Overexpression of BBF3 encoding a tobacco Dof transcription factor alters gene expression and cell death induction during N-mediated hypersensitivity to tobacco mosaic virus.

Autor: Suzuki, Taiga, Fujita, Mayu, Suzuki, Mio, Shigeta, Kaori, Nelson, Richard S., Matsushita, Yasuhiko, Sasaki, Nobumitsu
Předmět:
Zdroj: Journal of General Plant Pathology; Jan2024, Vol. 90 Issue 1, p2-13, 12p
Abstrakt: Dof (DNA binding with one finger) proteins are plant-specific transcription factors involved in gene regulation during abiotic and biotic stresses. Our previous studies suggested that tobacco Dof proteins, including BBF3, can upregulate the expression of the virus resistance N gene as well as resistance-related genes. In this study, we generated and characterized transgenic tobacco lines carrying the N gene that overexpressed BBF3 cDNA constitutively. In the absence of virus challenge, the BBF3 overexpression caused no developmental defects and no changes in the N transcript level, although the transcript levels of some defense-related genes were affected compared with levels in non-transgenic plants. TMV infection induced a hypersensitive reaction (HR) with larger necrotic lesions in transgenic lines than in non-transgenic plants, but there was no change in total virus accumulation per lesion in a standardized area. Activation of the N gene expression in non-transgenic plants during synchronously-induced HR was followed by downregulation of BBF3 gene expression. Constitutive overexpression of the BBF3 transgene resulted in higher accumulation of the N gene as well as HR marker genes (Hin1 and Hsr203j) and lower accumulation of salicylic acid- and jasmonic acid-signaling marker genes (PR1-a and PR-1b). In particular, the expression of PR-1b was remarkably suppressed in the BBF3-overexpressing transgenic lines. Dof-binding motifs were confirmed in the upstream regions of all target genes examined. Our results suggest that BBF3 has a role in modulating the expression of genes associated with virus elicitor recognition and defense responses resulting in larger areas of HR-associated cell death. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index
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