how rice plants deal with excess of an essential nutrient.Frontiers in plant science · 2024Review
- Bibliometric analysis of the research landscape on rice husks gasification (1995-2019).Environmental science and pollution research international · 2021Review
- Iron Biofortification in Rice: An Update on Quantitative Trait Loci and Candidate Genes.Frontiers in plant science · 2021Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MAIN
conclusionThe MIR gene is not an Oryza sativa orphan gene, but an Oryza genus-specific gene that evolved before AA lineage speciation by a complex origination process. Rice (Oryza sativa L.) is a model species and an economically relevant crop. The Oryza genus comprises 25 species, with genomic data available for several Oryza species, making it a model for genetics and evolution. The Mitochondrial Iron-Regulated (MIR) gene was previously implicated in the O. sativa Fe deficiency response, and was considered an orphan gene present only in rice. Here we show that MIR is also found in other Oryza species that belong to the Oryza sativa complex, which have AA genome type and constitute the primary gene pool for O. sativa breeding. Our data suggest that MIR originated in a stepwise process, in which sequences derived from an exon fragment of the raffinose synthase gene were pseudogenized into non-coding, which in turn originated the MIR gene de novo. All species with a putative functional MIR gene conserve their regulation by Fe deficiency, with the exception of Oryza barthii. In O. barthii, the MIR coding sequence was translocated to a different chromosomal position and separated from its regulatory region, leading to a lack of Fe deficiency responsiveness. Moreover, the MIR co-expression subnetwork cluster in O. sativa is responsive to Fe deficiency, evidencing the importance of the newly originated gene in Fe uptake. This work establishes that MIR is not an orphan gene as previously proposed, but a de novo originated gene within the genus Oryza. We also showed that MIR is undergoing genomic changes in one species (O. barthii), with an impact on Fe deficiency response.
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