Abstract
ABSTRACT Late blight in potato caused by Phytophthora infestans remains a major impediment to potato growers worldwide. Utilization of regulators that affect defence may augment control measures to achieve a basal defence against late blight. This work examines the effect of over-expressing the transcription factor StZFP2 in potato on P. infestans infection. StZFP2 is induced upon infestation by chewing insects such as Manduca sexta and the pathogen P. infestans. StZFP2 was transformed into potato under the control of the CaMV 35S promoter. Three over-expressing lines (OE-StZFP2) resulted in significantly lower lesion size five days after infection (DAI). The increased expression of StZFP2 slowed the spread of infection at 5DAI. Levels of StZFP2 and classic pathogen response marker genes, StPR-1b and StPR-2 were significantly lower in more resistant lines, suggesting that OE-StZFP2 affects this pathogen response.
Highlights
Late blight caused by Phytophthora infestans, responsible for the Irish potato famine remains a major disease threat to potatoes, the fourth most important food crop worldwide
To confirm that StZFP2 was affected by late blight infection in potato, detached leaflets from Kennebec were inoculated with P. infestans (US11) as described in the material and methods, harvested after 3DAI and snap frozen in liquid nitrogen
StZFP1 is the first Q-type ZFP described in potato and Tian et al (2010) showed that it was induced by P. infestans infection
Summary
Late blight caused by Phytophthora infestans, responsible for the Irish potato famine remains a major disease threat to potatoes, the fourth most important food crop worldwide. Attacking both tomato and potato, it ranks as the number one plant-pathogenic oomycete (Kamoun et al 2015). An additional aspect of defense signaling is detection of damage to plant cells, through damage-associated molecular patterns (DAMP). This can occur in conjunction with insect feeding, pathogen attack or through a mechanical non-biotic wound. DAMPs have their own unique DAMP receptors that activate expression of wound-responsive genes (for current reviews Gust et al 2017; Ranf 2017)
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