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The first viroid to be identified was potato spindle tuber viroid (PSTVd). Some 33 species have been identified.
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.
Virusoids are circular single-stranded RNAs dependent on plant viruses for replication and encapsidation. Since they depend on helper viruses, they are classified as satellites.
plant pathogens, of the order Viroidales, that consist of just a short section of RNA but without the protein coat typical of viruses
Avocado sunblotch viroid (ASBV) is an important disease affecting avocado trees. Infections result in lower yields and poorer quality fruit. ASBV is the smallest known viroid that infects plants and is transmitted by pollen and infected seeds or budwood. Trees infected with the viroid often show no symptoms other than a reduction in yield. However, they are still carriers and can pass the disease onto other plants.
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. In comparison, the genome of the smallest known viruses capable of causing an infection by themselves is around 2 kilobases in size. The human pathogen Hepatitis D virus is similar to viroids. Viroids are extremely small in size, ranging from 246 to 467 nucleotide (nt) long genome and consisting of fewer than 10,000 atoms. Viroids were discovered and given this name by Theodor Otto Diener, a plant pathologist at the Agricultural Research Service in Maryland, in 1971.
Viroid RNA does not code for any protein. 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. The first viroid to be identified was the potato spindle tuber viroid (PSTVd) . Some 33 species have been identified.
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. 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. Finally, transgenic expression of the noninfectious hpRNA of potato spindle tuber viroid develops all the corresponding viroid like symptoms. 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.
Virusoids are circular single-stranded RNAs dependent on plant viruses for replication and encapsidation. The genome of virusoids consists of several hundred nucleotides and only encodes structural proteins. Virusoids are similar to viroids in size, structure, and means of replication. Virusoids, while being studied in virology, are not considered as viruses but as subviral particles. Since they depend on helper viruses, they are classified as satellites.
The Pospiviroidae are a family of viroids, including the first viroid to be discovered, PSTVd. Their secondary structure is key to their biological activity. The classification of this family is based on differences in the conserved central region sequence. Pospiviroidae replication occurs in an asymmetric fashion via host cell RNA polymerase, RNase, and RNA ligase.
The Avsunviroidae are a family of viroids. At present three members are known. They consist of RNA genomes between 246-375 nucleotides in length. They are single stranded covalent circles and have intramolecular base pairing. All members lack a central conserved region. Replication occurs in the chloroplasts of plant cells. Key features of replication include no helper virus required and no proteins are encoded for. Unlike the other family of viroids, Pospiviroidae, Avsunviroidae are thought to replicate via a symmetrical rolling mechanism. It is thought the positive RNA strand acts as a template to form negative strands with the help of an enzyme thought to be RNA polymerase II. The negative RNA strands are then cleaved by ribozyme activity and circularizes. A second rolling circle mechanism forms a positive strand which is also cleaved by ribozyme activity and then ligated to become circular. The site of replication is unknown, but it is thought to be in the chloroplast and in the presence of Mg2+ ions.
Avocado sunblotch viroid (ASBV) is an important disease affecting avocado trees. Infections result in lower yields and poorer quality fruit. ASBV is the smallest known viroid that infects plants and is transmitted by pollen and infected seeds or budwood. Trees infected with the viroid often show no symptoms other than a reduction in yield. However, they are still carriers and can pass the disease onto other plants. Symptoms in more serious infections include depressed longitudinal streaks of yellow in the fruit. The fruit may also become red or white in color. Symptoms in the leaf are uncommon, but include bleached veins and petioles. Rectangular cracking patterns also occur in the bark of older branches. Infected but symptomless trees have a higher concentration of viroid particles than those showing symptoms. Symptomless trees also represent a greater danger in terms of spread of the viroid.
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The viroid begins producing an abnormal protein because of the mutation., The viroid can no longer be replicated efficiently by RNA polymerase II., The mutation prevents helper viruses from associating with the viroid., or The viroid siRNA no longer basepairs properly with the host cell’s mRNA.