[1]Arase S, Zhao C M, Akimitsu K, Yamamoto M, Ichii M. 2000. A recessive lesion mimic mutant of rice with elevated resistance to fungal pathogens. Journal of General Plant Pathology, 66, 109-116[2]Balague C, Lin B, Alcon C, Flottes G, Malmstrom S, Kohler C, Neuhaus G, Pelletier G, Gaymard F, et al. 2003. HLM1, an essential signaling component in the hypersensitive response, is a member of the cyclic nucleotide-gated channel ion channel family. The Plant Cell, 15, 365-379[3]Brodersen P, Petersen M, Pike H M, Olszak B, Skov S, Odum N, Jorgensen L B, Brown R E, Mundy J. 2002. Knockout of Arabidopsis accelerated-cell-death 11 encoding a sphingosine transfer protein causes activation of programmed cell death and defense. Genes and Development, 16, 490-502[4]Buschges R, Hollricher K, Panstruga R, Simons G, Wolter M, Frijters A, Daelen R V, Lee T V D, Diergaarde P, Groenendijk J, et al. 1997. The barley Mlo gene: A novel control element of plant pathogen resistance. Cell, 88, 695-705[5]Chen X F, Hao L, Pan J W, Zheng X X, Jiang G H, Jin Y, Gu Z M, Qian Q, Zhai W X, Ma B J. 2012. SPL5, a cell death and defense-related gene, encodes a putative splicing factor 3b subunit 3 (SF3b3) in rice. Molecular Breeding, 30, 339-349[6]Dangl J L, Dietrich R A, Richberg M H. 1996. Death don’t have no mercy: Cell death programs in plant-microbe interactions. The Plant Cell, 8, 1793-1807[7]Dietrich R A, Delaney T P, Uknes S J, Ward E R, Ryals J A, Dangl J L. 1994. Arabidopsis mutants simulating disease resistance response. Cell, 77, 565-577[8]Dietrich R A, Richberg M H, Schmidt R, Dean C, Dangl J L. 1997. A novel zinc finger protein is encoded by the Arabidopsis LSD1 gene and functions as a negative regulator of plant cell death. Cell, 88, 685-694[9]Greenberg J T. 1997. Programmed cell death in plant- pathogen interactions. Annual Review of Plant Physiology and Plant Molecular Biology, 48, 525-545[10]Gray J, Close P S, Briggs S P, Johal G S. 1997. A novel suppressor of cell death in plants encoded by the Lls1 gene of maize. Cell, 89, 25-31[11]Gray J, Janick-Buckner D, Buckner B, Close P S, Johal G S. 2002. Light-dependent death of maize lls1 cells is mediated by mature chloroplasts. Plant Physiology, 30, 1894-1907[12]Greenberg J T, Ausubel F M. 1993. Arabidopsis mutants compromised for the control of cellular damage during pathogenesis and aging. The Plant Journal, 4, 327-341[13]Hoisington D A, Neuffer M G, Walbot V. 1982. Disease lesion mimics in maize: 1. Effect of genetic background, temperature, developmental age, and wounding on necrotic spot formation with Les1. Developmental Biology, 93, 381-388[14]Hu G, Yalpani N, Briggs S P, Johal G S. 1998. A porphyrin pathway impairment is responsible for the phenotype of a dominant disease lesion mimic mutant of maize. The Plant Cell, 10, 1095-1106[15]Huang L, Sun Q, Qin F, Li C, Zhao Y, Zhou D X. 2007. Down-regulation of a SILENT INFORMATION REGULATOR2-related histone deacetylase gene, OsSRT1, induces DNA fragmentation and cell death in rice. Plant Physiology, 144, 1508-1519[16]Huang Q N, Shi Y F, Yang Y, Feng B H, Wei Y L, Chen J, Baraoidan M, Leung H, Wu J L. 2011. Characterization and genetic analysis of a light- and temperature-sensitive spotted-leaf mutant in rice. Journal of