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

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Physiogenic or Nonpathogenic Seed Disorders 251A comparative account of ultrastructure of asymptomatic and symptomatic cotyledonsis given by Singh and Mathur (1992). The cell walls are uniformly thickand more or less smooth in asymptomatic cotyledons. The fibrillar material is clear,and fine plasmodesmatal connections occur across the cell wall. The plasma membranelies close to the primary wall, and the cytoplasmic net is well organized,showing cell organelles such as endoplasmic reticulum, mitochondria, vacuoles,ribosomes, protein bodies, and starch grains. The aggregation of endoplasmic reticulum,mostly rough endoplasmic reticulum, and mitochondria is much more in theperipheral cytoplasm. The protein bodies vary in size and are deeply stained(Figure 9.2A).In symptomatic cotyledons the cell walls become broad, showing looseningof fibrillar material, and they are prominently sinuate with well-developed plasmodesmatalchannels connecting adjoining cells and the intercellular spaces(Figure 9.2B). The plasma membrane is deeply invaginated. The ribosomes andmitochondria are disfigured. The protein bodies are membrane bound, but the depositionof reserve material is poor and vacuolation in these bodies produces bizarreshapes (Figure 9.2B). Initially, the cell contents do not reveal the occurrence of oildroplets, but their appearance in the intercellular spaces is indicative of secretion.The starch grains are greatly corroded.Increased derangement leads to severe subcellular effects. The cell walls showfurther loosening of fibrils, broad plasmodesmatal channels, and accumulation of alarge amount of granular material beneath the cell wall (Figure 9.2C). Oily materialoccurs interspersed among these granules. The plasma membrane is dissociated fromthe cell wall and shows prominent breaks. The cytoplasmic net shows disintegration,small fragments of endoplasmic reticulum randomly dispersed, weakening or breakdownof the unit membrane around the cell organelles, and protein bodies. Theremains of protein bodies show great variation in shape (Figure 9.2B). Air spacesare greatly enlarged and show accumulation of a large amount of pigmented oilysecretion (Figure 9.2D).9.2 HUMIDITY EFFECTSClimatic stresses, particularly humidity, low or high, cause visible symptoms inseeds of crop plants (Table 9.1). The symptoms may be exomorphic, e.g., gray seedsof radish and white mustard, or endomorphic, discoloration (lettuce), transversecracks (pea and chickpea) and cavitation on adaxial face (pea and chickpea) ofcotyledons. Histology of hollow heart in pea and gray discolored seeds in whitemustard is known (Perry and Howell, 1965; Singh, 1974; Jørgensen, 1967).9.2.1 LOW HUMIDITY EFFECTS9.2.1.1 Hollow HeartHollow heart or cavitation (Figure 9.3A) on the adaxial face of cotyledons of pea(Pisum sativum) was first observed by Myers (1947, 1948) in seeds from NewZealand, Australia, and the United States. Perry and Howell (1965) examined more
252 Histopathology of Seed-Borne InfectionstsascwerpmipbBsgACastscwpDFIGURE 9.2 Ultrastructure of normal and marsh spot-affected cotyledons of pea. A, TEMphotomicrograph showing part of the normal cotyledon cell. Note the uniformly thick cellwall, plasma membrane, and the cytoplasmic net with cell organelles. B, TEM of marsh spotaffectedcotyledon cell showing changes in the cell wall, broadened plasmodemata, sinuateplasma membrane, vacuolated protein bodies, and pigmented contents in air spaces. C, D,TEM of severely affected cotyledons. C, Portion of cell beneath the cell wall showingaggregation of granular material. D, A portion showing broad cell wall with well-developedplasmodematal channels and air space with pigmented tanniferous material. (Abbreviations:as, air space; cw, cell wall; er, endoplasmic reticulum; mi, mitochondria; p, plasmodemata;pb, protein bodies; sg, starch grain; ts, tanniferous secretion.) (From Singh, D. and Mathur,R. 1992. Phytomorphology 42: 145–150.)
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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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TABLE 5.6Location of Mycelium of St
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7Seed Infection by VirusesViruses a
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Page 230 and 231: Seed Infection by Viruses 215ptowvv
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
Page 240 and 241: Seed Infection by Viruses 225Hunter
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