scholarly journals Simultaneous Downregulation of MTHFR and COMT in Switchgrass Affects Plant Performance and Induces Lesion-Mimic Cell Death

2017 ◽  
Vol 8 ◽  
Author(s):  
Sijia Liu ◽  
Chunxiang Fu ◽  
Jiqing Gou ◽  
Liang Sun ◽  
David Huhman ◽  
...  
Keyword(s):  
Cell Death ◽  
Plant Performance ◽  
Lesion Mimic

scholarly journals Uncoupled Expression of Nuclear and Plastid Photosynthesis-Associated Genes Contributes to Cell Death in a Lesion Mimic Mutant

2019 ◽  
Vol 31 (1) ◽  
pp. 210-230 ◽  
Author(s):  
Ruiqing Lv ◽  
Zihao Li ◽  
Mengping Li ◽  
Vivek Dogra ◽  
Shanshan Lv ◽  
...  
Keyword(s):  
Cell Death ◽  
Lesion Mimic ◽  
Lesion Mimic Mutant

scholarly journals LMM24 Encodes Receptor-Like Cytoplasmic Kinase 109, Which Regulates Cell Death and Defense Responses in Rice

2019 ◽  
Vol 20 (13) ◽  
pp. 3243 ◽  
Author(s):  
Yue Zhang ◽  
Qunen Liu ◽  
Yingxin Zhang ◽  
Yuyu Chen ◽  
Ning Yu ◽  
...  
Keyword(s):  
Cell Death ◽  
Molecular Mechanisms ◽  
Indica Rice ◽  
Defense Responses ◽  
Rice Cultivar ◽  
Histochemical Staining ◽  
Lesion Mimic ◽  
Ros Accumulation ◽  
Mutant Pool ◽  
Defense Response Genes

Lesion mimic mutants are excellent models for research on molecular mechanisms of cell death and defense responses in rice. We identified a new rice lesion mimic mutant lmm24 from a mutant pool of indica rice cultivar “ZhongHui8015”. The LMM24 gene was identified by MutMap, and LMM24 was confirmed as a receptor-like cytoplasmic kinase 109 by amino acid sequence analysis. The lmm24 mutant displayed dark brown lesions in leaves and growth retardation that were not observed in wild-type ZH8015. The results of histochemical staining and TUNEL assays showed enhanced ROS accumulation and cell death in lmm24. Chloroplast degradation was observed in lmm24 leaves, with decreased expression of photosynthesis-related genes and increased expression of the senescence-induced STAYGREEN (SGR) gene and other senescence-associated genes. Furthermore, lmm24 exhibited enhanced resistance to rice blast fungus Magnaporthe oryzae (M. oryzae) and up-regulation of defense response genes. Our data demonstrate that LMM24 regulates cell death and defense responses in rice.

Proteomics Analysis of Rice Lesion Mimic Mutant (spl1) Reveals Tightly Localized Probenazole-Induced Protein (PBZ1) in Cells Undergoing Programmed Cell Death

2008 ◽  
Vol 7 (4) ◽  
pp. 1750-1760 ◽  
Author(s):  
Sun Tae Kim ◽  
Sang Gon Kim ◽  
Young Hyun Kang ◽  
Yiming Wang ◽  
Jae-Yean Kim ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Proteomics Analysis ◽  
Lesion Mimic ◽  
Lesion Mimic Mutant ◽  
In Cells

scholarly journals Mutation Types of CYP71P1 Cause Different Phenotypes of Mosaic Spot Lesion and Premature Leaf Senescence in Rice

2021 ◽  
Vol 12 ◽  
Author(s):  
Yuhan Zheng ◽  
Jiangmin Xu ◽  
Fujun Wang ◽  
Yongchao Tang ◽  
Zheng Wei ◽  
...  
Keyword(s):  
Cell Death ◽  
Indica Rice ◽  
Photosynthetic Pigment ◽  
Single Amino Acid ◽  
Blue Staining ◽  
Premature Senescence ◽  
Lesion Mimic ◽  
Expression Of Genes ◽  
Single Amino Acid Change ◽  
Regulated Expression

