Mitochondrial degeneration in Texas cytoplasmic male-sterile corn anthers

Warmke, H. E.; Lee, Sheu‐Ling Janet

doi:10.1093/oxfordjournals.jhered.a108817

Cited by 125 publications

(62 citation statements)

References 17 publications

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“…Our finding that iar4L iar4 pollen is inviable is in agreement with a previous report that antisense expression of a sugar beet (Beta vulgaris) E1a-subunit in tobacco (Nicotiana tabacum) anther tapetum results in male sterility (Yui et al, 2003). Consistent with a high demand for mitochondrial acetyl-CoA during pollen development, both the number of mitochondria per cell and respiration rates increase significantly during pollen development (Warmke and Lee, 1977;Tadege and Kuhlemeier, 1997). The simplest explanation for the pollen and embryo lethality of iar4L iar4 double mutants is the presumptive lack of mitochondrial PDC activity.…”

Section: Discussionsupporting

confidence: 92%

Arabidopsis IAR4 Modulates Auxin Response by Regulating Auxin Homeostasis

et al. 2009

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In a screen for enhancers of tir1-1 auxin resistance, we identified two novel alleles of the putative mitochondrial pyruvate dehydrogenase E1a-subunit, IAA-Alanine Resistant4 (IAR4). In addition to enhancing the auxin response defects of tir1-1, iar4 single mutants exhibit numerous auxin-related phenotypes including auxin-resistant root growth and reduced lateral root development, as well as defects in primary root growth, root hair initiation, and root hair elongation. Remarkably, all of these iar4 mutant phenotypes were rescued when endogenous indole-3-acetic acid (IAA) levels were increased by growth at high temperature or overexpression of the YUCCA1 IAA biosynthetic enzyme, suggesting that iar4 mutations may alter IAA homeostasis rather than auxin response. Consistent with this possibility, iar4 mutants exhibit increased Aux/IAA stability compared to wild type under basal conditions, but not in response to an auxin treatment. Measurements of free IAA levels detected no significant difference between iar4-3 and wild-type controls. However, we consistently observed significantly higher levels of IAA-amino acid conjugates in the iar4-3 mutant. Furthermore, using stable isotope-labeled IAA precursors, we observed a significant increase in the relative utilization of the Trp-independent IAA biosynthetic pathway in iar4-3. We therefore suggest that the auxin phenotypes of iar4 mutants are the result of altered IAA homeostasis.Auxin regulates numerous aspects of plant development and physiology, including embryogenesis, vascular differentiation, organogenesis, tropic growth, and root and shoot architecture. In a simplified view, auxin biology can be broken down into three general areas: indole-3-acetic acid (IAA) biosynthesis and metabolism, the cell-to-cell transport of IAA, and the SCF TIR1

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Section: Discussionsupporting

confidence: 92%

Arabidopsis IAR4 Modulates Auxin Response by Regulating Auxin Homeostasis

et al. 2009

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“…Most plants were fertile and produced a normal amount of pollen grains, >90% of which were stained by the Alexander (23) The molecular mechanism by which URF13 causes male sterility in the cms-T maize is unknown (3). In male-sterile maize, tapetum mitochondria degenerate soon after meiosis (24). URF13 may impair mitochondrial development, either because the URF13 protein reduces mitochondrial performance, especially during this developmental stage when the demand for energy is high, or because an anther-specific substance interacts with URF13 to disturb mitochondrial activity in the same way as toxin or methomyl (2).…”

Section: Resultsmentioning

confidence: 99%

Targeting the maize T-urf13 product into tobacco mitochondria confers methomyl sensitivity to mitochondrial respiration.

