Abstract
Leprosis is a serious disease of citrus caused by Citrus leprosis virus C (CiLV-C, genus Cilevirus) whose transmission is mediated by false spider mites of the genus Brevipalpus. CiLV-C infection does not systemically spread in any of its known host plants, thus remaining restricted to local lesions around the feeding sites of viruliferous mites. To get insight into this unusual pathosystem, we evaluated the expression profiles of genes involved in defense mechanisms of Arabidopsis thaliana and Citrus sinensis upon infestation with non-viruliferous and viruliferous mites by using reverse-transcription qPCR. These results were analyzed together with the production of reactive oxygen species (ROS) and the appearance of dead cells as assessed by histochemical assays. After interaction with non-viruliferous mites, plants locally accumulated ROS and triggered the salicylic acid (SA) and jasmonate/ethylene (JA/ET) pathways. ERF branch of the JA/ET pathways was highly activated. In contrast, JA pathway genes were markedly suppressed upon the CiLV-C infection mediated by viruliferous mites. Viral infection also intensified the ROS burst and cell death, and enhanced the expression of genes involved in the RNA silencing mechanism and SA pathway. After 13 days of infestation of two sets of Arabidopsis plants with non-viruliferous and viruliferous mites, the number of mites in the CiLV-C infected Arabidopsis plants was significantly higher than in those infested with the non-viruliferous ones. Oviposition of the viruliferous mites occurred preferentially in the CiLV-C infected leaves. Based on these results, we postulated the first model of plant/Brevipalpus mite/cilevirus interaction in which cells surrounding the feeding sites of viruliferous mites typify the outcome of a hypersensitive-like response, whereas viral infection induces changes in the behavior of its vector.
Highlights
Most of the known plant viruses systemically infect their main plant hosts
This disease reveals an atypical pathosystem in which its etiological agent, Citrus leprosis virus C (CiLV-C), does not systemically spread in the host plants and half of the genes encoded by its genome are considered as orphans since they have no homologs in other viral species (Locali-Fabris et al, 2006; Tautz and Domazet-Lošo, 2011)
To shed light on citrus leprosis pathosystem, we evaluated the transcriptional profiles of marker genes of Arabidopsis defense pathways, reactive oxygen species (ROS) production and the occurrence of cell death upon infestation with either non-viruliferous or CiLV-C viruliferous mites
Summary
Most of the known plant viruses systemically infect their main plant hosts. Distinctively, Citrus leprosis virus C (CiLV-C), the causal agent of citrus leprosis, is unable to move long distances within any of its almost 50 natural or experimental host species belonging to at least 28 distant plant families (León et al, 2008; Nunes et al, 2012a,b; Arena et al, 2013; Garita et al, 2013, 2014). CiLV-C infection invariably produces chlorotic or necrotic lesions around the feeding sites of its mite vector Albeit it shows localized symptoms, citrus leprosis threatens citrus production in the Americas (Roy et al, 2015). Some insect eggs induce high level of SA, leading to a strong reduction of the JA-mediated defenses and, decreasing their interference on the future larva feeding (Little et al, 2007; Bruessow et al, 2010; Gouhier-Darimont et al, 2013; Hilfiker et al, 2014) Extracts from these eggs reduce the MYC protein levels in a SA-dependent manner (Schmiesing et al, 2016). We provide data about CiLV-C inoculation efficiency by the mite and indicate the plant reference genes to be used in the current and future transcriptomic studies involving the citrus leprosis pathosystem
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