<i>Potato spindle tuber viroid</i> Strains of Different Pathogenicity Induces and Suppresses Expression of Common and Unique Genes in Infected Tomato

Itaya, Asuka; Matsuda, Yoshie; Gonzales, Robert A.; Nelson, Richard S.; Ding, Biao

doi:10.1094/mpmi.2002.15.10.990

Cited by 116 publications

(107 citation statements)

References 76 publications

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“…Most studies have been limited to analyses of viroid structure and general plant symptoms (Schnölzer et al, 1985;Owens, 1990;Owens et al, 1991Owens et al, , 1995Owens et al, , 1996Hammond, 1992;Schmitz and Riesner, 1998). Changes in the global gene expression patterns of infected plants also have been described (Itaya et al, 2002). In general, however, we have little knowledge of how a specific PSTVd sequence or structure can evoke distinct changes in host gene expression that lead to alterations in specific cellular processes and the development of particular symptoms.…”

Section: S ćmentioning

confidence: 99%

“…The global gene expression pattern in an infected host has been examined by microarray analysis during viral infection (Whitham et al, 2003) and by macroarray analysis during viroid infection (Itaya et al, 2002). In general, there is a lack of understanding of how the altered expression of a partic- The number in each case is the mean Ϯ SE calculated from cell counts obtained from four complete transverse sections of the internode.…”

Section: The Possibility Of Linking Viroid Structure Host Gene Exprementioning

confidence: 99%

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Inhibition of Cell Growth and Shoot Development by a Specific Nucleotide Sequence in a Noncoding Viroid RNA

Qi¹,

Ding²

2003

Plant Cell

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129

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Viroids are small noncoding and infectious RNAs that replicate autonomously and move systemically throughout an infected plant. The RNAs of the family Pospiviroidae contain a central conserved region (CCR) that has long been thought to be involved in replication. Here, we report that the CCR of Potato spindle tuber viroid (PSTVd) also plays a role in pathogenicity. A U257A change in the CCR converted the intermediate strain PSTVd Int to a lethal strain that caused severe growth stunting and premature death of infected plants. PSTVd with nucleotide U257 changed to C or G did not cause such symptoms. The pathogenic effect of the U257A substitution was abolished by a C259U substitution in the same RNA. Analyses of the pathogenic effects of the U257A substitution in three other PSTVd variants established A257 as a new pathogenicity determinant that functions independently and synergistically with the classic pathogenicity domain. The U257A substitution did not alter PSTVd secondary structure, replication levels, or tissue tropism. The stunted growth of PSTVd Int U257A-infected tomato plants resulted from restricted cell expansion but not cell division or differentiation. This was correlated positively with the downregulated expression of an expansin gene, LeExp2 . Our results demonstrate that specific nucleotides in a noncoding, pathogenic RNA have a profound effect in altering distinct cellular responses, which then lead to well-defined alterations in plant growth and developmental patterns. The feasibility of correlating viroid RNA sequence/structure with the altered expression of specific host genes, cellular processes, and developmental patterns makes viroid infection a valuable system in which to investigate host factors for symptom expression and perhaps also to characterize the mechanisms of RNA regulation of gene expression in plants.

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Section: S ćmentioning

confidence: 99%

Section: The Possibility Of Linking Viroid Structure Host Gene Exprementioning

confidence: 99%

Inhibition of Cell Growth and Shoot Development by a Specific Nucleotide Sequence in a Noncoding Viroid RNA

Qi¹,

Ding²

2003

Plant Cell

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129

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“…PSTVd may interact with a double-stranded RNA-activated protein kinase to disturb cellular functions leading to diseases (Diener et al, 1993). Recent studies have demonstrated comprehensive alteration in host gene expression during PSTVd infection (Itaya et al, 2002). Altered expression of certain genes can be linked to specific defects in cellular processes that lead to a particular symptom (Qi and Ding, 2003).…”

Section: Implications Of the Intranuclear Localization Of Viroid Rnasmentioning

confidence: 99%

“…Viroids are self-replicating RNAs that infect plants. They can alter the expression of selective plant genes important to growth and development (Itaya et al, 2002;Qi and Ding, 2003). A viroid genome consists of a single-stranded, covalently closed circular, noncoding, and nonencapsidated RNA, with genome sizes ranging from 275 to 400 nucleotides (Hull, 2002).…”

Section: Introductionmentioning

confidence: 99%

Differential Subnuclear Localization of RNA Strands of Opposite Polarity Derived from an Autonomously Replicating Viroid[W]

