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

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Physiogenic or Nonpathogenic <strong>Seed</strong> Disorders 255and sides in such cotyledons have moderate and evenly distributed protoplasmiccontents. The epidermal cells lining the concavity contain homogeneous cytoplasmand normal interphase nuclei (Figure 9.3D, E).In chickpea (Cicer arietinum), the symptomatic cotyledons have epidermis andone or two subepidermal layers similar to those <strong>of</strong> the normal cotyledons. However,the mesophyll cells <strong>of</strong> deeper layers contain comparatively thin and weak cell wallsand prominently vacuolated more or less homogeneous cytoplasm. Comparativehistochemical studies revealed the occurrence <strong>of</strong> poor protein contents in the cells<strong>of</strong> the symptomatic zone, but the starch content was comparable to that <strong>of</strong> the normalcotyledons.9.2.1.2 Necrosis in Lettuce CotyledonsPhysiological necrosis, rot, or spotted cotyledons (Figure 9.4A, B), in seedlings <strong>of</strong>lettuce (Lactuca sativa) is a recognized abnormality (Dempsey and Harrington, 1951;Rogers, 1953; Cuddy and Lyall, 1959; Bass, 1970). Cotyledonary necrosis is rarelyevident in freshly harvested seeds. It is not evident immediately in imbibed, excisedembryos, and it takes several days to manifest. It is influenced by storage conditions,and the process <strong>of</strong> deterioration is gradual. Initial deterioration causes only delay inmidrib greening, but severe effects result in weak growth <strong>of</strong> the embryonic axis andthe cotyledons, which fail to emerge from the seed coat (Dempsey and Harrington,1951; Bass, 1970). Finley (1959) has experimentally shown that it is caused byphysiological drought due to moisture stress at temperature <strong>of</strong> 32°C or above overan extended period.Smith (1989) has given a comparative account <strong>of</strong> ultrastructure <strong>of</strong> normal andsymptomatic cotyledons with particular reference to the mobilization <strong>of</strong> reservesduring germination. The ultrastructure <strong>of</strong> cotyledonary cells reveals the presence <strong>of</strong>electron-dense protein bodies with phytin-like deposits, many lipid bodies, plastids,elongated mitochondria, microbodies, and a prominent nucleus with a compactnucleolus (Figure 9.4C). The anatomy <strong>of</strong> symptomatic cotyledons shows that thenecrotic patch, according to size and severity, represents a region <strong>of</strong> localized celldeath. This necrosis is predominantly localized in the midrib region and in thetransverse section is seen to be symmetrical (Figure 9.4D). The epidermal cells andthe provascular cells are apparently more resistant to deterioration than the palisadeor mesophyll cells. The affected mesophyll cells fail to mobilize food reserves andshow distortion <strong>of</strong> cytoplasmic contents. The cells develop irregularity in the plasmalemma,fretted protein bodies with numerous inclusions and confluence <strong>of</strong> lipidbodies. While manifestations <strong>of</strong> membrane damage, such as discontinuity, myelinlikefigures adjacent to the plasmalemma, and/or withdrawal <strong>of</strong> the plasmalemmafrom the cell wall, are seen (Figure 9.4E), it is speculated that the delayed mobilization<strong>of</strong> reserves may be the result <strong>of</strong> membrane lesions (Smith, 1989).9.2.1.3 Cracking <strong>of</strong> CotyledonsOnly macro-morphological observations are known. McCollum (1953), Pirson(1966), Pollock, Roos, and Manalo (1969), and Kietreiber (1969) observed seedlings

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