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Registro Completo |
Biblioteca(s): |
Embrapa Milho e Sorgo. |
Data corrente: |
27/03/2000 |
Data da última atualização: |
09/06/2018 |
Tipo da produção científica: |
Resumo em Anais de Congresso |
Autoria: |
PACCOLA-MEIRELLES, L.D.; CASELA, C. R.; FERREIRA, A. S.; MEIRELLES, W. F.; MARRIEL, I. E. |
Afiliação: |
WALTER FERNANDES MEIRELLES, CNPMS; IVANILDO EVODIO MARRIEL, CNPMS. |
Título: |
Detecção e identificação de uma bactéria associada a mancha foliar por Phaeosphaeria em milho. |
Ano de publicação: |
1999 |
Fonte/Imprenta: |
Fitopatologia Brasileira, Brasília, v. 24, p. 314-315, ago. 1999. Suplemento. |
Idioma: |
Português |
Notas: |
Edição dos resumos do 32º Congresso Brasileiro de Fitopatologia, Curitiba, 1999. |
Conteúdo: |
x |
Palavras-Chave: |
Disease; Identification; Maize. |
Thesagro: |
Bactéria; Doença; Identificação; Mancha Foliar; Milho; Phaeosphaeria Maydis; Zea Mays. |
Categoria do assunto: |
H Saúde e Patologia |
URL: |
https://ainfo.cnptia.embrapa.br/digital/bitstream/item/41025/1/Deteccao-identificacao.pdf
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Marc: |
LEADER 00919nam a2200289 a 4500 001 1483558 005 2018-06-09 008 1999 bl uuuu u00u1 u #d 100 1 $aPACCOLA-MEIRELLES, L.D. 245 $aDetecção e identificação de uma bactéria associada a mancha foliar por Phaeosphaeria em milho.$h[electronic resource] 260 $aFitopatologia Brasileira, Brasília, v. 24, p. 314-315, ago. 1999. Suplemento.$c1999 500 $aEdição dos resumos do 32º Congresso Brasileiro de Fitopatologia, Curitiba, 1999. 520 $ax 650 $aBactéria 650 $aDoença 650 $aIdentificação 650 $aMancha Foliar 650 $aMilho 650 $aPhaeosphaeria Maydis 650 $aZea Mays 653 $aDisease 653 $aIdentification 653 $aMaize 700 1 $aCASELA, C. R. 700 1 $aFERREIRA, A. S. 700 1 $aMEIRELLES, W. F. 700 1 $aMARRIEL, I. E.
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Embrapa Milho e Sorgo (CNPMS) |
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| Acesso ao texto completo restrito à biblioteca da Embrapa Mandioca e Fruticultura. Para informações adicionais entre em contato com cnpmf.biblioteca@embrapa.br. |
Registro Completo
Biblioteca(s): |
Embrapa Mandioca e Fruticultura. |
Data corrente: |
25/08/2020 |
Data da última atualização: |
25/08/2020 |
Tipo da produção científica: |
Artigo em Periódico Indexado |
Circulação/Nível: |
A - 1 |
Autoria: |
ARENA, G. D.; RAMOS-GONZALEZ, P. L.; FALK, B. W.; CASTEEL, C. L.; ASTUA, J. de F.; MACHADO, M. A. |
Afiliação: |
GABRIELLA D. ARENA, Centro de Citricultura Sylvio Moreira; PEDRO LUIS RAMOS-GONZALEZ, Instituto Biológico; BRYCE W. FALK, University of California; CLARE L. CASTEEL, CASTEEL; JULIANA DE FREITAS ASTUA, CNPMF; MARCOS A. MACHADO, Centro de Citricultura Sylvio Moreira. |
Título: |
Plant immune system activation upon Citrus Leprosis Virus c infection is mimicked by the ectopic expression of the P61 viral protein. |
Ano de publicação: |
2020 |
Fonte/Imprenta: |
Frontiers in Plant Science, August, 2020. |
Idioma: |
Inglês |
Conteúdo: |
Citrus leprosis virus C (CiLV-C, genus Cilevirus, family Kitaviridae) is an atypical virus that does not spread systemically in its plant hosts. Upon its inoculation by Brevipalpus mites, only localized lesions occur, and the infection remains limited to cells around mite feeding sites. Here, we aimed to gain insights into the putative causes of viral unfitness in plants by expanding the limited knowledge of the molecular mechanisms underlying plant/kitavirid interactions. Firstly, we quantified the CiLV-C viral RNAs during the infection in Arabidopsis thaliana plants using RT-qPCR and systematized it by defining three stages of distinguishing subgenomic and genomic RNA accumulation: i) 0–24 h after infestation, ii) 2–4 days after infestation (dai), and iii) 6–10 dai. Accordingly, the global plant response to CiLV-C infection was assessed by RNA-Seq at each period. Results indicated a progressive reprogramming of the plant transcriptome in parallel to the increasing viral loads. Gene ontology enrichment analysis revealed the induction of cell growth-related processes at the early stages of the infection and the triggering of the SA-mediated pathway, ROS burst and hypersensitive response (HR) at the presymptomatic stage. Conversely, infected plants downregulated JA/ET-mediated pathways and processes involved in the primary metabolism including photosynthesis. Marker genes of unfolded protein response were also induced, suggesting a contribution of the endoplasmic reticulum stress to the cell death caused by the viral infection. Finally, we transiently expressed CiLV-C proteins in Nicotiana benthamiana plants to undertake their roles in the elicited plant responses. Expression of the CiLV-C P61 protein consistently triggered ROS burst, upregulated SA- and HR-related genes, increased SA levels, reduced JA levels, and caused cell death. Mimicry of responses typically observed during CiLV-C–plant interaction indicates P61 as a putative viral effector causing the