Mollicutes are simplified bacteria having no cell walls and few organelles, but viruses are simpler as they are composed only of the genetic material of nucleic acid coding for its protein coat. Not having organelles causes many biologists to refer to them as ‘particles’ instead of living organisms. The nucleic acid center of the particle may be DNA or RNA, both coding for production of the protein coat. Not having the other cellular components such as ribosomes for protein synthesis, nor a supply of amino acids or energy source, viruses are completely dependent upon being parasitic of living cells. The nucleic acid component links into the host cells protein synthesis system to reproduce the virus particle.
Most plant viruses also infect insect species that feed on plants. Aphids, leafhoppers, beetles and mites are common vectors of corn viruses. Some are easily moved into leaf tissue by humans rubbing diseased tissue on non-diseased leaves. Many virus particles are able to move cell to cell through cell wall holes (plasmadesmata). Corn viruses commonly become most damaging after they reach the growing point, from which they infect the new cells. Most reach the growing point through the phloem.
Symptoms usually show as a mosaic chlorosis on leaves and dwarfness of the plants, but a few have darker green plants (maize rough dwarf disease). Some virus diseases are most severe when plants are infected with two viruses. Corn Lethal Necrosis severity is linked to Maize chlorotic mottle virus plus maize dwarf mosaic virus or wheat streak mosaic virus.
Resistance, either complete or partial, has been identified in corn to all known viruses. In some cases, it has required considerable effort to identify resistance sources when a disease is new to an area but the diversity in corn germplasm has always succeeded. For example, corn lethal necrosis suddenly showed up in Kansas but within a few years it was found that some older USA public inbreds were resistant. Likewise, it took only a few years for resistance to be found to this disease when it popped up in East Africa. The mechanism of resistance is not always clear but probably includes inhibiting the spread of the virus to the growing point. There is evidence that it could involve detection of the virus protein, turning on production of the resistance mechanism. It also could involve interfering with the translation of the virus nucleic acid code, resulting in inability to replicate the coat protein of the virus. This type of reaction is involved in some viruses that infect bacteria (these viruses are called bacteriophages). In this case the bacteria change the virus DNA or RNA code by making a simple nucleic acid switch, destroying the nature of the virus protein. This is the basis of the CRISPR technology now being proposed as a method of changing genes in higher plants.
Corn virus disease distribution and occurrence is greatly affected by environments affecting vector insects, alternative hosts and corn development. Another example of new challenges is inevitable, but the genetic diversity of corn will ultimately overcome the threat.
Visit us at the ASTA in Chicago, Dec 9-12 (booth G207)
About Corn Journal
The purpose of this blog is to share perspectives of the biology of corn, its seed and diseases in a mix of technical and not so technical terms with all who are interested in this major crop. With more technical references to any of the topics easily available on the web with a search of key words, the blog will rarely cite references but will attempt to be accurate. Comments are welcome but will be screened before publishing. Comments and questions directed to the author by emails are encouraged.