Before we take a look at the progress made in the development of hybrid (disease resistance) varieties of barley, we have to understand the very fundamentals based on which these varieties were prepared. To develop disease resistance in barley crop, Hordeum vulgar L, the researchers focused on the host and pathogen systems. In this type of system generally the pathogen benefits from the host as it feeds and grows whereas the host suffers and withers eventually due to the malfunctioning of the natural system.
The type of disease caused and the lesions observed depend on the extent of interaction that takes place between the host and the pathogen. A poorly or weakly developed lesion shows us that the relationship was incompatible between the two, whereas a well-developed lesion shows signs of compatibility.
Different varieties of host when infected with an individual culture of pathogen results in different types of lesions proving the fact that these interactions are conditioned by genes.
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The necessity for studying the genetics of both the host and pathogen was shown by studies conducted by Flor (Flor, 1955). These studies were based on the relationship of genes conditioning the reaction of flax, and the corresponding genes conditioning pathogenicity of flax rust fungus.
These studies concluded that for each gene conditioning the reaction of the host there is a corresponding gene conditioning the pathogenicity of the pathogen (J.G.Moseman). The same relationship has been proved between barley and powdery mildew fungus (Erysiphe graminis f.). The genetic studies of either the host or the pathogen can provide the information regarding the genetics of the other organism and the development of the powdery mildew fungus.
Within the past decade, two viral diseases namely the Barley yellow dwarf and Barley stripe mosaic have become more active in many areas of the world. Barley yellow dwarf has been reported in many countries such as England, Norway, Australia and United states. Barley stripe mosaic has been reported from Japan, Canada and The States. Another point to note is that these diseases are common for all the members of the grass family. In the United States major losses are incurred from this disease in Oats than in barley.
BARLEY YELLOW DWARF DISEASE
Barley yellow dwarf was first identified by Oswald and Houston in 1951; it has been a major disease in most parts of the world especially in The United States. Around 80 percent reduction in yield has been measured experimentally in susceptible varieties of barley, wheat and oats (Bruehl, 1961).
Barley yellow dwarf virus (BYDV) is characterized by a single-stranded RNA virus; this virus is transmitted by aphids. The isolates that have been divided into two subgroups:
This group contains three strains mainly MAV, SGV and PAV.
This group contains two strains RMV and RPV.
MAV strain carried by Sitobion Avenae.
SGV and PAV carried by Rhopalosiphum padi, S.avenae and Metopolophium dirhodum.
These strains are carried by Rhopalosiphum padi and Rhopalosiphum padi
These strains have been classified as less severe.
These strains cause severe form of the disease.
The symptoms of barley yellow dwarf disease differ with the affected crop, plant age at the time of infection, present environmental conditions, and the virus strain, and can be confused with other related diseases or physiological disorders. The symptoms begin to appear in approximately 14 days after the time of infection.
Characteristic symptoms that have been found to be associated with the Barley Yellow Dwarf disease are Discoloration i.e. yellowing or reddening of the leaf and Dwarfing. Varieties that are susceptible show progressive symptom development in the form of bright yellow blots, with the colour developing from the tip of the leaf and progressing downward throughout the blade. Other symptoms include stunting/dwarfing (hence the name yellow dwarf), reduction in root growth, delayed heading or no heading, and a visible reduction in yield. It is observed that the heads of the affected plants tend to remain erect and due to colonization by saprophytic fungi they become black and discolored. Due to this infection, the leaves have reduced photosynthetic ability.
BARLEY YELLOW DWARF-Virus.
Aphids are known to be vectors of the BYDV (Barley Yellow Dwarf Virus). When aphids feeds on the plant, BYD virions get transferred to the aphid's hind gut, the coat protein present on the surface of the virus is recognized by the hindgut epithelium cells of the aphid, after which the virion is allowed to pass into the hemolymph of the aphid, where it remains indefinitely, but cannot multiply within the aphid. The virus is transported into the aphids salivary gland so as to be released into salivary canals and ducts. The virus is later excreted in the aphid saliva during feeding.
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Gildow and colleages in the year 1999 worked on the model for transmission of the virus through the aphids. They pointed out the three main barriers that the virus must overcome within the aphid for the transmission to take place.
Firstly, after the ingestion, the virus needs to undergo specific binding with the epithelial cells of the hindgut, successful binding results in the virus being membrane transported to the haemocoel .
Once transported to the haemocoel, the protein coat domain interacts with symbionin, an endo symbiotic bacterial protein (Young and Filichkin, 1999). Symbionin protects the virus from degradation within the haemocoel and allow its survival for a significant time within the aphid. Another interaction with the read through domain of the coat protein allows the virus to move from the haemocoel of the insect into the basal lamina of the salivary gland followed by endocytosis across the plasma lemma. The saliva then produced during feeding contains the virus which later gets transferred to phloem of the plant. This model elaborates the events that occur during transmission and can be useful in developing techniques to control the disease.
The Barley yellow dwarf virus particles are structurally isometric and are about 30 nm when measured using shadowed preparations , 23-25nm when observed in thin sections and 20 nm if negatively stained preparations of virus are used. Gill and Chong studied the ultrastructural changes induced by MAV and RPV which are vector specific and PAV which is non-specific in oat cells.
Below here we see a thin section of BYDV infected phloem parenchyma cells of barren brome (Bromus Sterilis L.). This is image of the cell which has been infected with a severe strain of BYDV which is transmitted by R.padi. This infection was achieved by exposing eight day old seedlings to the virus by the means of aphids.