HR-like symptoms associated with the infection. Our data strengthen the hypothesis that symptoms of CiLV-C infection might be the outcome of a hypersensitive-like response during an incompatible interaction. Consequently, the locally restricted infection of CiLV-C, commonly observed across infections by kitavirids, supports the thesis that these viruses, likely arising from an ancestral arthropod-infecting virus, are unable to fully circumvent plant defenses. MenosCitrus leprosis virus C (CiLV-C, genus Cilevirus, family Kitaviridae) is an atypical virus that does not spread systemically in its plant hosts. Upon its inoculation by Brevipalpus mites, only localized lesions occur, and the infection remains limited to cells around mite feeding sites. Here, we aimed to gain insights into the putative causes of viral unfitness in plants by expanding the limited knowledge of the molecular mechanisms underlying plant/kitavirid interactions. Firstly, we quantified the CiLV-C viral RNAs during the infection in Arabidopsis thaliana plants using RT-qPCR and systematized it by defining three stages of distinguishing subgenomic and genomic RNA accumulation: i) 0–24 h after infestation, ii) 2–4 days after infestation (dai), and iii) 6–10 dai. Accordingly, the global plant response to CiLV-C infection was assessed by RNA-Seq at each period. Results indicated a progressive reprogramming of the plant transcriptome in parallel to the increasing viral loads. Gene ontology enrichment analysis revealed the induction of cell growth-related processes at the early stages of the infection and the triggering of the SA-mediated pathway, ROS burst and hypersensitive response (HR) at the presymptomatic stage. Conversely, infected plants downregulated JA/ET-mediated pathways and processes involved in the primary metabolism including photosynthesis. Marker genes of unfolded protein response were also induced, suggesting a contribution of the endoplasmic reticulum st... Mostrar Tudo |
Thesagro: |
Fruta Cítrica. |
Categoria do assunto: |
-- |
Marc: |
LEADER 03074naa a2200193 a 4500 001 2124551 005 2020-08-25 008 2020 bl uuuu u00u1 u #d 100 1 $aARENA, G. D. 245 $aPlant immune system activation upon Citrus Leprosis Virus c infection is mimicked by the ectopic expression of the P61 viral protein.$h[electronic resource] 260 $c2020 520 $aCitrus leprosis virus C (CiLV-C, genus Cilevirus, family Kitaviridae) is an atypical virus that does not spread systemically in its plant hosts. Upon its inoculation by Brevipalpus mites, only localized lesions occur, and the infection remains limited to cells around mite feeding sites. Here, we aimed to gain insights into the putative causes of viral unfitness in plants by expanding the limited knowledge of the molecular mechanisms underlying plant/kitavirid interactions. Firstly, we quantified the CiLV-C viral RNAs during the infection in Arabidopsis thaliana plants using RT-qPCR and systematized it by defining three stages of distinguishing subgenomic and genomic RNA accumulation: i) 0–24 h after infestation, ii) 2–4 days after infestation (dai), and iii) 6–10 dai. Accordingly, the global plant response to CiLV-C infection was assessed by RNA-Seq at each period. Results indicated a progressive reprogramming of the plant transcriptome in parallel to the increasing viral loads. Gene ontology enrichment analysis revealed the induction of cell growth-related processes at the early stages of the infection and the triggering of the SA-mediated pathway, ROS burst and hypersensitive response (HR) at the presymptomatic stage. Conversely, infected plants downregulated JA/ET-mediated pathways and processes involved in the primary metabolism including photosynthesis. Marker genes of unfolded protein response were also induced, suggesting a contribution of the endoplasmic reticulum stress to the cell death caused by the viral infection. Finally, we transiently expressed CiLV-C proteins in Nicotiana benthamiana plants to undertake their roles in the elicited plant responses. Expression of the CiLV-C P61 protein consistently triggered ROS burst, upregulated SA- and HR-related genes, increased SA levels, reduced JA levels, and caused cell death. Mimicry of responses typically observed during CiLV-C–plant interaction indicates P61 as a putative viral effector causing the HR-like symptoms associated with the infection. Our data strengthen the hypothesis that symptoms of CiLV-C infection might be the outcome of a hypersensitive-like response during an incompatible interaction. Consequently, the locally restricted infection of CiLV-C, commonly observed across infections by kitavirids, supports the thesis that these viruses, likely arising from an ancestral arthropod-infecting virus, are unable to fully circumvent plant defenses. 650 $aFruta Cítrica 700 1 $aRAMOS-GONZALEZ, P. L. 700 1 $aFALK, B. W. 700 1 $aCASTEEL, C. L. 700 1 $aASTUA, J. de F. 700 1 $aMACHADO, M. A. 773 $tFrontiers in Plant Science, August, 2020.
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