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Title

The immune repressor BIR1 contributes to antiviral defense and undergoes transcriptional and post-transcriptional regulation during viral infections

AuthorsGuzmán-Benito, Irene; Donaire, Livia ; Amorim-Silva, Vítor; Vallarino, José G.; Esteban, Alicia; Wierzbicki, Andrzej T.; Ruiz-Ferrer, Virginia; Llave, César
KeywordsAntiviral defense
BAK1
BIR1
Plant innate immunity
Plant viruses
Post-transcriptional silencing
RNA-directed DNA methylation
SOBIR1
Issue Date20-May-2019
PublisherJohn Wiley & Sons
CitationNew Phytologist 224: 421–438 (2019)
AbstractBIR1 is a receptor‐like kinase that functions as a negative regulator of basal immunity and cell death in Arabidopsis.Using Arabidopsis thaliana and Tobacco rattle virus (TRV), we investigate the antiviral role of BIR1, the molecular mechanisms of BIR1 gene expression regulation during viral infections, and the effects of BIR1 overexpression on plant immunity and development.We found that SA acts as a signal molecule for BIR1 activation during infection. Inactivating mutations of BIR1 cause strong antiviral resistance that is not due to constitutive cell death or SA defense priming in the bir1‐1 mutant. RNA‐directed DNA methylation (RdDM) and post‐transcriptional silencing are both required to negatively regulate BIR1 expression upon viral induction. BIR1 overexpression causes severe developmental defects, cell death and premature death that correlate with the constitutive activation of plant immune responses.Our findings suggest that BIR1 acts as a negative regulator of antiviral defense in plants, and indicate that RNA silencing contributes, alone or in conjunction with other regulatory mechanisms, to define a threshold expression for proper BIR1 function beyond which an autoimmune response may occur. This work provides novel mechanistic insights into the regulation of BIR1 homeostasis that may be common for other plant immune components.
Description68 p.-7 fig.-10 fig. supl.-1 tab. supl.
Publisher version (URL)https://doi.org/10.1111/nph.15931
URIhttp://hdl.handle.net/10261/182471
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