Reactive oxygen species (ROS) play important roles in defence response of host plants versus pathogens. While generation and detoxification of ROS is well understood, how varied ability of different isolates of pathogens to overcome host ROS, or ROS contribution to a particular isolate's pathogenicity, remains largely unexplored. Here, we report that transcriptional regulation of the ROS pathway, in combination with the insulin pathway, increases the pathogenicity of invasive species
Bursaphelenchus xylophilus
. The results showed a positive correlation between fecundity and pathogenicity of different nematode isolates. The virulent isolates from introduced populations in Japan, China and Europe had significantly higher fecundity than native avirulent isolates from the USA. Increased expression of
Mn-SOD
and reduced expression of
catalase
/
GPX-5
and H
2
O
2
accumulation during invasion are associated with virulent strains. Additional H
2
O
2
could improve fecundity of
Bu. xylophilus
. Furthermore, depletion of
Mn-SOD
decreased fecundity and virulence of
Bu. xylophilus
, while the insulin pathway is significantly affected. Thus, we propose that destructive pathogenicity of
Bu. xylophilus
to pines is partly owing to upregulated fecundity modulated by the insulin pathway in association with the ROS pathway and further enhanced by H
2
O
2
oxidative stress. These findings provide a better understanding of pathogenic mechanisms in plant–pathogen interactions and adaptive evolution of invasive species.
This article is part of the theme issue ‘Biotic signalling sheds light on smart pest management’.
Weighing empirical and hypothetical evidence for assessing potential invasive species range limits: a review of the case of Burmese pythons in the USA
