Histopathology of Seed-Borne Infections - Applied Research Center ...

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Seed Infection by Viruses 2073. The movement of virus through plasmodesmata may take place on accountof the capacity of the virus to alter the structure of plasmodesmata or maybe facilitated by the spread and movement proteins coded by the virus(Meshi et al., 1987; Wolf et al., 1989).4. Long-distance movement of virus occurs through conducting tissues, particularlythe phloem. The existence of functional plasmodesmata betweenmesophyll cells and phloem has been observed, providing a symplasticpathway for the movement of viruses. The open ends of the vascularelements in the leaf mesophyll may also provide sites for the phloemloading with virus. The virus moves rapidly over long distances as evidentfrom the classic experiments of Samuel (1934) on tobacco mosaic virus(TMV) in tomato. Samuel inoculated one terminal leaflet and then followedthe spread of the virus in the infected plant with the help ofinfectivity tests and found a systematic spread of the pathogen downwardas well as upward. Schippers (1963) examined the spread of BCMV inbean plants. He inoculated the middle leaflet of the first compound leafon the main stem and thereafter determined its presence in flower budsand ovaries at different nodes (Figure 7.1). Five days after inoculation,the virus was detected for the first time in buds and ovaries from nodesfour and five and from axillary shoots at nodes one and three. After 6days of inoculation, the virus also could be detected in floral buds andovaries at nodes zero and two (Figure 7.1). This showed upward as wellas downward transport of virus in the plant.5. An important question is the form in which the virus moves from cell tocell systematically in the plant. Three options are possible: (1) as virusparticle; (2) as virus nucleic acid; and (3) as virus-specific nucleoprotein.It is also possible that the virus may move in more than one form. TheTMV infection spreads from cell to cell in the absence of protein coat intomato (Siegel, Zaitlin, and Sehgal, 1962; Dawson, Bubrick, andGranthan, 1988) but for long-distance transport, virus particles areprobably essential (Saito, Yamanaka, and Okada, 1990). BSMV causesinfection in the absence of the protein coat and may become systemic(Maule, 1991).7.3.2 OVULE AND SEEDNeergaard (1979) and Mathews (1991) believe that the viruses may not enter ovuleson account of the lack of plasmodesmatal connections with the surrounding tissues.Neergaard (1979) further concluded that (1) the virus may not be capable of establishinga compatible relationship with the gametes or the embryo sac of the host;(2) the virus is lethal to the gametes, thus causing sterility and preventing productionof infected seed;and (3) the virus is not capable of infecting male and female gametesor the young embryo, either due to lack of virulence to these stages of the host ordue to their resistance. Such conclusions seem to have been made mainly on thebasis of detrimental effects of virus infection on the floral, fruit, and seed parts.Caldwell (1962) has observed that tomato aspermy virus is not seed-transmitted in
208 Histopathology of Seed-Borne Infectionsnode54321005days after inoculation6inoculated leafletbud in which virus could be demonstratedFIGURE 7.1 Bean common mosaic virus (BCMV) transmission in Phaseolus vulgaris.Transport of virus to flower buds and their ovaries situated at the basal nodes of axillaryshoots and at nodes four and five of the main stem, after 5 and 6 days of inoculation of themiddle leaflet of the second fully unfolded compound leaf. (From Schippers, B. 1963. ActaBot. Neerl. 12: 433–497.)tomato plants because it causes sterility of pollen and ovule. Virus infection affectsproduction and quality of pollen in several other cases (Yang and Hamilton, 1974;Mink, 1993). However, the recent histopathological studies using electron microscopyhave shown that the invasion, as well as the effects of virus infection, dependon the virus or its strain, host cultivar, and the environment.Three alternatives for virus invasion of the ovule and seed are recognized. Wherevirus invades the shoot and floral meristem or causes early invasion of fertile floralappendages, the virus may occur in anthers and pollen grains and in ovule and femalegametophyte at all stages of development. Bennett (1969) calls it ovule infectionfrom the mother plant. Mathews (1991) believes that virus transmission through thefemale gametophyte is probably more efficient for most seed-borne viruses thantransmission through pollen. The following have noted the presence of virus particlesin anthers and ovules and male and female gametophytes during their development:Yang and Hamilton (1974) for tobacco ring spot virus (TRSV) in soybean;
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Histopathology ofSeed-Borne Infecti
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PrefaceThe book deals with only one
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The AuthorsDalbir Singh, Ph.D., for
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ContentsChapter 1 Introduction ....
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4.3.2 Routes for Infection from Ova
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8.4 Survival in Seed ..............
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2 Histopathology of Seed-Borne Infe
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4 Histopathology of Seed-Borne Infe
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2Reproductive Structuresand Seed Fo
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Reproductive Structures and Seed Fo
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14 Histopathology of Seed-Borne Inf
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3Structure of SeedsThe seed habit i
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Structure of Seeds 49(1971) of usin
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Structure of Seeds 51is found in as
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Structure of Seeds 53dry seed of Ly
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Structure of Seeds 553.3.2 SEED COA
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Structure of Seeds 57Endosperm: One
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Structure of Seeds 59scendembepsmuA
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Structure of Seeds 61Endosperm: Sca
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Structure of Seeds 63Chalaza simple
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Structure of Seeds 65stystypmerA Bc
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Structure of Seeds 67epsent endCADB
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Structure of Seeds 69perhscendembpe
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Structure of Seeds 71eposgepi′epo
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Structure of Seeds 73(Zea and Sorgh
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Structure of Seeds 75Baker, D.M. an
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Structure of Seeds 77Maheshwari Dev
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Structure of Seeds 79Vries, M.A. de
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100 Histopathology of Seed-Borne In
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TABLE 5.6Location of Mycelium of St
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Page 224 and 225: Seed Infection by Viruses 209Wilcox
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Page 232 and 233: Seed Infection by Viruses 2177.4.2
Page 234 and 235: Seed Infection by Viruses 219seed(s
Page 236 and 237: Seed Infection by Viruses 221AMV fo
Page 238 and 239: Seed Infection by Viruses 223REFERE
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