Microarray analysis of the interaction between the aphid Rhopalosiphum padi and host plants reveals both differences and similarities between susceptible and partially resistant barley lines

Abstract

The bird cherry-oat aphid (Rhopalosiphum padi L.) is an important pest on cereals causing plant growth reduction without specific leaf symptoms. Breeding of barley (Hordeum vulgare L.) for R. padi resistance shows that there are several resistance genes, reducing aphid growth. To identify candidate sequences for resistance-related genes, we performed microarray analysis of gene expression after aphid infestation in two susceptible and two partially resistant barley genotypes. One of the four lines is a descendant of two of the other genotypes. There were large differences in gene induction between the four lines, indicating substantial variation in response even between closely related genotypes. Genes induced in aphid-infested tissue were mainly related to defence, primary metabolism and signalling. Only 24 genes were induced in all lines, none of them related to oxidative stress or secondary metabolism. Few genes were down-regulated, with none being common to all four lines. There were differences in aphid-induced gene regulation between resistant and susceptible lines. Results from control plants without aphids also revealed differences in constitutive gene expression between the two types of lines. Candidate sequences for induced and constitutive resistance factors have been identified, among them a proteinase inhibitor, a serine/threonine kinase and several thionins.

The constitutive expression and induction of three β-1,3-glucanases by bird cherry-oat aphid in relation to aphid resistance in 15 barley breeding lines

“…This contig was more abundant in S than in R lines in all comparisons where there were significant differences between lines, suggesting that it is related to barley susceptibility to R. padi. Based on previous investigations by Delp et al (2009) using four different barley genotypes, we expected that the expressions of both contig1636_at and contig1639_at would relate to susceptibility. The sequence corresponding to contig1637_s_at was expected to be induced by aphids, but to exhibit no difference between resistant or susceptible lines.…”

“…The sequence corresponding to contig1637_s_at was included as a reference since it was induced by aphids both in R and S genotypes in the previous study by Delp et al (2009). In this work, we also extend the characterization of the barley breeding lines with data concerning aphid host acceptance.…”

“…In a more recent study, we investigated the constitutive expression of putative resistance-related genes in 23 different barley genotypes with varying resistance to R. padi (Mehrabi et al 2014). These genotypes are related to three of the four genotypes in the study by Delp et al (2009). The study showed that the contig1636_at was present in all genotypes, as determined by genomic PCR, but constitutively expressed only in nine genotypes, seven of which are susceptible and two resistant to R. padi (Mehrabi et al 2014).…”

“…To compare the temporal pattern of induction of b-1,3-glucanase transcripts in different genotypes, we calculated the relative induction for each time point: (the average with aphids minus the average without aphids)/the average at t = 0 and used the same criteria as in Delp et al (2009) to determine whether the induction was considered significant or not (Table 3). Contig1636_at was induced by aphids in four out of the five genotypes found to express the sequence constitutively.…”

Benzoxazinoid Metabolites Regulate Innate Immunity against Aphids and Fungi in Maize

“…It is, therefore, plausible that plants with a dysfunctional Bx1 gene can accumulate BX levels from the stress-inducible IGL enzyme. Consequently, the bx1 single mutant is unsuitable to assess the contribution of BXs to resistance against JA-eliciting attackers, such as R. padi and S. turtica (Delp et al, 2009;Erb et al, 2009). We, therefore, created Bx1 wild-type and bx1 mutant plants in the genetic background of a dysfunctional Igl gene.…”