Lesion mimic mutants (LMMs) are ideal materials for studying programmed cell death and defense response in plants. Here we report investigations on two LMMs (msl-1 and msl-2) from the indica rice cultivar JG30 treated by ethyl methyl sulfone. Both of the mutants showed similar mosaic spot lesions at seedling stage, but they displayed different phenotypes along with development of the plants. At tillering stage, larger orange spots appeared on leaves of msl-2, while only small reddish-brown spots exhibit on leaves of msl-1. At heading stage, the msl-2 plants were completely dead, while the msl-1 plants were still alive even if showed apparent premature senility. For both the mutants, the mosaic spot lesion formation was induced by light; DAB and trypan blue staining showed a large amount of hydrogen peroxide accumulated at the lesion sites, accompanied by a large number of cell death. Consequently, reactive oxygen species were enriched in leaves of the mutants; SOD and CAT activities in the scavenging enzyme system were decreased compared with the wild type. In addition, degraded chloroplasts, decreased photosynthetic pigment content, down-regulated expression of genes associated with chloroplast synthesis/photosynthesis and up-regulated expression of genes related to senescence were detected in the mutants, but the abnormality of msl-2 was more serious than that of msl-1 in general. Genetic analysis and map-based cloning revealed that the lesion mimic and premature senescence traits of both the mutants were controlled by recessive mutated alleles of the SL (Sekiguchi lesion) gene, which encodes the CYP71P1 protein belonging to cytochrome P450 monooxygenase family. The difference of mutation sites and mutation types (SNP-caused single amino acid change and SNP-caused early termination of translation) led to the different phenotypes in severity between msl-1 and msl-2. Taken together, this work revealed that the CYP71P1 is involved in regulation of both premature senescence and cell death in rice, and its different mutation sites and mutation types could cause different phenotypes in terms of severity.

A major suppressor of cell death, slm1, modifies the expression of the maize (Zea mays L.) lesion mimic mutation les23

Genome ◽  
2004 ◽  
Vol 47 (5) ◽  
pp. 961-969 ◽  
Author(s):  
Bryan W Penning ◽  
Gurmukh S Johal ◽  
Michael D McMullen
Keyword(s):  
Cell Death ◽  
Quantitative Trait ◽  
Chromosome 2 ◽  
Genetic Modifiers ◽  
Lesion Mimic ◽  
Cell Death Pathway ◽  
Delayed Initiation ◽  
Significant Locus ◽  
Trait Locus ◽  
Lesion Severity

Disease lesion mimics provide an excellent biological system to study the genetic basis of cell death in plants. Many lesion mimics show variation in phenotype expression in different genetic backgrounds. Our goal was to identify quantitative trait loci (QTL) modifying lesion mimic expression thereby identifying genetic modifiers of cell death. A recessive lesion mimic, les23, in a severe-expressing line was crossed to the maize inbred line Mo20W, a lesion-suppressing line, and an F2 population was developed for QTL analysis. In addition to locating les23 to the short arm of chromosome 2, this analysis detected significant loci for modification of lesion expression. One highly significant locus was found on the long arm of chromosome 2. The Mo20W allele at this QTL significantly delayed initiation of the lesion phenotype and decreased the final lesion severity. Other QTL with lesser effect affected severity of lesion expression without affecting lesion initiation date. Our results demonstrate that dramatic change in lesion phenotype can be controlled by a single major QTL. The presumed function of this QTL in normal plants is to regulate some aspect of the cell death pathway underlying the les23 phenotype.Key words: genetic background, quantitative trait locus, phenotype suppression, Mo20W, corn.

scholarly journals SPL36 Encodes a Receptor-like Protein Kinase that Regulates Programmed Cell Death and Defense Responses in Rice

Rice ◽  
2021 ◽  
Vol 14 (1) ◽  
Author(s):  
R. A. O. Yuchun ◽  
J. I. A. O. Ran ◽  
W. A. N. G. Sheng ◽  
W. U. Xianmei ◽  
Y. E. Hanfei ◽  
...  
Keyword(s):  
Cell Death ◽  
Salt Stress ◽  
Protein Kinase ◽  
Programmed Cell Death ◽  
Stress Responses ◽  
Defense Responses ◽  
Base Substitution ◽  
Wild Type ◽  
Salt Stress Response ◽  
Lesion Mimic