Integrative Plant Biology, 53, 671-681[17]Huang Q N, Yang Y, Shi Y F, Chen J, Wu J L. 2010. Spotted-leaf mutants of rice (Oryza sativa). Rice Science, 17, 247-256[18]Ishikawa A, Okamoto H, Iwasaki Y, Asahi T. 2001. A deficiency of coproprophyrinogen III oxidase causes lesion formation in Arabidopsis. The Plant Journal, 27, 89-99[19]Jung Y H, Lee J H, Agrawal G K, Rakwal R, Kim J A, Shim J K, Lee S K, Jeon J S, Koh H J, Lee Y H, et al. 2005. The rice (Oryza sativa) blast lesion mimic mutant, blm, may confer resistance to blast pathogens by triggering multiple defense-associated signaling pathways. Plant Physiology and Biochemistry, 43, 397-406[20]Kachroo A, Venugopal S C, Lapchyk L, Falcone D, Hildebrand D, Kachroo P. 2004. Oleic acid levels regulated by glycerolipid metabolism modulate defense gene expression in Arabidopsis. Proceedings of the National Academy of Sciences of the United States of America, 101, 5152-5157[21]Kauffman H E, Reddy A P K, Hsieh, S P V, Merca S D. 1973. An improved technique for evaluating resistance of rice varieties to Xanthomonas oryzae. Plant Disease Report, 57, 537-541[22]Kiyosawa S. 1970. Inheritance of a particular sensitivity of the rice variety, Sekiguchi-Asahi, to pathogens and chemicals, and linkage relationship with blast resistance. Bulletin of the National Institute of Agricultural Sciences (Japanese Series D Physiology and Genetics), 21, 61-71[23]Lin A H, Wang Y Q, Tang J Y, Xue P, Li C L, Liu L C, Hu B, Yang F Q, Loake G J, Chu C C, et al. 2012. Nitric oxide and protein S-nitrosylation are integral to hydrogen peroxide-induced leaf cell death in rice. Plant Physiology, 158, 451-464[24]Liu G, Wang L, Zhou H, Leung H, Wang G L, He C. 2004. Physical mapping of a rice lesion mimic gene, Spl1, to a 70-kb segment of rice chromosome 12. Molecular Genetics and Genomics, 272, 108-115[25]Lorrain S, Lin B, Auriac M C, Kroj T, Saindrenan P, Nicole M, Balague C, Roby D. 2004. Vascular associated death1, a novel GRAM domain-containing protein, is a regulator of cell death and defense responses in vascular tissues. The Plant Cell, 16, 2217-2232[26]Lu Y J, Zheng K L. 1992. A simple method for isolation of rice DNA. Chinese Journal of Rice Science, 6, 47-48[27](in Chinese) Lyngkjaer M F, Newton A C, Atzema J L, Baker S J. 2000. The barley mlo-gene: An important powdery mildew resistance source. Agronomie, 20, 745-756[28]Mizobuchi R, Hirabayashi H, Kaji R, Nishizawa Y, Yoshimura A, Satoh H, Ogawa T, Okamoto M. 2002. Isolation and characterization of rice lesion-mimic mutants with enhanced resistance to rice blast and bacterial blight. Plant Science, 163, 345-353[29]Mori M, Tomita C, Sugimoto K, Hasegawa M, Hayashi N, Dubouzet J G, Ochiai H, Sekimoto H, Hirochika H, Kikuchi S. 2007. Isolation and molecular characterization of a Spotted leaf 18 mutant by modified activation-tagging in rice. Plant Molecular Biology, 63, 847-860[30]Mou Z L, He Y K, Dai Y, Liu X F, Li J Y. 2000. Deficiency in fatty acid synthase leads to premature cell death and dramatic alterations in plant morphology. The Plant Cell, 12, 405-417[31]Qiao Y L, Jiang W Z, Lee J H, Park B S, Choi M S, Piao R, Woo M O, Roh J H, Han L Z, Paek N C, et al. 2010. Spl28 encodes a clathrin-associated adaptor protein complex 1, medium