Qi¹,

Ding²

2003

The Plant Cell

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The wide variety of RNAs produced in the nucleus must be localized correctly to perform their functions. However, the mechanism of this localization is poorly understood. We report here the differential subnuclear localization of RNA strands of opposite polarity derived from the replicating Potato spindle tuber viroid (PSTVd). During replication, ( ؉ )-and ( ؊ )-strand viroid RNAs are produced. We found that in infected cultured cells and plants, the ( ؊ )-strand RNA was localized in the nucleoplasm, whereas the ( ؉ )-strand RNA was localized in the nucleolus as well as in the nucleoplasm with distinct spatial patterns. Furthermore, the presence of the ( ؉ )-PSTVd in the nucleolus caused the redistribution of a small nucleolar RNA. Our results support a model in which (1) the synthesis of the ( ؊ )-and ( ؉ )-strands of PSTVd RNAs occurs in the nucleoplasm, (2) the ( ؊ )-strand RNA is anchored in the nucleoplasm, and (3) the ( ؉ )-strand RNA is transported selectively into the nucleolus. Our results imply that the eukaryotic cell has a machinery that recognizes and localizes the opposite strands of an RNA, which may have broad ramifications in the RNA regulation of gene expression and the infection cycle of pathogenic RNAs and in the development of RNA-based methods to control gene expression as well as pathogen infection.

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“…Viroid infection, which entails replication and movement, may interfere with the host regulation machinery and induce wide modifications in host gene expression (Itaya et al, 2002) that ultimately lead to the onset of macroscopic symptoms. Although downregulation of a specific tomato (Solanum lycopersicum) gene involved in cell expansion has been correlated with the stunting phenotype induced by severe PSTVd strains (Qi and Ding, 2003a), the primary molecular event has not been identified.…”

Section: Introductionmentioning

confidence: 99%

A Viroid RNA with a Specific Structural Motif Inhibits Chloroplast Development

Rodio¹,

Delgado

Stradis³

et al. 2007

The Plant Cell

101

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Peach latent mosaic viroid (PLMVd) is a chloroplast-replicating RNA that propagates in its natural host, peach (Prunus persica), as a complex mixture of variants, some of which are endowed with specific structural and pathogenic properties. This is the case of variant PC-C40, with an insertion of 12 to 13 nucleotides that folds into a hairpin capped by a U-rich loop, which is responsible for an albino-variegated phenotype known as peach calico (PC). We have applied a combination of ultrastructural, biochemical, and molecular approaches to dissect the pathogenic effects of PC-C40. Albino sectors of leaves infected with variant PC-C40 presented palisade cells that did not completely differentiate into a columnar layer and altered plastids with irregular shape and size and with rudimentary thylakoids, resembling proplastids. Furthermore, impaired processing and accumulation of plastid rRNAs and, consequently, of the plastid translation machinery was observed in the albino sectors of leaves infected with variant PC-C40 but not in the adjacent green areas or in leaves infected by mosaic-inducing or latent variants (including PC-C40D, in which the 12-to 13-nucleotide insertion was deleted). Protein gel blot and RT-PCR analyses showed that the altered plastids support the import of nucleus-encoded proteins, including a chloroplast RNA polymerase, the transcripts of which were detected. RNA gel blot and in situ hybridizations revealed that PLMVd replicates in the albino leaf sectors and that it can invade the shoot apical meristem and induce alterations in proplastids, bypassing the RNA surveillance system that restricts the entry of a nucleus-replicating viroid and most RNA viruses. Therefore, a non-protein-coding RNA with a specific structural motif can interfere with an early step of the chloroplast developmental program, leading ultimately to an albino-variegated phenotype resembling that of certain variegated mutants in which plastid rRNA maturation is also impaired. Our results highlight the potential of viroids for further dissection of RNA trafficking and pathogenesis in plants.

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Potato spindle tuber viroid Strains of Different Pathogenicity Induces and Suppresses Expression of Common and Unique Genes in Infected Tomato

Cited by 116 publications

References 76 publications

Inhibition of Cell Growth and Shoot Development by a Specific Nucleotide Sequence in a Noncoding Viroid RNA

Inhibition of Cell Growth and Shoot Development by a Specific Nucleotide Sequence in a Noncoding Viroid RNA

Differential Subnuclear Localization of RNA Strands of Opposite Polarity Derived from an Autonomously Replicating Viroid[W]

A Viroid RNA with a Specific Structural Motif Inhibits Chloroplast Development

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