Jump to content

Viroid

From Wikipedia, the free encyclopedia

This is an old revision of this page, as edited by Dienerto (talk | contribs) at 18:48, 24 November 2014. The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.

Viroid
Scientific classification
(unranked):
Subviral agents
(unranked):
Viroid
Families

Pospiviroidae
Avsunviroidae

Viroids are the smallest infectious pathogens known, consisting solely of short strands of circular, single-stranded RNA without protein coats. They are mostly plant pathogens, some of which are of economical importance. Viroid genomes are extremely small in size, ranging from 246 to 467 nucleobases; they thus consist of fewer than 10,000 atoms.[1] In comparison, the genome of the smallest known viruses capable of causing an infection by themselves are around 2,000 nucleobases in size. The human pathogen hepatitis D virus is a defective RNA virus similar to viroids.[2]

Viroids, the first known sub-viral pathogens, were discovered, initially characterized, and named by Theodor Otto Diener, plant pathologist at the U.S Department of Agriculture's Research Center in Beltsville, Maryland, in 1971.[3][4] The first viroid to be identified was Potato spindle tuber viroid (PSTVd). Some 33 species have been identified.

Viroids do not code for any protein.[5] Their replication mechanism uses RNA polymerase II, a host cell enzyme normally associated with synthesis of messenger RNA from DNA, which instead catalyzes "rolling circle" synthesis of new RNA using the viroid's RNA as template. Some viroids are ribozymes, having catalytic properties which allow self-cleavage and ligation of unit-size genomes from larger replication intermediates.[6]

With Diener’s 1989 hypothesis[7]---suggesting that viroids may represent “living relics” from a hypothetical, ancient, and non-cellular RNA world, before the evolution of DNA or protein---viroids have attained significance beyond plant virology to evolutionary biology by representing the most plausible molecules capable of explaining crucial intermediate steps in the evolution of life from inanimate matter. Although Diener’s hypothesis lay dormant for 25 years, it was resurrected in 2014 and its plausibility further enhanced by additional characteristics of viroids and viroid-like satellite viruses.Cite error: The opening <ref> tag is malformed or has a bad name (see the help page).<Flores, R., Gago-Zachert, S., Serra, P., Sanjuan, R., Elena, S.F. (2014). "Viroids: Survivors from the RNA World?". Ann.Rev.Microbiol.68:395–414 (2014.

Taxonomy

Transmission

Viroid infections are transmitted by cross contamination following mechanical damage to plants as a result of horticultural or agricultural practices. Some are transmitted by aphids and they can also be transferred from plant to plant by leaf contact.[10]

Replication

Viroids replicate in the nucleus (Pospiviroidae) or chloroplasts (Avsunviroidae) of plant cells in three steps through an RNA-based mechanism. They require RNA polymerase II, a host cell enzyme normally associated with synthesis of messenger RNA from DNA, which instead catalyzes "rolling circle" synthesis of new RNA using the viroid's RNA as template. Some viroids are ribozymes, having catalytic properties which allow self-cleavage and ligation of unit-size genomes from larger replication intermediates.[11]

Viroids and RNA silencing

There has long been confusion over how viroids are able to induce symptoms in plants without encoding any protein products within their sequences. Evidence now suggests that RNA silencing is involved in the process. First, changes to the viroid genome can dramatically alter its virulence.[12] This reflects the fact that any siRNAs produced would have less complementary base pairing with target messenger RNA. Secondly, siRNAs corresponding to sequences from viroid genomes have been isolated from infected plants.[13] Finally, transgenic expression of the noninfectious hpRNA of potato spindle tuber viroid develops all the corresponding viroid-like symptoms.[14]

This evidence indicates that when viroids replicate via a double stranded intermediate RNA, they are targeted by a dicer enzyme and cleaved into siRNAs that are then loaded onto the RNA-induced silencing complex. The viroid siRNAs actually contain sequences capable of complementary base pairing with the plant's own messenger RNAs, and induction of degradation or inhibition of translation causes the classic viroid symptoms.[15]

Living relics of the RNA World?