Chaumont

Bernier

Buxant

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

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The URF13 protein, which is encoded by the maize mitochondrial T-urfl3 gene, is thought to be responsible for pathotoxin and methomyl sensitivity and male sterility. We have investigated whether T-ufl3 confers toxin sensitivity and male sterility when expressed in another plant species.The coding sequence of T-urfl3 was fused to a mitochondrial targeting presequence, placed under the control of the cauliflower mosaic virus 35S promoter, and introduced into tobacco byAgrobacterium tumefaciens-mediated transformation.Plants expressing high levels of URF13 were methomyl sensitive. Subcellular analysis indicated that URF13 is mainly associated with the mitochondria. Adding methomyl to isolated mitochondria stimulated NADH-linked respiration and uncoupled oxidative phosphorylation, indicating that URF13 was imported into the mitochondria, and conferred toxin sensitivity. Most control plants, which expressed the T-urfl3 construct lacking the mitochondrial presequence, were methomyl sensitive and contained URF13 in a membrane fraction. Subcellular fractionation by sucrose gradient centrifugation showed that URF13 sedimented at several positions, suggesting the protein is associated with various organelles, including mitochondria. No methomyl effect was observed in isolated mitochondria, however, indicating that URF13 was not imported and did not confer toxin sensitivity to the mitochondria. Thus, URF13 confers toxin sensitivity to transgenic tobacco with or without import into the mitochondria. There was no correlation between the expression of URF13 and male sterility, suggesting either that URF13 does not cause male sterility in transgenic tobacco or that URF13 is not expressed in sufficient amounts in the appropriate anther cells.

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“…In cms-T anthers, degeneration of the tapetum occurs prematurely, beginning at the dyad (Yang, 1989) to the early microspore stages (Warmke and Lee, 1977). Mitochondria in the tapetal cells and middle wall layer show signs of structural disorganization, becoming enlarged with a less dense matrix and more diffuse cristae (Gengenbach et al, 1973;Watrud et al, 1975b;Gregory et al, 1977Gregory et al, , 1978Wannke and Lee, 1977;Yang, 1989).…”

Section: Of the Tapetummentioning

confidence: 99%

The Genetics, Pathology, and Molecular Biology of T-Cytoplasm Male Sterility in Maize

Wise

Bronson

Schnable

et al. 1999

Advances in Agronomy

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This chapter reviews the genetics, pathology, and molecular biology of T-cytoplasm male sterility in maize. The chapter discusses the role of cytoplasmic male sterility systems in facilitating the production of hybrid seeds. The effects of widespread planting of T-cytoplasm maize on the severe 1970 epidemic and effect of a mitochondria1 gene on disease susceptibility and male sterility are discussed. It also discusses the involvement of nuclear cytoplasmic interactions in restoration of cms-T, the perspectives of cms-T researchers, and future directions. In cms-T plants, male sterility is associated with premature breakdown of the mitochondria-rich, tapetal cell layer of the anther; this layer is crucial to pollen production because it supplies nutrients to the developing microspores. In many species, cms is associated with the expression of novel open-reading frames in the mitochondrial genome. The studies provided a foundation for further research that resulted in the cloning of the T-urf13 and Rf2 genes from maize and the ChPKSl gene from C. heterostrophus, and the generation of models for the topology of urf13 in the inner mitochondrial membrane, Rfl-mediated processing of T-urfl3 transcripts, and the evolution of toxin biosynthesis in C. heterostrophus and M. zeae-maydis. Disciplines Agronomy and Crop Sciences | Botany | Plant Breeding and Genetics | Plant Pathology CommentsThis is a chapter from Advances in Agronomy 65 (1999): 79,

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Mitochondrial degeneration in Texas cytoplasmic male-sterile corn anthers

Cited by 125 publications

References 17 publications

Arabidopsis IAR4 Modulates Auxin Response by Regulating Auxin Homeostasis

Arabidopsis IAR4 Modulates Auxin Response by Regulating Auxin Homeostasis

Targeting the maize T-urf13 product into tobacco mitochondria confers methomyl sensitivity to mitochondrial respiration.

The Genetics, Pathology, and Molecular Biology of T-Cytoplasm Male Sterility in Maize

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