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      The Phenotype of the Soybean Disease-Lesion Mimic (dlm) Mutant is Light-Dependentand Associated with Chloroplast Function

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      https://www.riss.kr/link?id=A104495606

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      다국어 초록 (Multilingual Abstract)

      The dlm (disease lesion mimic) mutant of soybean (Glycine max L. Merr) shows the similar lesion of a soybean disease caused by a fungus, Corynespora cassilcola. The lesion was examined at cellular and molecular level. Trypan blue staining result indicated that cell death was detectable in the entire region of leaves excluding veins when the lesions had already been developed. We found that the mesophyll cells of palisade layer in the dlm mutant appeared to be wider apart from each other. The chloroplasts of the dlm mutant cells contained bigger starch granules than those in normal plants. We also found that the lesion development of dlm plant was light-dependent and the starch degradation during the dark period of diurnal cycle was impaired in the mutant. Three soybean pathogenesis- related genes, PR-1a, PR-4, and PR-10, were examined for their expression patterns during the development of disease lesion mimic. The expression of all three genes was up-regulated to some extent upon the appearance of the disease lesion mimic. Although the exact function of DLM protein remains elusive, our data would provide some insight into mechanism
      underling the cell death associated with the dlm mutation.
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      The dlm (disease lesion mimic) mutant of soybean (Glycine max L. Merr) shows the similar lesion of a soybean disease caused by a fungus, Corynespora cassilcola. The lesion was examined at cellular and molecular level. Trypan blue staining result indic...

      The dlm (disease lesion mimic) mutant of soybean (Glycine max L. Merr) shows the similar lesion of a soybean disease caused by a fungus, Corynespora cassilcola. The lesion was examined at cellular and molecular level. Trypan blue staining result indicated that cell death was detectable in the entire region of leaves excluding veins when the lesions had already been developed. We found that the mesophyll cells of palisade layer in the dlm mutant appeared to be wider apart from each other. The chloroplasts of the dlm mutant cells contained bigger starch granules than those in normal plants. We also found that the lesion development of dlm plant was light-dependent and the starch degradation during the dark period of diurnal cycle was impaired in the mutant. Three soybean pathogenesis- related genes, PR-1a, PR-4, and PR-10, were examined for their expression patterns during the development of disease lesion mimic. The expression of all three genes was up-regulated to some extent upon the appearance of the disease lesion mimic. Although the exact function of DLM protein remains elusive, our data would provide some insight into mechanism
      underling the cell death associated with the dlm mutation.

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      참고문헌 (Reference)

      1 "keys for deciphering cell death and defensepathways in plants" 8 : 263-271, 2003

      2 "ed. by J. R. Wilcox pp. 687-727. AmericanSociety of Agronomy"

      3 "and sequence diversity of the Mlo family inplants. J. Biol. Chem. 274" 274 : 34993-35004, 1999

      4 "a novel controlelement of plant pathogen resistance. Cell 88" Diergaarde 88 : 695-705, 1997

      5 "X.1997. The cpr5 mutant of Arabidopsis expresses both NPR1-dependent and NPR1-independent resistance. Plant Cell 9" 9 : 1573-1584, 1997

      6 "X. 1998. UncouplingPR gene expression from NPR1 and bacterial resistance characterization of the dominant Arabidopsis cpr6-1 mutant.Plant Cell 10" 10 : 557-569, 1998

      7 "X. 1994. A mutation in Arabidopsis that leads toconstitutive expression of systemic acquired resistance. PlantCell 6" 1845-1857.

      8 "T. 2001. Adeficiency of coproprophyrinogen III oxidase causes lesionformation in Arabidopsis. Plant J. 27" 27 : 89-99, 2001

      9 "T. 1999. Reactive oxygen intermediates as mediators of programmedcell death in plants and animals. Biochem. Pharmacol.57" 57 : 231-245, 1999

      10 "T. 1999. Molecular characterization of the maizeRp1-D rust resistance haplotype and its mutants. Plant Cell11" 11 : 1365-1376, 1999

      1 "keys for deciphering cell death and defensepathways in plants" 8 : 263-271, 2003

      2 "ed. by J. R. Wilcox pp. 687-727. AmericanSociety of Agronomy"

      3 "and sequence diversity of the Mlo family inplants. J. Biol. Chem. 274" 274 : 34993-35004, 1999

      4 "a novel controlelement of plant pathogen resistance. Cell 88" Diergaarde 88 : 695-705, 1997

      5 "X.1997. The cpr5 mutant of Arabidopsis expresses both NPR1-dependent and NPR1-independent resistance. Plant Cell 9" 9 : 1573-1584, 1997

      6 "X. 1998. UncouplingPR gene expression from NPR1 and bacterial resistance characterization of the dominant Arabidopsis cpr6-1 mutant.Plant Cell 10" 10 : 557-569, 1998

      7 "X. 1994. A mutation in Arabidopsis that leads toconstitutive expression of systemic acquired resistance. PlantCell 6" 1845-1857.

