Involvement of S2 episomal sequences in the generation of NCS4 deletion mutation in maize mitochondria

Newton, Kathleen J.; Mariano, Jennifer; Gibson, Carmela M.; Kuzmin, Eugene; Gabay-Laughnan, S.

doi:10.1002/(sici)1520-6408(1996)19:3<277::aid-dvg11>3.0.co;2-x

Cited by 40 publications

(15 citation statements)

References 25 publications

(3 reference statements)

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“…Thus far, a complete deletion of the rpl16 gene in mitochondria has not been isolated, presumably due to its lethality (Newton et al, 1996). In the Arabidopsis maternal distorted leaf mutant, rearrangement in two mitochondrial DNA fragments associated with the rps3-rpl16 polycistron resulted in a deletion of part of the intron and exon b of rps3 that is upstream of rpl16 but without affecting the rpl16 coding region.…”

Section: Abortion Of Emp5-1 Mutant Seed Development Is Caused By Defementioning

confidence: 99%

“…The mutant showed poor growth, distorted rough leaves, and aborted flowering organs (Sakamoto et al, 1996). A deletion of the 59 untranslated region sequences, including the promoter for the transcription unit of the rps3-rpl16 polycistron in maize nonchromosomal stripe3 (ncs3) and ncs4 mutants, caused severe stunted and striped leaves and male fertility, respectively (Hunt and Newton, 1991;Newton et al, 1996). The mRNA abundance corresponding to the rps3/rpll6 coding region was specifically reduced in these mutants.…”

Section: Abortion Of Emp5-1 Mutant Seed Development Is Caused By Defementioning

confidence: 99%

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Empty Pericarp5Encodes a Pentatricopeptide Repeat Protein That Is Required for Mitochondrial RNA Editing and Seed Development in Maize

et al. 2013

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In flowering plants, RNA editing is a posttranscriptional mechanism that converts specific cytidines to uridines in both mitochondrial and plastidial transcripts, altering the information encoded by these genes. Here, we report the molecular characterization of the empty pericarp5 (emp5) mutants in maize (Zea mays). Null mutation of Emp5 results in abortion of embryo and endosperm development at early stages. Emp5 encodes a mitochondrion-targeted DYW subgroup pentatricopeptide repeat (PPR) protein. Analysis of the mitochondrial transcripts revealed that loss of the EMP5 function abolishes the C-to-U editing of ribosomal protein L16 at the rpl16-458 site (100% edited in the wild type), decreases the editing at nine sites in NADH dehydrogenase9 (nad9), cytochrome c oxidase3 (cox3), and ribosomal protein S12 (rps12), and surprisingly increases the editing at five sites of ATP synthase F0 subunit a (atp6), apocytochrome b (cob), nad1, and rpl16. Mutant EMP5-4 lacking the E+ and DYW domains still retains the substrate specificity and editing function, only at reduced efficiency. This suggests that the E+ and DYW domains of EMP5 are not essential to the EMP5 editing function but are necessary for efficiency. Analysis of the ortholog in rice (Oryza sativa) indicates that rice EMP5 has a conserved function in C-to-U editing of the rice mitochondrial rpl16-458 site. EMP5 knockdown expression in transgenics resulted in slow growth and defective seeds. These results demonstrate that Emp5 encodes a PPR-DYW protein that is required for the editing of multiple transcripts in mitochondria, and the editing events, particularly the Cto-U editing at the rpl16-458 site, are critical to the mitochondrial functions and, hence, to seed development in maize.

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Section: Abortion Of Emp5-1 Mutant Seed Development Is Caused By Defementioning

confidence: 99%

Section: Abortion Of Emp5-1 Mutant Seed Development Is Caused By Defementioning

confidence: 99%

Empty Pericarp5Encodes a Pentatricopeptide Repeat Protein That Is Required for Mitochondrial RNA Editing and Seed Development in Maize

et al. 2013

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“…The NCS4 and NCS6 mutations were found in the WF9 nuclear genotype and a fertile revertant maize mitochondrial genotype of the CMS-S group (Lauer et al, 1990;Newton et al, 1996). Although plants carrying the mitochondrial deletions are heteroplasmic, the mutations themselves are exceptionally stable, with no alterations detectable over many years of propagation.…”

