Mechanism of viroid pathogenesis: Differential activation of the interferon-induced, double-stranded RNA-activated, Mr 68 000 protein kinase by viroid strains of varying pathogenicity

Diener, T.O.; Hammond, Rosemarie W.; Black, T.; Katze, Michael G.

doi:10.1016/0300-9084(93)90058-z

Cited by 53 publications

(31 citation statements)

References 32 publications

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“…This implies that the highly structured viroid RNA or replicative intermediates may interact with selected host factors to regulate replicative processes and symptom development. Recently, Diener et al (1993) found that the mPKR is capable of being activated by viroid strains in a manner directly related to their ability to incite severe disease symptoms. These data, together with the observation that pPKR phosphorylation levels are induced during viroid infection , support a possible role for pPKR in pathogenesis.…”

Section: Discussionmentioning

confidence: 99%

Identification of a Plant-Encoded Analog of PKR, the Mammalian Double-Stranded RNA-Dependent Protein Kinase

Langland¹,

Jin²,

Jacobs³

et al. 1995

Plant Physiol.

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Plant virus or viroid infection stimulates the phosphorylation of a plant-encoded protein of M, 68,000 to 70,000 (now termed pPKR) that is associated with double-stranded RNA-stimulated protein kinase activity. Using various biochemical and immunological comparisons, we have demonstrated that this plant protein is an analog of the mammalian PKR enzymes. pPKR is both cytosolic and ribosome associated, similar to mammalian PKR, and appears to be capable of phosphorylating exogenous histones. Monoclonal antiserum to the human PKR as well as antiserum to a conserved double-stranded RNA-binding domain present on mammalian PKR demonstrated cross-reactivity with pPKR. Likewise, polyclonal antiserum to the pPKR detected the mouse and human PKR in western blot analysis. Northern blot analysis of a mammalian PKR cDNA detected a specific 2.5-kb transcript present in plant poly(A)' RNA.

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Section: Discussionmentioning

confidence: 99%

Identification of a Plant-Encoded Analog of PKR, the Mammalian Double-Stranded RNA-Dependent Protein Kinase

Langland¹,

Jin²,

Jacobs³

et al. 1995

Plant Physiol.

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“…These observations pose interesting questions on the primary molecular mechanism, which might involve direct interaction of the mature viroid RNA containing the PC determinant with a host factor needed for plastid rRNA maturation or viroid-induced silencing of a specific host gene product also mediating this process. Direct interactions between invading RNAs and host factors have been proposed to regulate symptom expression not only in nuclear viroids (Diener et al, 1993) but also in viral satellite RNAs (Taliansky and Robinson, 1997) and viruses (Rodríguez-Cerezo et al, 1991). This scenario is particularly attractive in this instance because the PC determinant maps at a hairpin, a structural element frequently involved in RNA-RNA and RNA-protein interactions.…”

Section: The Ability Of a Non-protein-coding Rna To Perturb Cellular mentioning

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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“…There is already an example of how subtle nucleotide differences without obvious effect on the PSTVd secondary structure have significant impact on interactions with host factors. Diener et al (1993) showed that PSTVd Mild and PSTVd Severe , which differ by two nucleotides in the lower portion of the classic pathogenicity domain, have a 10-fold difference in activating the interferon-induced, double-stranded RNA-activated protein kinase (P68). Whether such differential activation of P68 is directly responsible for the development of some viroid symptoms remains to be investigated.…”

Section: Roles Of Rna Sequences In Viroid and Viral Pathogenicitymentioning

confidence: 99%

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

Qi¹,

Ding²

2003

Plant Cell

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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Mechanism of viroid pathogenesis: Differential activation of the interferon-induced, double-stranded RNA-activated, Mr 68 000 protein kinase by viroid strains of varying pathogenicity

Cited by 53 publications

References 32 publications

Identification of a Plant-Encoded Analog of PKR, the Mammalian Double-Stranded RNA-Dependent Protein Kinase

Identification of a Plant-Encoded Analog of PKR, the Mammalian Double-Stranded RNA-Dependent Protein Kinase

A Viroid RNA with a Specific Structural Motif Inhibits Chloroplast Development

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

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