      8 "T. 2001. Adeficiency of coproprophyrinogen III oxidase causes lesionformation in Arabidopsis. Plant J. 27" 27 : 89-99, 2001

      9 "T. 1999. Reactive oxygen intermediates as mediators of programmedcell death in plants and animals. Biochem. Pharmacol.57" 57 : 231-245, 1999

      10 "T. 1999. Molecular characterization of the maizeRp1-D rust resistance haplotype and its mutants. Plant Cell11" 11 : 1365-1376, 1999

      11 "T. 1996. Diseaselesion mimicry caused by mutations in the rust resistance generp1. Plant Cell 8" 8 : 1367-1376, 1996

      12 "S. H. 2001. Recombination between paraloguesat the rp1 rust resistance locus in maize. Genetics158" 158 : 423-438, 2001

      13 "R. W. 2001. Negative regulationof defense responses in plants by a conserved MAPKK kinase.Proc. Natl. Acad. Sci. USA 98" 98 : 373-378, 2001

      14 "P. 2000. Regulators of cell deathin disease resistance. Plant Mol. Biol. 44" 44 : 371-385, 2000

      15 "M. O. 2000. The biochemistry of apoptosis. Nature407" 407 : 770-776, 2000

      16 "J.2002. Knockout of Arabidopsis ACCELERATED-CELLDEATH11encoding a sphingosine transfer protein causesactivation of programmed cell death and defense. Genes Dev.16" 16 : 490-502, 2002

      17 "J.-K. 2005. Polymorphism andexpression of isoflavone synthase genes from soybean cultivars.Mol. Cells. 19" 19 : 67-73, 2005

      18 "J. T.2001. The Arabidopsis-accelerated cell death gene ACD2encodes red chlorophyll catabolite reductase and suppressesthe spread of disease symptoms. Proc. Natl. Acad. Sci. USA98" 98 : 771-776, 2001

      19 "J. T. 1999. The gain-of-function Arabidopsis acd6mutant reveals novel regulation and function of the salicylicacid signaling pathway in controlling cell death" 11 : 1695-1708, 1999

      20 "J. T. 1997. Programmed cell death in plant-pathogeninteractions. Annu. Rev. Plant Physiol. Plant Mol. Biol. 48" 48 : 525-545, 1997

      21 "J. L. 1999. LSD1 regulates salicylic acid induction ofcopper zinc superoxide dismutase in Arabidopsis thaliana.Mol. Plant-Microbe Interact. 12" 12 : 1022-1026, 1999

      22 "J. L. 1996. Initiation of runawaycell death in an Arabidopsis mutant by extracellularsuperoxide. Science 273" 273 : 1996

      23 "J. E. 1998. Inheritance of a disease lesion mimic mutant insoybean. J. Heredity 89" 89 : 363-365, 1998

      24 "J. C. 2004. Pathogenesis-relatedgene expression by specific calmodulin isoforms is dependenton NIM1 a key regulator of systemic acquired resistance.Mol. Cells 18" 18 : 207-213, 2004

      25 "J. 2000. Deficiency infatty acid synthase leads to premature cell death and dramaticalterations in plant morphology. Plant Cell 12" 12 : 405-417, 2000

      26 "J. -K. 2004. Circadian regulation of rice" 17 : 10-16, 2004

      27 "H. W. 1964. An electron microscopestudy of tobacco mosaic virus lesions in Nicotiana glutinosaL. J. Cell Biol. 23" 499-509,

      28 "G. S. 1998. A porphyrinpathway impairment is responsible for the phenotype of adominant disease lesion mimic mutant of maize. Plant Cell10" 10 : 1095-1105, 1998

      29 "G. B. 2004. Molecular mechanismsinvolved in bacterial speck disease resistance of tomato. PlantPathol. J. 20" 20 : 7-12, 2004

      30 "F. M. 2000. Simulationof fungal-mediated cell death by fumonisin B1 andselection of fumonisin B1-resistant" 12 : 2000

      31 "E. J. 2005. Many ways to exit Cell death categories in plants. Trends Plant Sci. 10" 10 : 117-122, 2005

      32 "E. F. 1999. Activated oxygenand free oxygen radicals in pathology" 1999 : 167-178, 37

      33 "E. 1999. Inhibition of protoporphyrinogen oxidaseexpression in Arabidopsis causes a lesion-mimic phenotypethat induces systemic acquired resistance. Plant J. 17" 17 : 667-678, 1999

      34 "D. R. 2000. The “harmless” release of cytochromec. Cell Death Diff. 7" Von Ahsen 7 : 1192-1199, 2000

      35 "B.1998. Defense responses to tetrapyrrole-induced oxidativestress in transgenic plants with reduced uroporphyrinogendecarboxylase or coproporphyrinogen oxidase activity. PlantPhysiol. 116" 116 : 107-116, 1998

      36 "B. 1999. Expression of uroporphyrinogendecarboxylase or coproporphyrinogen oxidase antisense RNAin tobacco induces pathogen defense responses conferringincreased resistance to tobacco mosaic virus. J. Biol. Chem.274" 274 : 4231-4238, 1999

      37 "A. M. 2001. Programmed cell death in development anddefense. Plant Physiol. 125" 125 : 94-97, 2001

      38 "A. J. 1994. The HypersensitiveResponse Reaction in Plants to Pathogens" A Resistance Phenomenon.American Phytopathological Society Press

      39 "A. 2004. The metabolicimbalance underlying lesion formation in Arabidopsis thalianaoverexpressing farnesyl diphosphate synthase leads to oxidative stress and is triggered by the developmentaldecline of endogenous HMGR activity. Planta 219" 219 : 982-992, 2004

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      학술지 이력

      학술지 이력
      연월일 이력구분 이력상세 등재구분
      2023 평가예정 해외DB학술지평가 신청대상 (해외등재 학술지 평가)
      2020-01-01 평가 등재학술지 유지 (해외등재 학술지 평가) KCI등재
      2010-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2008-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2006-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2003-01-01 평가 등재학술지 선정 (등재후보2차) KCI등재
      2000-07-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
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      학술지 인용정보

      학술지 인용정보
      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 1.14 0.32 0.84
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      0.69 0.57 0.477 0.17
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