Section: Plant Materials and Mitochondrial Isolationmentioning

confidence: 99%

“…NCS5 and NCS6 plants carry different deletions of the 5 Ј end of the cox2 gene, which encodes a subunit of respiratory complex IV (CIV; cytochrome oxidase) (Lauer et al, 1990;Newton et al, 1990). NCS3 and NCS4 are two different deletions of the mitochondrial gene encoding the RPS3 ribosomal protein and are associated with very reduced levels of mitochondrial protein synthesis (Hunt and Newton, 1991;Newton et al, 1996). Another type of plant mitochondrial defect, cytoplasmic male sterility (CMS), causes respiratory failure specifically during pollen development (reviewed by Conley and Hanson, 1995;Schnable and Wise, 1998).…”

Section: Introductionmentioning

confidence: 99%

Differential Expression of Alternative Oxidase Genes in Maize Mitochondrial Mutants

et al. 2002

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We have examined the expression of three alternative oxidase ( aox ) genes in two types of maize mitochondrial mutants. Nonchromosomal stripe (NCS) mutants carry mitochondrial DNA deletions that affect subunits of respiratory complexes and show constitutively defective growth. Cytoplasmic male-sterile (CMS) mutants have mitochondrial DNA rearrangements, but they are impaired for mitochondrial function only during anther development. In contrast to normal plants, which have very low levels of AOX, NCS mutants exhibit high expression of aox genes in all nonphotosynthetic tissues tested. The expression pattern is specific for each type of mitochondrial lesion: the NADH dehydrogenase-defective NCS2 mutant has high expression of aox2 , whereas the cytochrome oxidase-defective NCS6 mutant predominantly expresses aox3 . Similarly, aox2 and aox3 can be induced differentially in normal maize seedlings by specific inhibitors of these two respiratory complexes. Translation-defective NCS4 plants show induction of both aox2 and aox3 . AOX2 and AOX3 proteins differ in their ability to be regulated by reversible dimerization. CMS mutants show relatively high levels of aox2 mRNAs in young tassels but none in ear shoots. Significant expression of aox1 is detected only in NCS and CMS tassels. The induction pattern of maize aox genes could serve as a selective marker for diverse mitochondrial defects.

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“…This literature includes many examples of aberrant recombination induced by tissue culture conditions (Kanazawa et al, 1994) upon alloplasmic substitution, wide hybridization (Kaul, 1988;Dieterich et al, 2003), or spontaneously (Marienfeld and Newton, 1994;Newton et al, 1998). In many of these cases, the genomic rearrangement activity was detected as the induction or loss of cytoplasmic male sterility (CMS).…”

Section: Introductionmentioning

confidence: 99%

Plant Mitochondrial Recombination Surveillance Requires Unusual RecA and MutS Homologs

et al. 2007

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For >20 years, the enigmatic behavior of plant mitochondrial genomes has been well described but not well understood. Chimeric genes appear, and occasionally are differentially replicated or expressed, with significant effects on plant phenotype, most notably on male fertility, yet the mechanisms of DNA replication, chimera formation, and recombination have remained elusive. Using mutations in two important genes of mitochondrial DNA metabolism, we have observed reproducible asymmetric recombination events occurring at specific locations in the mitochondrial genome. Based on these experiments and existing models of double-strand break repair, we propose a model for plant mitochondrial DNA replication, chimeric gene formation, and the illegitimate recombination events that lead to stoichiometric changes. We also address the physiological and developmental effects of aberrant events in mitochondrial genome maintenance, showing that mitochondrial genome rearrangements, when controlled, influence plant reproduction, but when uncontrolled, lead to aberrant growth phenotypes and dramatic reduction of the cell cycle.

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Involvement of S2 episomal sequences in the generation of NCS4 deletion mutation in maize mitochondria

Cited by 40 publications

References 25 publications

Empty Pericarp5Encodes a Pentatricopeptide Repeat Protein That Is Required for Mitochondrial RNA Editing and Seed Development in Maize

Empty Pericarp5Encodes a Pentatricopeptide Repeat Protein That Is Required for Mitochondrial RNA Editing and Seed Development in Maize

Differential Expression of Alternative Oxidase Genes in Maize Mitochondrial Mutants

Plant Mitochondrial Recombination Surveillance Requires Unusual RecA and MutS Homologs

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