The epidemiology of tomato mosaic: Sources of TMV in commercial tomato crops under glass

Of the several possible sources of tomato mosaic virus, seeds and root debris in the soil are considered to be of greatest importance. A survey of 374,000 seedlings on ten commercial holdings found 0.05% of them infected, and although these were removed virus had been spread to other young plants which did not show infection when transplanted into the growing houses, seven of twenty-two of which contained a few infected plants when sampled shortly after planting. Virus overwintering on clothing, and debris on structures, are thought to be of minor importance, and smoking tobacco is seldom a source of infection for the tomato crop. A further survey of seventy-eight samples from tomato crops in Britain confirmed the 1960-61 survey: all were infected with tomato strains of TMV, none with tobacco strains, but one of the 187 infected seedlings referred to above was carrying a tobacco strain. Petunia was not as satisfactory as a special cultivar of White Burley tobacco for distinguishing between the tobacco and tomato TMV isolates. Observations and tests on a commercial holding showed that TMV was readily carried from plants in infected glasshouses into clean ones by workers, and once introduced, spread rapidly within the crop.     

The adaptation of tomato mosaic virus to resistant tomato plants

Tomato mosaic virus derived from susceptible tomato plants (the standard virus) was cultured in resistant plants. Sap from non-inoculated leaves of resistant tomato plants infected with virus from the resistant host was more infective and contained more virus particles than leaf sap of resistant plants infected with the standard virus. Leaves of resistant tomatoes infected with virus from the resistant host also showed more obvious symptoms. Susceptible plants infected with virus from resistant plants not only showed fewer symptoms than when infected with standard virus, but samples were less infective and contained less virus up to 26 weeks, when values for infectivity were similar. This modification in activity was not reversible and was obtained with two lines of tomato having different types of resistance. Passage of virus from resistant plants through susceptible plants did not impair its ability to infect resistant plants.     

The epidemiology of tomato brown root rot

In the absence of nematodes, three different symptoms of disease, parts of the brown root rot complex (BRR), occurred on tomato roots surviving in soils infested with GSF (= grey sterile fungus) and Colletotrichum atramentarium (Berk. & Br.) Taubenh. In heavily infested soils brown lesions occurred throughout cropping, appearing within a week of planting. Corkiness and black dot, caused by GSF and C. atramentarium respectively, rarely occurred until the third month after planting but towards the end of the season the incidence of black dot sometimes suddenly increased greatly. Observations of crops growing in plots treated with different soil partial sterilants suggested that GSF was more damaging than C. atramentarium. Yield was not related to the incidence of black dot but was inversely proportional to the occurrences of brown lesions and corkiness. The relation with brown lesions was significant within 8 weeks of planting, when most brown lesions gave cultures of GSF, but later more of these lesions gave cultures of C. atramentarium than of GSF. Pathogenicity tests with pure cultures of GSF and C. atramentarium were done on agar media and by artificially infesting partially sterilized soils. Roots of undamaged seedlings on agar media developed 10 mm. brown lesions within 2 weeks of inoculating 10-day-old tomatoes with most GSF cultures isolated from: (1) rotted roots of Lycopersicon esculentum, Solanum capsicastrum, Capsicum annuum var. longum and C. frutescens; (2) browned zones of Lycopersicon hirsutum roots; and (3) apparently healthy roots of Cucumis sativus. After inoculation with C. atramentarium, small (c. 2 mm.) pink lesions developed, whereas none formed using Pyrenochaeta spp. In soil tests the greater root damage done by GSF, including root loss, was reflected in decreased aerial growth and smaller fruit yields; C. atramentarium affected neither. In the second year of soil infestation GSF decreased yields during 6 weeks of picking from 1.96 kg. in the uninoculated controls to 1.02 kg./plant. The pattern of damage done by GSF changed as plants aged. In soil, brown lesions occurred within a few days of planting but corkiness did not appear for 2–3 months, when stem lesions and leaf yellowing often developed simultaneously. A 50% root loss after 21 weeks did not affect fruit yields whereas a 40% loss within 11 weeks of planting was reflected by a 45% yield decrease.     

Strain-genotype interaction of tobacco mosaic virus in tomato

The symptoms and virus content of isogenic tomato genotypes differing by three tobacco mosaic virus (TMV) resistance factors, Tm-I, Tm-2 and Tm-2², were studied in relation to various isolates of TMV and four strains were identified. The common strain induced no symptoms on plants with any of the factors for resistance, one strain caused symptoms on Tm-I plants, one on Tm-2 plants and one on both Tm-I and Tm-2 plants and also on Tm-I Tm-2 plants. No strain induced symptoms on Tm-2² plants. The gene, Tm-I, was found to be dominant or incompletely dominant for preventing symptom development but was recessive or intermediate for limiting virus multiplication of the common strain. Both Tm-2 and Tm-2² were dominant for a hypersensitive response to the common strain. Virus multiplication was temperature-dependent. The background or varietal genotype did not affect virus multiplication. A systemic necrosis of Tm-2² plants occurred only when heterozygous Tm-2² was not protected by other factors against specific strains of TMV. The complexity of the host genotype, pathogen genotype and environment interactions are outlined and the exploitation of the resistance factors in tomato breeding discussed.     

The movement of tobacco mosaic viruses and potato virus X through tomato plants

Tomato aucuba mosaic virus, tobacco mosaic virus and potato virus X took 3'5-4, 5 and 3 days respectively to move from inoculated tomato leaflets into the petioles and stems
On reaching the stem each virus usually first moved downward, but in some plants both upward and downward movement occurred simultaneously and in a few
upward movement occurred first.
All three viruses travelled through the stem at approximately the same rate. Each was capable of travelling more than 80 cm. during the first 12 hr. after entering the stem, giving a minimal average rate of about 8 cm. per hr.
Uninfected pieces of stem invariably occurred between infected pieces. Maximum lengths of stem through which virus particles had apparently passed without causing infection, were 44.5, 49 and 39 cm. for the three viruses.     

Agrobacterium-mediated inoculation of plants with tomato golden mosaic virus DNAs

We have adapted the agroinfection procedure of Grimsley and co-workers [4,5] to develop a simple, efficient, reproducible infectivity assay for the insect-transmitted, split-genome geminivirus, tomato golden mosaic virus (TGMV). Agrobacterium T-DNA vectors provide efficient delivery of both components of TGMV when used in mixed inoculation of wild-type host plants. A greater increase in infection efficiency can be obtained by Agrobacterium delivery of the TGMV A component to permissive transgenic plants. These permissive plants contain multiple tandem copies of the B component integrated into the host genome. An inoculum containing as few as 2000 Agrobacterium cells can produce 100% infection under these conditions. Further, our results show that there is a marked effect of the configuration of the TGMV A components within the T-DNA vector on time of symptom development. We have also found that transgenic plants carrying tandem copies of the A component do not complement the B component. Possible mechanisms to explain these results and the potential use of this system to further study the functions of the geminivirus components in infection are discussed.