Diener’s 1989 hypothesis[16] claimed that viroids' unique properties make them more plausible candidates than introns or other RNAs considered in the past as “living relics” of a hypothetical, pre-cellular RNA world. If so, viroids have attained potential significance beyond plant plant pathology to evolutionary biology, by representing the most plausible macromolecules known capable of explaining crucial intermediate steps in the evolution of life from inanimate matter to life as we know it today. Diener's hypothesis lay dormant until 2014, when it was resurrected by Flores et al.[17] who summarized Diener’s arguments supporting his hypothesis and combined them with two additional ones (numbers 2 and 4 below). These properties include:

  1. viroid’s small size, imposed by error-prone replication;
  2. their high guanine and cytosine content, which increases stability and replication fidelity;
  3. their circular structure, which assures complete replication without genomic tags;
  4. existence of structural periodicity, which permits modular assembly into enlarged genomes;
  5. their lack of protein-coding ability, consistent with a ribosome-free habitat; and
  6. replication mediated in some by ribozymes—the fingerprint of the RNA world.[18][19]

History

In the 1920s, symptoms of a previously unknown potato disease were noticed in farmers’ New York and New Jersey fields. Because tubers on affected plants become elongated and misshaped, they named it the potato spindle tuber disease.[20]

The symptoms appeared on plants onto which pieces from affected plants had been budded—that the disease therefore was caused by a transmissible pathogenic agent. However, a fungus or bacterium could not be found consistently associated with symptom-bearing plants, and therefore, it was assumed the disease was caused by a virus. Despite numerous attempts over the years to isolate and purify the assumed virus, using increasingly sophisticated methods, these were unsuccessful when applied to extracts from potato spindle tuber disease-afflicted plants.[21]

In 1971 Theodor O. Diener, a plant pathologist at the U.S. Department of Agriculture’s Pioneering Laboratory for Plant Virology at Beltsville, Maryland, showed that the agent was not a virus, but a totally unexpected novel type of pathogen, one-80th the size of typical viruses, for which he proposed the term “viroid.”[22] Parallel to agriculture-directed studies, more basic scientific research elucidated many of viroids’ physical, chemical, and macromolecular properties. They were shown to consist of short stretches (a few hundred nucleobases) of single-stranded RNA and, unlike viruses, do not have a protein coat. Compared with other infectious plant pathogens, viroids are extremely small in size, ranging from 246 to 467 nucleobases; they thus consist of fewer than 10,000 atoms. In comparison, the genome of the smallest known viruses capable of causing an infection by themselves are around 2,000 nucleobases long.[23]

In 1976, Sänger et al.[24] presented evidence that potato spindle tuber viroid is a “single-stranded, covalently closed, circular RNA molecule, existing as a highly base-paired rod-like structure"—believed to be the first such molecule described. Circular RNA, unlike linear RNA, forms a covalently closed continuous loop, in which the 3' and 5' ends present in linear RNA molecules have been joined together. Sänger et al. also provided evidence for the true circularity of viroids by finding that the RNA could not be phosphorylated at the 5’ terminus. Then, in other tests, they failed to find even one free 3’ end, which ruled out the possibility of the molecule having two 3’ ends. Viroids thus are true circular RNAs.

The single-strandedness and circularity of viroids was confirmed by electron microscopy[25] and the complete nucleotide sequence of potato spindle tuber viroid was determined in 1978.[26] PSTV was the first pathogen of a eukaryotic organism for which the complete molecular structure has been established. Over thirty plant diseases have since been identified as viroid-, not virus-caused, as had been assumed.[27][23]