AbstractLesion mimic mutants spontaneously produce disease spots in the absence of biotic or abiotic stresses. Analyzing lesion mimic mutants’ sheds light on the mechanisms underlying programmed cell death and defense-related responses in plants. Here, we isolated and characterized the rice (Oryza sativa) spotted leaf 36 (spl36) mutant, which was identified from an ethyl methanesulfonate-mutagenized japonica cultivar Yundao population. spl36 displayed spontaneous cell death and enhanced resistance to rice bacterial pathogens. Gene expression analysis suggested that spl36 functions in the disease response by upregulating the expression of defense-related genes. Physiological and biochemical experiments indicated that more cell death occurred in spl36 than the wild type and that plant growth and development were affected in this mutant. We isolated SPL36 by map-based cloning. A single base substitution was detected in spl36, which results in a cysteine-to-arginine substitution in SPL36. SPL36 is predicted to encode a receptor-like protein kinase containing leucine-rich domains that may be involved in stress responses in rice. spl36 was more sensitive to salt stress than the wild type, suggesting that SPL36 also negatively regulates the salt-stress response. These findings suggest that SPL36 regulates the disease resistance response in rice by affecting the expression of defense- and stress-related genes.

scholarly journals Golgi anti-apoptotic proteins are evolutionarily conserved ion channels that regulate cell death in plants

2019 ◽  
Author(s):  
Maija Sierla ◽  
David L. Prole ◽  
Nuno Saraiva ◽  
Guia Carrara ◽  
Natalia Dinischiotu ◽  
...  
Keyword(s):  
Cell Death ◽  
Ion Channels ◽  
Programmed Cell Death ◽  
Stress Responses ◽  
Fluorescent Protein ◽  
Yellow Fluorescent Protein ◽  
Lesion Mimic ◽  
Evolutionarily Conserved ◽  
Apoptotic Proteins ◽  
Regulate Cell Death

ABSTRACTProgrammed cell death regulates developmental and stress responses in eukaryotes. Golgi anti-apoptotic proteins (GAAPs) are evolutionarily conserved cell death regulators. Human and viral GAAPs inhibit apoptosis and modulate intracellular Ca2+fluxes, and viral GAAPs form cation-selective channels. Although most mammalian cell death regulators are not conserved at the sequence level in plants, the GAAP gene family shows expansion, with five paralogues (AtGAAP1-5) in the Arabidopsis genome. We pursued molecular and physiological characterization of AtGAAPs making use of the advanced knowledge of their human and viral counterparts. Structural modeling of AtGAAPs predicted the presence of a channel-like pore, and electrophysiological recordings from purified AtGAAP3 reconstituted into lipid bilayers confirmed that plant GAAPs can function as ion channels. AtGAAP1 and AtGAAP4 localized exclusively to the Golgi within the plant cell, while AtGAAP2, AtGAAP3 and AtGAAP5 also showed tonoplastic localization. Gene expression analysis revealed differential spatial expression and abundance of transcript forAtGAAPparalogues in Arabidopsis tissues. We demonstrate that AtGAAP1-5 inhibit Bax-induced cell death in yeast. However, overexpression of AtGAAP1 induces cell death inNicotiana benthamianaleaves and lesion mimic phenotype in Arabidopsis. We propose that AtGAAPs function as Golgi-localized ion channels that regulate cell death by affecting ionic homeostasis within the cell.HighlightArabidopsis Golgi anti-apoptotic proteins (GAAPs) share functional conservation with their human and viral counterparts in cell death regulation and ion channel activityAbbreviationsAtGAAP,Arabidopsis thalianaGAAP; BI-1, Bax inhibitor-1; CFP, cyan fluorescent protein; CMLV, camelpox virus; ER, Endoplasmic reticulum; GAAP, Golgi anti-apoptotic protein; GFP, green fluorescent protein; hGAAP, human GAAP; LFG, Lifeguard; LMM, lesion mimic mutant; PCD, programmed cell death; TMBIM, transmembrane Bax inhibitor-1 motif-containing; TMDs, transmembrane domains; vGAAP, viral GAAP; YFP, yellow fluorescent protein

Overexpression of SGR Results in Oxidative Stress and Lesion-mimic Cell Death in Rice Seedlings

2011 ◽  
Vol 53 (5) ◽  
pp. 375-387 ◽  
Author(s):  
Huawu Jiang ◽  
Yaping Chen ◽  
Meiru Li ◽  
Xinglan Xu ◽  
Guojiang Wu
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Rice Seedlings ◽  
Lesion Mimic

scholarly journals Ethylene Is One of the Key Elements for Cell Death and Defense Response Control in the Arabidopsis Lesion Mimic Mutant vad1

2007 ◽  
Vol 145 (2) ◽  
pp. 465-477 ◽  
Author(s):  
Olivier Bouchez ◽  
Carine Huard ◽  
Séverine Lorrain ◽  
Dominique Roby ◽  
Claudine Balagué
Keyword(s):  
Cell Death ◽  
Defense Response ◽  
Response Control ◽  
Lesion Mimic ◽  
Lesion Mimic Mutant
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