subunit μ1(AP1M1) and is responsible for spotted leaf and early senescence in rice (Oryza sativa). New Phytologist, 185, 258-274[32]Shi Y F, Chen J, Liu W Q, Huang Q N, Shen B, Leung H, Wu J L. 2009. Genetic analysis and gene mapping of a new rolled leaf gene in rice (Oryza sativa L.). Science in China (Series C Life Sciences), 52, 885-890[33]Sun C H, Liu L C, Tang J Y, Lin A H, Zhang F T, Fang J, Zhang G F, Chu C C. 2011. RLIN1, encoding a putative coproporphyrinogen Ⅲ oxidase, is involved in lesion initiation in rice. Journal of Genetics and Genomics, 38, 29-37[34]Takahashi A, Agrawal G K, Yamazaki M, Onosato K, Miyao A, Kawasaki T, Shimamoto K, Hirochika H. 2007. Rice Pti1a negatively regulates RAR1-dependent defense responses. The Plant Cell, 19, 2940-2951[35]Tang J Y, Zhu X D, Wang Y Q, Liu L C, Xu B, Li F, Fang J, Chu C C. 2011. Semi-dominant mutations in the CC-NB- LRR-type R gene, NLS1, lead to constitutive activation of defense responses in rice. The Plant Journal, 66, 996- 1007. Thordal-Christensen H, Zhang Z G, Wei Y D, Collinge D B. 1997. Subcellular localization of H2O2 in plant. H2O2 accumlation in papillae and hypersensitive response during the barley-powdery mildew interaction. The Plant Journal, 11, 1187-1194[36]Tong X H, Qi J F, Zhu X D, Mao B Z, Zeng L J, Wang B H, Li Q, Zhou G X, Xu X J, Lou Y G, et al. 2012. The rice hydroperoxide lyase OsHPL3 functions in defense responses by modulating the oxylipin pathway. The Plant Journal, 71, 763-775[37]Walbot V, Hoisington D A, Neuffer M G. 1983. Disease lesion mimics in maize. In: Kosuge T, Meredith C eds., Genetic Engineering of Plants. Plenum, New York. pp. 431-442[38]Wang L J, Pei Z Y, Tian Y C, He C Z. 2005. OsLSD1, a rice zinc finger protein, regulates programmed cell death and callus differentiation. Molecular Plant-Microbe Interactions, 18, 375-384[39]Wang Z H, Jia Y L. 2006. Induction and preliminary analysis of a rice lesion mimic mutant lmm1. Journal of Nuclear Agricultural Sciences, 20, 255-258[40](in Chinese) Wu C J, Bordeos A, Madamba M R S, Baraoidan M, Ramos M, Wang G L, Leach J E, Leung H. 2008. Rice lesion mimic mutants with enhanced resistance to diseases. Molecular Genetics and Genomics, 279, 605-619[41]Wu J L, Wu C J, Lei C L, Baraoidan M, Bordeos A, Madamba M R S, Ramos-Pamplona M, Mauleon R, Portugal A, Ulat V J, et al. 2005. Chemical- and irradiation-induced mutants of indica rice IR64 for forward and reverse genetics. Plant Molecular Biology, 59, 85-97[42]Yamanouchi U, Yano M, Lin H, Ashikari M, Yamada K. 2002. A rice spotted leaf gene, Spl7, encodes a heat stress transcription factor protein. Proceedings of the National Academy of Sciences of the United States of America, 99, 7530-7535[43]Yin Z C, Chen J, Zeng L R, Goh M L, Leung H, Khush G, Wang G L. 2000. Characterizing rice lesion mimic mutants and identifying a mutant with broad-spectrum resistance to rice blast and bacterial blight. Molecular Plant-Microbe Interactions, 13, 869-876[44]Zeng L R, Qu S H, Bordeos A, Yang C W, Baraoidan M, Yan H Y, Xie Q, Nahm B H, Leung H, Wang G L. 2004. Spotted leaf 11, a negative regulator of plant cell death and defence, encodes a U-box/armadillo repeat protein endowed with E3 ubiquitin ligase activity. The Plant Cell, 16, 2795-2808 |