See also

2

References

  1. ^ Wolfram, S. "A New Kind of Science:web:www.wolframscience.com/nksonlineast//page-1179a.
  2. ^ Makino S, Chang MF, Shieh CK et al. (1987). "Molecular cloning and sequencing of a human hepatitis delta (delta) virus RNA". Nature 329 343–6.
  3. ^ Diener TO "Potato spindle tuber "virus". IV. A replicating, low molecular weight RNA" Virology 45, 411–28m(1971
  4. ^ "Tracking the Elusive Viroid" web|url=http://www.ars.usda.gov/is/timeline/viroid.htm 2007.
  5. ^ Tsagris EM, de Alba AE, Gozmanova M, Kalantidis K Cell. Microbiol. 10, 2168–7910 (2008).
  6. ^ name="Davos"/> Daròs JA, Elena SF, Flores R "Viroids: an Ariadne's thread into the RNA labyrinth" EMBO Rep.06, 593–8 (2006),
  7. ^ Diener TO "Circular RNAs: Relics of precellular evolution?" Proc.Natl.Acad.Sci.USA," 86, 9370–9374 (1989}.
  8. ^ Brian W. J. Mahy, Marc H. V. Van Regenmortel M, Desk Encyclopedia of Plant and Fungal Virology, 71–81 (2008)
  9. ^ a b c d e f g h Cite error: The named reference nt was invoked but never defined (see the help page).
  10. ^ De Bokx, J. A. and P. G. M. Piron (1981). "Transmission of potato spindle tuber viroid by aphids." Netherlands Journal of Plant Pathology 87(2), 31-34.
  11. ^ Cite error: The named reference Daros was invoked but never defined (see the help page).
  12. ^ Elizabeth Dickson, Hugh D. Robertson, C. L. Niblett, R. K. Horst & Milton Zaitlin; Robertson; Niblett; Horst; Zaitlin (1979). "Minor differences between nucleotide sequences of mild and severe strains of potato spindle tuber viroid". Nature. 277 (5691): 60–62. Bibcode:1979Natur.277...60D. doi:10.1038/277060a0.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  13. ^ Papaefthimiou I, Hamilton A, Denti M, Baulcombe D, Tsagris M, Tabler M; Hamilton; Denti; Baulcombe; Tsagris; Tabler (2001). "Replicating potato spindle tuber viroid RNA is accompanied by short RNA fragments that are characteristic of post-transcriptional gene silencing". Nucleic Acids Res. 29 (11): 2395–400. doi:10.1093/nar/29.11.2395. PMC 55696. PMID 11376158.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  14. ^ Wang MB, Bian XY, Wu LM; Wu; Liu; Smith; Isenegger; Wu; Masuta; Vance; Watson; Rezaian; Dennis, ES; Waterhouse, PM; et al. (2004). "On the role of RNA silencing in the pathogenicity and evolution of viroids and viral satellites". Proc. Natl. Acad. Sci. U.S.A. 101 (9): 3275–80. Bibcode:2004PNAS..101.3275W. doi:10.1073/pnas.0400104101. PMC 365780. PMID 14978267. {{cite journal}}: Explicit use of et al. in: |author2= (help); Unknown parameter |displayauthors= ignored (|display-authors= suggested) (help)CS1 maint: multiple names: authors list (link)
  15. ^ Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 22678590, please use {{cite journal}} with |pmid=22678590 instead.
  16. ^ Cite error: The named reference Proc.Natl.Acad.Sci.USA,1989-TOD was invoked but never defined (see the help page).
  17. ^ Flores, R., Gago-Zachert, S., Serra, P., Sanjuan, R., Elena, S.F. (2014) "Viroids: Survivors from the RNA World?". Annual Review of Microbiology 68: 395–414. Retrieved November 1, 2014.
  18. ^ Cite error: The named reference Flores was invoked but never defined (see the help page).
  19. ^ Zimmer, Carl (September 25, 2014). "A Tiny Emissary From the Ancient Past". New York Times. Retrieved November 22, 2014.
  20. ^ Owens, R.A. and J.Th.J. Verhoeven. 2009. Potato spindle tuber. The Plant Health Instructor. DOI: 10.1094/PHI-I-2009-0804-01
  21. ^ "ARS Research Timeline – Tracking the Elusive Viroid". 2006-03-02. Retrieved 2014-11-22.
  22. ^ Cite error: The named reference pmid5095900 was invoked but never defined (see the help page).
  23. ^ a b Pommerville, Jeffrey C (2014). Fundamentals of Microbiology. Burlington, MA: Jones and Bartlett Learning. p. 482. ISBN 978-1-284-03968-9.
  24. ^ Sänger, HL; Klotz, G; Riesner, D; Gross, HJ; Kleinschmidt, AK (1976) . "Single-stranded covalently closed circular RNA molecules, existing as highly base-paired rod-like structures". Proc.Natl.Acad.Sci.USA 73 (11): 3852–56. PMID 1069269
  25. ^ Sogo, JM, Koller T, Diener TO. (1973) “Potato spindle tuber viroid. X. Visualization and size determination by electron microscopy.” Virology.(1973) 55(1):70–80.
  26. ^ Gross HJ, Domdey H, Lossow C, Jank P, Raba M, Alberty H, Sänger HL .“(1978) “Nucleotide sequence and secondary structure of potato spindle tuber viroid.” Nature.273, :203–208.
  27. ^ Hammond, R. W. and Owens, R. A. 2006. Viroids: New and Continuing Risks for Horticultural and Agricultural Crops. Oniine. APSnet Features. doi: 10.1094/APSnetFeature-2006-1106
Retrieved from "https://en.wikipedia.org/enwiki/w/index.php?title=Viroid&oldid=635271981"