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D.S. Achor and L.G. Albrigo

Permanent chlorosis of leaves on plants fertilized with urea containing high levels of the contaminant biuret has been observed in several crops including citrus. Little has been reported as to the cellular changes that result from such chlorosis. Branches from `Ruby Red' grapefruit (Citrus paradisi Macfadyn) and `Hamlin' orange [C. sinensis (L.) Osbeck] were sprayed with urea solutions containing 1.05% biuret. As visible symptoms developed, leaf tissue samples were prepared for transmission electron microscopy. For comparison purposes, leaves from similar trees showing chlorosis from age-related senescence and Zn deficiency were also sampled. The progressive development of chlorosis in biuret-affected leaves was characterized by: the loss of starch, thylakoidal and granal membranes in chloroplasts along with the enlargement and increase in number of plastoglobuli or lipid bodies. The lipid bodies were liberated alone or in association with membrane vesicles to the cytoplasm and vacuoles. The number and volume of the individual chloroplasts became smaller. Concurrent loss of cytoplasmic content and the enlargement of the vacuolar space were also observed in the biuret affected leaf tissue. Similar findings were observed in the cells of senescent leaves. In cells of leaves showing nutritional deficiency, losses in cytoplasmic content and vacuolar enlargement were observed but there was neither complete loss of thylakoidal or granal membranes nor the release of lipids from the plastids. It was concluded that 1) the cytological characteristics of the biuret-affected samples were more similar to age-related senescent samples than to chlorosis from Zn deficiency and 2) that complete loss of the lipid bodies from the chromoplasts to the cytoplasm and vacuole in the biuret-affected samples and in age-related senescence in citrus leaves was responsible for the permanent nature of the chlorosis.

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D.S. Achor, L.G. Albrigo, and C.W. McCoy

Upper surface leaf lesions on `Sunburst' mandarin [(Citrus reticulata Blanco × (C. paradisi Macf. × C. reticulate)] associated with feeding by the citrus rust mite [Phyllocoptruta oleivora (Ashm.)] are more severe than those on other citrus cultivars. Development of leaf lesions on `Sunburst' mandarin and two other cultivars were examined by light and electron microscopy. Damaged leaves treated with a fungicide confirmed that the anatomical changes on `Sunburst' are an enhanced wound periderm response to feeding injury by rust mite and not the result of fungal invasion.

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D.S. Achor, H. Browning, and L.G. Albrigo

Young expanding leaves of `Ambersweet' [Citrus reticulata Blanco × C. paradisi Macf. × C. reticulata) × C. sinensis (L) Osb.] with feeding injury by third larval stage of citrus leafminer (Phyllocnistis citrella) were examined by light and electron microscopy for extent of injury and tissue recovery over time. Results confirmed that injury is confined to the epidermal layer, leaving a thin covering over the mine tunnel that consisted of the cuticle and outer cell wall. Wound recovery consisted of two possible responses: the production of callus tissue or the formation of wound periderm. The production of callus tissue developed within 3 days of injury when the uninjured palisade or spongy parenchyma below the injured epidermis produced callus tissue through periclinal or diagonal cell divisions. After 1 month, the entire epidermis was replaced by callus tissue. In the absence of secondary microbial invasion, this callus tissue developed a thick cuticle, followed by development of a covering of platelet wax after 4 months. Alternatively, wound periderm formed if the outer cuticular covering was torn before the cuticle had developed sufficiently to prevent the exposed cells from being desiccated or invaded by fungi, bacteria, or other insects. The wound periderm consisted of a lignified layer of collapsed callus cells, a suberized phellem layer, and a multilayered phelloderm-phellogen. Since there were always cellular collapse or fungi and bacteria associated with wound periderm formation, it was determined to be a secondary effect, not a direct effect of leafminer feeding.