Abstract

The heavy metal, cadmium (Cd), has become a new threat to rice production in paddy fields. Cd is absorbed by rice roots and translocated to shoots, where it accumulates in different tissues. Rice is also commonly attacked by insect herbivores, but the effects of low-level Cd exposure on the performance of rice pests and the underlying mechanisms remain unexplored. We investigated brown planthopper (BPH) performance on Cd-exposed rice in the laboratory and field. Low-level Cd exposure did not significantly affect rice growth but decreased hatching rate and extended hatching duration of BPH eggs. No direct toxic effect of low Cd exposure on BPH eggs were found in in vitro developmental rate assays. By transcriptome analysis, a total of 747 rice genes were differentially expressed in Cd-exposed plants under BPH attack. Interestingly, BPH-elicited jasmonate (JA) and phenylpropanoid pathway genes were up-regulated by Cd exposure. Consistently, the levels of JAs and JA-mediated phenylpropanoid derivatives were also increased. Furthermore, Cd exposure did not affect BPH performance on mutant plants impaired in JA biosynthesis ( aoc-2 ) and signaling ( myc2–5 ), suggesting that JA is required to influence BPH performance under Cd exposure. In the field, herbivore populations were reduced on Cd-treated plants compared with control plants. This study revealed that low-level Cd exposure primes JA-mediated defense responses in rice and thereby affects herbivore performance. • Low-level Cd exposure enhanced rice resistance to BPH in the laboratory and field. • BPH-elicited JA and phenylpropanoid levels were primed by low-level Cd exposure. • JA signaling is required for enhanced BPH resistance under Cd exposure.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call