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Viroids
V irulent P hage 2107 the trait or disease to both males and females. It is also seen in mitochondrial inheritance but here, although both males and females can be affected, only females transmit the trait. This is because only eggs and not sperm transmit mitochondria to the zygote. Example pedigrees may be seen at http: //www. gla.ac.uk/medicalgenetics/encyclopedia.htm See also: Mitochondrial Inheritance
Viroids C Beamish and E Kutter Copyright ß 2001 Academic Press doi: 10.1006/rwgn.2001.1367
Viroids might be considered `naked viruses' ± viruses without their space ships. They are infectious circular RNA molecules only about 300 nucleotides long, with no protein coats. Cells somehow take them up, replicate them extensively and then release them. Sometimes they harm their host cell, sometimes not. They cause a variety of problematic diseases in higher plants. For example, in potato spindle-tuber disease, a viroid causes the potatoes to become cracked, gnarled, and elongated. Viroids also damage coconut palms, hops, peaches, cucumbers, and avocados. They are transmitted between plants mechanically or through pollen or ovules. In addition to their large economic impact on plant crops, these RNAs are of great interest to molecular biologists because they are the smallest and simplest replicating molecules known, and because it is possible that they are a sort of living fossils, reflecting precellular evolution in a hypothetical RNA world. Viroids were discovered in 1971 by T.O. Diener, a plant pathologist. It is still not clear how they cause disease, especially since they may cause severe problems in one plant and no particular symptoms in a related species. They encode no proteins. Perhaps they bind to something in the cell and disrupt some regulatory mechanism. The RNA of many viroids contains sections of nucleotide sequence complementary to key regions at the boundaries of RNA introns; maybe that is how they damage cells. They also have nucleotide sequences similar to some seen in transposons and retroviruses. Two quite distinct groups of viroids have been identified. Group A viroids (such as peach latent mosaic viroid) replicate in chloroplasts, while group B viroids multiply in the nucleus of the host cell. Viroid replication involves either symmetric or asymmetric rolling circle replication mediated by an RNA-directed RNA
polymerase, long thought to be unique to plant cells. (Now it seems that there may be a similar animal-cell enzyme that is involved in replicating hepatitis delta virus RNA.) The infecting circular monomer is copied to make a long linear multimeric minus strand. In the symmetric mode, the multimeric minus strand is cut and sealed to make minus circular monomers. These then act as templates to form the plus-strand monomers by the same set of three reactions. All group B viroids studied to date use the symmetric mode. In the asymmetric mode, seen for group A viroids, the minus strand serves directly as a template to make linear multimeric plus strands. These are cleaved through autocatalysis involving a so-called `hammerhead' ribozyme structure and sealed into closed circles. Such hammerhead structures have also been seen in other RNA molecules that have enzyme-like properties. No hammerheads are seen in the group B viroids and no self cleavage has yet been observed, but neither has a cellular enzyme yet been identified that is responsible for their cleavage. Thus, a still-unidentified form of autocatalysis may be involved.
Further Reading
Diener TO (1991) Subviral pathogens of plants: viroids and viroid-like satellite RNAs. FASEB Journal 5 (13): 2808 ±2813. Scott A (1985) Pirates of the Cell. Oxford: Blackwell. Sanger HL (1989) Viroid function: viroid replication. In Diener TO (ed.) The Viroids, pp. 117±166. New York: Plenum Press.
See also: Rolling Circle Replication
Virology See: Virus
Virulent Phage E Thomas Copyright ß 2001 Academic Press doi: 10.1006/rwgn.2001.1370
A virulent phage will always substantially alter the physiology of the cell it infects and lyse its bacterial host at the completion of its infection cycle. Because of this distinguishing characteristic, virulent phages are also known as lytic phages. Coliphages T4 and T7 are classic example of virulent phages. The life cycle of virulent phages (Figure 1) is initiated with adsorption of the phage to some specific set of macromolecules it uses as receptors on a bacterial host. Once adsorption has occurred, the viral DNA enters the
Viroids C Beamish and E Kutter Copyright ß 2001 Academic Press doi: 10.1006/rwgn.2001.1367
Viroids might be considered `naked viruses' ± viruses without their space ships. They are infectious circular RNA molecules only about 300 nucleotides long, with no protein coats. Cells somehow take them up, replicate them extensively and then release them. Sometimes they harm their host cell, sometimes not. They cause a variety of problematic diseases in higher plants. For example, in potato spindle-tuber disease, a viroid causes the potatoes to become cracked, gnarled, and elongated. Viroids also damage coconut palms, hops, peaches, cucumbers, and avocados. They are transmitted between plants mechanically or through pollen or ovules. In addition to their large economic impact on plant crops, these RNAs are of great interest to molecular biologists because they are the smallest and simplest replicating molecules known, and because it is possible that they are a sort of living fossils, reflecting precellular evolution in a hypothetical RNA world. Viroids were discovered in 1971 by T.O. Diener, a plant pathologist. It is still not clear how they cause disease, especially since they may cause severe problems in one plant and no particular symptoms in a related species. They encode no proteins. Perhaps they bind to something in the cell and disrupt some regulatory mechanism. The RNA of many viroids contains sections of nucleotide sequence complementary to key regions at the boundaries of RNA introns; maybe that is how they damage cells. They also have nucleotide sequences similar to some seen in transposons and retroviruses. Two quite distinct groups of viroids have been identified. Group A viroids (such as peach latent mosaic viroid) replicate in chloroplasts, while group B viroids multiply in the nucleus of the host cell. Viroid replication involves either symmetric or asymmetric rolling circle replication mediated by an RNA-directed RNA
polymerase, long thought to be unique to plant cells. (Now it seems that there may be a similar animal-cell enzyme that is involved in replicating hepatitis delta virus RNA.) The infecting circular monomer is copied to make a long linear multimeric minus strand. In the symmetric mode, the multimeric minus strand is cut and sealed to make minus circular monomers. These then act as templates to form the plus-strand monomers by the same set of three reactions. All group B viroids studied to date use the symmetric mode. In the asymmetric mode, seen for group A viroids, the minus strand serves directly as a template to make linear multimeric plus strands. These are cleaved through autocatalysis involving a so-called `hammerhead' ribozyme structure and sealed into closed circles. Such hammerhead structures have also been seen in other RNA molecules that have enzyme-like properties. No hammerheads are seen in the group B viroids and no self cleavage has yet been observed, but neither has a cellular enzyme yet been identified that is responsible for their cleavage. Thus, a still-unidentified form of autocatalysis may be involved.
Further Reading
Diener TO (1991) Subviral pathogens of plants: viroids and viroid-like satellite RNAs. FASEB Journal 5 (13): 2808 ±2813. Scott A (1985) Pirates of the Cell. Oxford: Blackwell. Sanger HL (1989) Viroid function: viroid replication. In Diener TO (ed.) The Viroids, pp. 117±166. New York: Plenum Press.
See also: Rolling Circle Replication
Virology See: Virus
Virulent Phage E Thomas Copyright ß 2001 Academic Press doi: 10.1006/rwgn.2001.1370
A virulent phage will always substantially alter the physiology of the cell it infects and lyse its bacterial host at the completion of its infection cycle. Because of this distinguishing characteristic, virulent phages are also known as lytic phages. Coliphages T4 and T7 are classic example of virulent phages. The life cycle of virulent phages (Figure 1) is initiated with adsorption of the phage to some specific set of macromolecules it uses as receptors on a bacterial host. Once adsorption has occurred, the viral DNA enters the