Mitochondrial RNA editing truncates a chimeric open reading frame associated with S male-sterility in maize

Crosses between Triticum timopheevi, as maternal donor, and T. aestivum can lead to cytoplasmic male sterile (cms) plants. The T. timopheevi derived mitochondrial DNA from parental, cms, and fertility-restored lines differs from that of T. aestivum derived mtDNA in the coxI gene region. Our previous results for cms lines showed that there is an open reading frame, orf256, upstream from coxI in T. timopheevi derived mtDNA that is not present in T. aestivum DNA. The 5′ flanking region and the first 33 nucleotides of the coding region of orf256 are identical to the corresponding region of T. aestivum coxI, whereas the rest of orf256, including the 3′ flank, is not related to coxI. Also, the organization of orf256 and coxI on a HindIII fragment from T. timopheevi derived mtDNA are identical in T. timopheevi, cms, and fertility-restored lines. We now report that the DNA sequence of orf256 is identical in T. timopheevi, cms, and fertility-restored lines. Major transcripts in cms and fertility-restored lines encode both orf256 and coxI with 5′ termini like coxI mRNA of T. aestivum, whereas parental mitochondria from T. timopheevi have major transcripts with 5′ termini within the orf256 coding region. Mitochondria from cms and fertility-restored lines have the potential to produce a protein that would not be present in parental T. timopheevi or in T. aestivum.Key words: cytoplasmic male sterility, wheat, mitochondrial DNA, mitochondrial RNA, coxI.

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Mitochondrial Dual-coding Genes in Trypanosoma brucei

10.1101/187732 ◽

2017 ◽

Author(s):

Laura E. Kirby ◽

Donna Koslowsky

Keyword(s):

Trypanosoma Brucei ◽

Rna Editing ◽

Genetic Drift ◽

Mitochondrial Genes ◽

Open Reading Frame ◽

Dual Coding ◽

Mutational Bias ◽

Reading Frame ◽

African Trypanosomes ◽

Reading Frames

AbstractTrypanosoma brucei is transmitted between mammalian hosts by the tsetse fly. In the mammal, they are exclusively extracellular, continuously replicating within the bloodstream. During this stage, the mitochondrion lacks a functional electron transport chain (ETC). Successful transition to the fly, requires activation of the ETC and ATP synthesis via oxidative phosphorylation. This life cycle leads to a major problem: in the bloodstream, the mitochondrial genes are not under selection and are subject to genetic drift that endangers their integrity. Exacerbating this, T. brucei undergoes repeated population bottlenecks as they evade the host immune system that would create additional forces of genetic drift. These parasites possess several unique genetic features, including RNA editing of mitochondrial transcripts. RNA editing creates open reading frames by the guided insertion and deletion of U-residues within the mRNA. A major question in the field has been why this metabolically expensive system of RNA editing would evolve and persist. Here, we show that many of the edited mRNAs can alter the choice of start codon and the open reading frame by alternative editing of the 5’ end. Analyses of mutational bias indicate that six of the mitochondrial genes may be dual-coding and that RNA editing allows access to both reading frames. We hypothesize that dual-coding genes can protect genetic information by essentially hiding a non-selected gene within one that remains under selection. Thus, the complex RNA editing system found in the mitochondria of trypanosomes provides a unique molecular strategy to combat genetic drift in non-selective conditions.Author SummaryIn African trypanosomes, many of the mitochondrial mRNAs require extensive RNA editing before they can be translated. During this process, each edited transcript can undergo hundreds of cleavage/ligation events as U-residues are inserted or deleted to generate a translatable open reading frame. A major paradox has been why this incredibly metabolically expensive process would evolve and persist. In this work, we show that many of the mitochondrial genes in trypanosomes are dual-coding, utilizing different reading frames to potentially produce two very different proteins. Access to both reading frames is made possible by alternative editing of the 5’ end of the transcript. We hypothesize that dual-coding genes may work to protect the mitochondrial genes from mutations during growth in the mammalian host, when many of the mitochondrial genes are not being used. Thus, the complex RNA editing system may be maintained because it provides a unique molecular strategy to combat genetic drift.

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