Figure Electron Micrograph of Bromis sterilis L. cells infected with barley yellow dwarf virus. Note the large Osmiophilic lipid globule(O.G) and the rhombic crystalline array which is enveloped in an endoplasmic reticulum cisterna(E.R). (V) virus particles.
Considering the genomic composition of the viruses, The Luteovirus BYDV subtypes and the Polerovirus CYDV-RPV particles are both made up of 180 protein subunits which consists of a mixture of predominant 22 kD population and a small number of 50 to 55 kD read through proteins (D'Arcy et al. 2000). Among the other characteristics which distinguishes the two, the Polerovirus genus contains a VPg genome-linked protein and a 5' ORF (Open Reading Frame), designated ORF 0, both of which are absent in members of the Luteovirus subtypes. The RdRp genes of Luteovirus and Polerovirus also exhibit a great deal of differences, the two genera differ in sequences at their 3' termini. The Luteovirus genome (Fig. 4) consists of five major ORFs that appear to be expressed in infected plants
Figure The genetic composition of the Barley Yellow Dwarf Virus and the Cereal Yellow Dwarf virus. Black lines indicate single stranded positive sense genomic(sRNA) and subgenomic (sgRNA). The white boxes represent the protein products of the genes and their respective weight in kilo daltons(K).
Resistance to BYDV/CYDV
The research for breeding BYDV resistive varieties of barley has been carried out for more than 50 years, yet the practice of using alternative control measures were given more priority than resistance breeding especially in UK (Plumb, 2002). Breeding of varieties which provide strain specific resistance requires evaluation and selection which usually varies due to the fact that the process is based on the assessment of yield and the appearance of symptom instead of quantitative assays which determines the virus strain. As concluded by Burnett et.al (1995), that tolerance rather than resistance better describes what has been traditionally measured in field studies.
Ryd2 aka Yd2 is the gene commonly used in breeding for BYD tolerance. This semi dominant gene was first found in barleys that originated in Ethiopia (Schaller and Rasmusson, 1959) and was found to be located on the 3H chromosome (Schaller, 1964). Another gene known as yd1, is recessive by nature and was discovered in Rojo barley although comparatively yd1 has a lower level of tolerance than yd2 (Suneson 1955). Due to this, there is only a limited amount of research work carried out on yd1. In 2004, a novel gene was discovered, this gene was located in one of the Ethiopian Barley lines (L94) near the centromere of the chromosome 6H in the Ethiopian Barley line L94 and was named Ryd3. The dominancy of this gene is yet not known, but the resistance appeared is comparable to Ryd2.
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The Ryd2 gene however remains the most commonly used gene to develop resistance. Experiments conducted by Schaller and colleagues at Davis, California resulted in the following conclusion:
Out of the 6689 varieties of barley that were tested for resistance to BYDV, 117 varieties were classified as resistant. Out of this 117, 113 varieties were introduced from Abyssinia, 3 were hybrids with Abyssinian types as parent and one was from China. None of these varieties however, was found to be free of the BYDV, as indicated by the appearance of disease symptoms. Therefore tolerance rather than resistance was evident and the majority of those with tolerance may have possessed Ryd2 or even Ryd3 gene.
Another variety known as the post winter barley has been released which is "somewhat resistant" to BYDV and has no relation whatsoever with Ryd2 or the Ethiopian barley. (Grafton et al.1982)
Subsequently, further research showed us that the Yd2 gene is linked with four genetic markers on the chromosome 3; namely streaked vs. normal leaves, lax vs. dense spike xanthan, vs. normal seedling and uzu vs. normal growth.
Also some evidence has been gathered that makes the effectiveness of the Ryd2 gene vary with the genetic background (eg. Catherall et.al 1970) Some breeders have found that Ryd2 is less effective in later maturing germplasm (Catherall and Hayes, 1966; B8. Resistance Mechanisms in Barley Jones and Catherall, 1970). The effectiveness of Ryd2 gene can be measured by quantitative analysis of the accumulation of the virus in the host plant. It has been verified that the Ryd2 gene can reduced this accumulation showing sign of resistance.(Ranieri et al. 1993; Larkin et al. 1991; Skaria et al.1985). However, the reduction in virus accumulation is effective only against BYDV (eg. Luteovirus) and not against CYD virus.
There are several deductions made so as to figure out the function of Ryd2. Larkin et.al in 1991 showed that Ryd2 does not function in leaf protoplasts; also suggesting in a way that replication itself is not restricted. There is a possibility that Ryd2 can restrict the movement of virus from cell to cell or it can be expressed in phloem cells which are not well represented in the protoplast cells. Thus it has been concluded that Ryd2 gene restricts virus accumulation rather than virus replication or spread.
Collins in the year 1996 mapped the Ryd2 gene, these studies suggested that Ryd2 coseggregated with RFLP markers Xwg889 and XYIp on the long arm of chromosome 3, which is located at .5cM from the centromere. Sequencing revealed that Yip alleles differ by just a single nucleotide in barley with or without Ryd2, and the tight linkage between Yip and Ryd2 gave an opportunity to develop specific marker fior Ryd2 selection. In 1998, Paltridge developed YLM which was a PCR based marker. The precise mechanism by which Ryd2 functions is not known. It is known that the tightly-linked Ylp encodes a vacuolar H+-translocating ATPase subunit E (Ford et al. 1998; Dietz et al. 1995), but a role for this peptide in resistance remains speculative.