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Abstract

Single-node stem cuttings of Dieffenbachia amoena, Gentil were stored at 16 to 37° C and at 25 to 100% relative humidities. The cuttings required at least 2 days to produce suberin on cell walls near the cut surface, at least 6 days to form phellogen beneath suberized cells and at least 9 days to form a periderm layer. For periderm formation the optimum temperatures were 28 to 34 °C and optimum relative humidities 91 to 100%.

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periderm of the roots was peeled back to reveal any successful fungal penetration and the extent of colonization ( Fig. 1E ). Observations were made at 21 d, as new periderm formation occurs in 2 to 3 weeks post infection or injury ( Biggs 1986 ; Devkota

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. Periderm formation was determined by counting shoot internodes that changed color from green to tan or brown 4 weeks after ABA application. Periderm formation was expressed as the ratio of number of brown to total number of internodes per shoot. Leaf

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least over the shorter distance to the base of a crack. This being the case, the natural “filling” or “healing” of any cuticular cracks might keep pace with their rate of formation with the result that a periderm need not be formed and the temporary

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Abstract

Cured storage roots of sweet potato [Ipomoea batatas (L.) Lam. cv. Centennial] were wounded and recured for 12 days with or without 2,5-norbornadiene, AOA, or CoCl2 treatments. Ethylene production, wound lignification, and wound periderm formation were measured 0, 3, 6, 9, and 12 days after wounding. Ethylene production preceded wound lignification and wound periderm formation by 24 to 48 hr, respectively. Blocking ethylene action with 2,5-norbornadiene increased ethylene production, blocked wound periderm formation for up to 12 days, and strongly suppressed and delayed lignification. Blocking ethylene synthesis with AOA or CoCl2 decreased ethylene production to 10% of the control. Lignification and wound periderm formation were also suppressed and initiation delayed. These results suggest that ethylene is involved in lignification and periderm formation in wounded sweet potato roots. Chemical names used: bicyclo[2.2.l]hepta-2,5-diene (2,5-norbornadiene); (aminooxy) acetic acid (AOA).

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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.

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Abstract

Details of mango (Mangifera indica L.) stem anatomy and formation of the bud union were observed in 4 combinations of 2 scions and 3 stocks chip budded at 5 stages of stock growth from first flush to 1 year old. ‘Haden’, ‘Saigon’, and ‘Turpentine’ stems of equivalent age and growth rate were indistinguishable anatomically. Four stages in formation of the bud union were: pre-callus, where 4 days after budding only a wound periderm was present; callus, where 8 days after budding proliferation from tissues mainly near the cambium resulted in firm attachment of the components; cambial bridge, where 12 days after budding cambial layers from stock and scion formed a bridge and vascular tissues were differentiated within 36-48 days; and, the healed union, where after 6-8 months several cylinders of new tissues were present and the lateral shift of the scion to align with the stock had begun.

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Abstract

Five-year-old ‘Riesling’ grape (Vitis vinifera) vines growing in the Okanagan Valley of British Columbia were subjected to three crop levels (full crop, two clusters per shoot, and one cluster per shoot) in combination with no shoot thinning or thinning to 24 shoots per meter of row. Reduction in crop level improved vine size and cane periderm formation slightly. Yield per vine was linearly related to crop level, but berry weight, berries per cluster, and cluster weight increased with decreasing crop level. °Brix and pH increased and titratable acidity decreased with reduction in crop level. Thinning to 24 shoots per meter of row provided some improvement in yield components and °Brix. Crop loads below 10 kg of fruit per kilogram of cane prunings are necessary to achieve adequate fruit maturity under Okanagan conditions.

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Abstract

Freshly harvested sweet potatoes [Ipomoea batatas (L.) Lam. c. Jewel] are cured by holding them at 80–95% relative humidity and 29.4°C for 5 to 7 days. Curing heals wounds inflicted during harvest, thus minimizing loss from microbial decay during subsequent storage. The wound healing process was followed by applying a saturated solution of phloroglucinol in strong acid (PG) to the underside of detached wound tissue and scoring the intensity of the color developed. Microscopic examination of companion tissue with PG showed that color intensity was due to the layers of cells in which PG positive material was deposited. Wound periderm formation was observed to occur simultaneously with development of the most intense color, indicating that the test may be useful in the evaluation of curing progress.

Open Access

The fungus Aureobasidium pullulans is ubiquitous and can cause russet of fruit in New York orchards. The details of russet induction by this fungus are not well known. We inoculated `McIntosh' apple fruits with a suspension of A. pullulans spores (10 million colony-forming units/mL) 1–2 weeks postbloom or later at about 30 days postbloom. We dropped inoculum into plastic “microwells” attached to the fruit surface. The cuticle of uninoculated fruit (wells filled with water only) had no russet by autumn. Skin susceptibility to russet diminished with fruit age. The cuticle of inoculated young fruit began to break down in a few days, likely through direct cuticular digestion. Further erosion and breaching of the protective cuticle caused underlying epidermal cells to die. Within 1–2 weeks, cuticle disruption and epidermal cell death were widespread. This stimulated the fruit to initiate a repair process that involved periderm formation (russet), where many rows of cells were produced in nearby tissue to seal off the injury. This type of repair is not stretchable, so as young fruit expanded, additional skin splits and checks developed. This breakdown–repair process repeated itself, which created a scurfy skin. Older fruit did not expand as much after inoculation as did young fruit, and so they developed few obvious leathery patches of periderm. Older cuticle also resisted digestion better than did the young fruit cuticle, but we do not know if resistance resulted from increased cuticle thickness in older fruit or a change in cuticular compounds during fruit growth. Regardless, A. pullulans applied to older fruit did not progress beyond the early phase of cuticle digestion, even after 3 weeks postinoculation.

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