Microarray analysis of Etrog citron (Citrus medica L.) reveals changes in chloroplast, cell wall, peroxidase and symporter activities in response to viroid infection

Abstract

Viroids are small (246-401 nucleotides), single-stranded, circular RNA molecules that infect several crop plants and can cause diseases of economic importance. Citrus are the hosts in which the largest number of viroids have been identified. Citrus exocortis viroid (CEVd), the causal agent of citrus exocortis disease, induces considerable losses in citrus crops. Changes in the gene expression profile during the early (pre-symptomatic) and late (post-symptomatic) stages of Etrog citron infected with CEVd were investigated using a citrus cDNA microarray. MaSigPro analysis was performed and, on the basis of gene expression profiles as a function of the time after infection, the differentially expressed genes were classified into five clusters. FatiScan analysis revealed significant enrichment of functional categories for each cluster, indicating that viroid infection triggers important changes in chloroplast, cell wall, peroxidase and symporter activities.

A remarkable synergistic effect at the transcriptomic level in peach fruits doubly infected by prunus necrotic ringspot virus and peach latent mosaic viroid

“…To date, the effects of viroid infection on the host transcriptome have been reported for four viroids. These studies used PCR-based cDNA library subtraction [15]; differential display RT-PCR and quantitative real-time RT-PCR [31,32] or cDNA microarray [17,33] to detect host gene expression changes. Currently, a number of studies explore gene expression changes in virus-infected plants using DNA microarrays.…”

“…These studies reveal a significant impact of the viral/viroidal infection on host gene expression. Among the cellular processes affected upon infection are defense/stress responses, cell wall structure, chloroplast function, hormone signaling, protein metabolism, silencing and diverse other functions [2,5,10-17]. Moreover, infection leads to the modulated expression of various key regulators such as numerous transcription factors, antioxidants, metabolic enzymes and transporters [18].…”

Cytopathic Effects Incited by Viroid RNAs and Putative Underlying Mechanisms

“…Altered accumulation and phosphorylation of host proteins were identified in early studies (for a review see Navarro et al, 2012a), which more recently have been complemented by genome-wide transcriptome analyses (Qi and Ding, 2003; Wang et al, 2011; Owens et al, 2012; Rizza et al, 2012). Although it remains to be conclusively established whether the genes with altered expression are actually involved in symptom elicitation, these studies have supplied interesting information for further dissecting the molecular interplay between viroids and their hosts.…”

“…Some years ago, the stunting and restricted cell wall expansion induced by PSTVd in tomato was correlated to the down-regulation of an expansin gene (LeExp2 ; Qi and Ding, 2003). More recently, genome-wide analyses have shown important transcriptional changes in response to infections by CEVd in Etrog citron (Rizza et al, 2012) and PSTVd in tomato (Owens et al, 2012). Notwithstanding the different viroid-host combinations and experimental designs of these studies, it is worth noting that overexpression of genes coding for proteins involved in cell wall remodeling (i.e., pectinesterases) and down-regulation of genes involved in chloroplast metabolism and biogenesis, were observed in both cases.…”

“…Alternatively, post-translational triggering of signaling cascades by RNA-activated phosphorylation of host proteins has been proposed as the primary event of viroid pathogenesis (Hiddinga et al, 1988; see for a review Owens and Hammond, 2009). In addition to many studies supporting the ability of viroids to modify host gene expression during infection (Conejero et al, 1990; Itaya et al, 2002; Tessitori et al, 2007; Wang et al, 2011; Owens et al, 2012; Rizza et al, 2012; see for a review Owens and Hammond, 2009), other hypotheses based on the interference of viroid RNAs with the plant RNA silencing machinery have been proposed for their pathogenesis in the last few years (see below). Models on how viroids may elicit macroscopic symptoms have been described in previous reviews (Flores et al, 2005; Ding, 2009; Owens and Hammond, 2009; Navarro et al, 2012a).…”