Nicotiana benthamiana exportin 1 is required for elicitor-induced phytoalexin production, cell death induction, and resistance against potato late blight pathogen Phytophthora infestans
The oomycete Phytophthora infestans is the causal agent of potato late blight, one of the most devastating pathogens for potato. To investigate the plant mechanisms for resistance against P. infestans , the Solanaceae model plant Nicotiana benthamiana was employed in this study. Previously, we repor...
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Veröffentlicht in: | Journal of general plant pathology : JGPP 2019-09, Vol.85 (5), p.347-355 |
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Sprache: | eng |
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Zusammenfassung: | The oomycete
Phytophthora infestans
is the causal agent of potato late blight, one of the most devastating pathogens for potato. To investigate the plant mechanisms for resistance against
P. infestans
, the Solanaceae model plant
Nicotiana benthamiana
was employed in this study. Previously, we reported that NbNup75, a nuclear pore complex protein, is required for the resistance against
P. infestans
, suggesting that nuclear-pore-mediated transport is involved in the induction of defense responses. In this study, we investigated the role of
N. benthamiana
exportin 1
NbXpo1
in disease resistance. Mammalian and yeast exportin 1 proteins are known as a regulator for nuclear-pore-mediated export of proteins and RNAs.
NbXpo1
-silenced
N. benthamiana
showed minor growth defects and significantly decreased resistance to
P. infestans
. Gene silencing of
NbXpo1
compromised defense responses induced by the elicitor INF1 (a secretory protein of
P. infestans
), such as production of the phytoalexin capsidiol and induction of cell death. In
NbXpo1
-silenced plants, the genes for capsidiol biosynthesis,
NbEAS
, and defense-related MAP kinase,
NbWIPK
, were significantly downregulated, while genes encoding the plant defensin,
NbPDF
, and anti-microbial protein thionin,
NbTHI
, were upregulated. These results indicate that
N. benthamiana
Xpo1 is involved in activating a specific group of defense-related genes. |
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ISSN: | 1345-2630 1610-739X |
DOI: | 10.1007/s10327-019-00855-9 |