4.6 Article

Capsicum annuum basic transcription factor 3 (CaBtf3) regulates transcription of pathogenesis-related genes during hypersensitive response upon Tobacco mosaic virus infection

期刊

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2011.12.074

关键词

Hypersensitive response (HR); Nascent polypeptide-associated complex (NAC); Tobacco mosaic virus (TMV)-P-o; Virus-induced gene silencing (VIGS); Capsicum annuum basic transcription factor 3 (CaBtf3)

资金

  1. Science Research Center-Engineering Research Center (Plant Signaling Network Research Center) of the Ministry of Education, Science and Technology [R11-2003-008-02001-0]
  2. National Research Foundation
  3. MEST [2009-0085565]
  4. Rural Development Administration, Republic of Korea [PJ007850]
  5. National Research Foundation of Korea [2009-0085565, 과C6A2204] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

向作者/读者索取更多资源

Hypersensitive response (HR) cell death upon plant virus infection is an excellent plant strategy for inhibiting viral movement and obtaining systemic acquired resistance (SAR) against further infection. Various host factors are involved in these HR processes, either directly as viral resistance proteins or indirectly. We characterized a gene encoding the CaBtf3 [beta-nascent polypeptide-associated complex (NAC) subunit] of NAC from the hot pepper plant. NAC contacts nascent polypeptides to prevent aggregation and degradation of newly synthesized proteins by controlling cotranslational protein folding. CaBtf3 protein fused to green fluorescent protein predominantly localized to the nucleus. Silencing phenotype of CaBtf3 upon the Tobacco mosaic virus (TMV)-P-o inoculation exhibited reduced HR cell death and decreased expression of some HR-associated genes, but increased TMV coat protein levels compared with TRV2 control plants. Furthermore, silencing of NbBtf3, a highly homologous gene of CaBtf3, also led to the reduced Bax- and Pto-mediated cell death. The results indicate that CaBtf3 might be involved in HR cell death and could function as a transcription factor in the nucleus by transcriptional regulation of HR-related gene expression. (C) 2011 Elsevier Inc. All rights reserved.

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