Viroid

related topics
{acid, form, water}
{disease, patient, cell}
{specie, animal, plant}
{food, make, wine}
{math, number, function}

Pospiviroidae
Avsunviroidae

Viroids are plant pathogens that consist of a short stretch (a few hundred nucleobases) of highly complementary, circular, single-stranded RNA without the protein coat that is typical for viruses.[1] The smallest discovered is a 220 nucleobase scRNA (small cytoplasmic RNA) associated with the rice yellow mottle sobemovirus (RYMV).[2] In comparison, the genome of the smallest known viruses capable of causing an infection by themselves are around 2 kilobases in size. The human pathogen hepatitis D is similar to viroids.[3]

Viroids were discovered and given this name by Theodor Otto Diener, a plant pathologist at the Agricultural Research Service in Maryland, in 1971.[4][5][6]

Viroid RNA does not code for any protein.[7] The replication mechanism involves RNA polymerase II, an 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.[8]

The first viroid to be identified was the potato spindle tuber viroid (PSTVd). Some 33 species have been identified.

  1   CGGAACUAAA CUCGUGGUUC CUGUGGUUCA CACCUGACCU CCUGAGCAGA AAAGAAAAAA
 61   GAAGGCGGCU CGGAGGAGCG CUUCAGGGAU CCCCGGGGAA ACCUGGAGCG AACUGGCAAA
121   AAAGGACGGU GGGGAGUGCC CAGCGGCCGA CAGGAGUAAU UCCCGCCGAA ACAGGGUUUU
181   CACCCUUCCU UUCUUCGGGU GUCCUUCCUC GCGCCCGCAG GACCACCCCU CGCCCCCUUU
241   GCGCUGUCGC UUCGGCUACU ACCCGGUGGA AACAACUGAA GCUCCCGAGA ACCGCUUUUU
301   CUCUAUCUUA CUUGCUUCGG GGCGAGGGUG UUUAGCCCUU GGAACCGCAG UUGGUUCCU
Secondary structure

PSTviroid.png

Contents

[edit] Taxonomy

[edit] 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.[10] 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.[11] Finally, transgenic expression of the noninfectious hpRNA of potato spindle tuber viroid develops all the corresponding viroid like symptoms.[12]

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 is what causes the classic viroid symptoms.

Full article ▸

related documents
Peptide
Inositol triphosphate
Hydroxyl
Leucine
Stereochemistry
Northern blot
Thiomargarita namibiensis
Soman
Diene
Respirometer
Lithium carbonate
Structural biology
Nonmetal
Valine
Acetic acid bacteria
Chemisorption
Pentose
Alpha-ketoglutaric acid
Lonsdaleite
Ferric
Ulexite
Threonine
Aquamarine
Monosaccharide
Kirkendall effect
Acetoacetic acid
Coenzyme A
Euchromatin
Steam
Chalcogen