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`Granny Smith' apples (Malus × domestica Borkh) and `d'Anjou' pears (Pyrus communis L.) were dipped in a 2.5%, 5%, or 10% stripped corn oil (α-tocopherol <3 mg·kg-1) emulsions, 2000 mg·L-1 diphenylamine (DPA), respectively, at harvest and stored in air at 0 °C for 8 months. Untreated fruit served as controls. In oil-treated apples and pears, ethylene and α-farnesene production rates were lower in early storage and higher in late storage than in control. Control fruit developed 34% scald in `Granny Smith' apples and 23% scald in `d'Anjou' pears after 6 months storage, whereas fruit treated with oil at 5% or 10%, or with DPA at 2000 mg·L-1 were free from scald. After 8 months storage, oil at 10% was as effective as DPA in controlling scald in pears, whereas in apples, fruit treated with 10% oil developed 18% scald and DPA-treated fruit were scald-free. DPA-treated apples developed 32% senescent scald, while 5% or 10% oil-treated fruit had none. Oil-treated fruit were greener, firmer, and contained more titratable acidity after 8 months of storage than control or DPA-treated apples and pears. In `Granny Smith', 100% of the controls and 79% of the DPA-treated fruit developed coreflush after 8 months of storage, but both 5% and 10% oil-treated fruit were free from coreflush. In `d'Anjou', 34% of the controls and 27% of the DPA-treated fruit showed decay after 8 months of storage, compared with 5% decay in 5% oiltreated fruit, and no decay in 10% oil-treated fruit.
Effects of Lovastatin treatment on ethylene production, α-farnesene biosynthesis, and scald development were studied using `Delicious' and `Granny Smith' apples and `d'Anjou' pears stored in air at 0 °C. During 6 months of storage, Lovastatin did not affect internal ethylene concentration, but reduced α-farnesene production in a concentration-dependent manner in both apples and pears. Lovastatin reduced scald at 0.63 mmol·L-1 and inhibited scald completely at 1.25 or 2.50 mmol·L-1 in `Delicious' and `Granny Smith' apples. In `d'Anjou' pears, Lovastatin at concentrations from 0.25 to 1.25 mmol·L-1 inhibited scald completely. After 8 months of storage, the inhibition of scald in both apples and pears by Lovastatin was concentration-dependent, but none of the concentrations eliminated scald. Compared with 11.8 mmol·L-1 diphenylamine (DPA), Lovastatin treatment reduced scald to the same level at 1.25 mmol·L-1 in `d'Anjou' pear and 2.50 mmol·L-1 in `Delicious' and `Granny Smith' apples. Compared to the controls, Lovastatin did not affect fruit color, firmness, soluble solid contents, or titratable acidity during storage in either apple or pear.
In `Delicious' and `Granny Smith' apples, fruit did not produce α-farnesene until internal ethylene reached about 1 μL•L-1. The correlation between internal ethylene and α-farnesene production was highly significant (r 2 = 0.71 and 0.76, respectively) and fitted the exponential growth equation. Aminoethoxyvinylglycine (AVG) inhibited both internal ethylene and α-farnesene production, while ethephon stimulated them. When applied to discs from preclimacteric fruit peel, cycloheximide and actinomycin D inhibited ethylene and α-farnesene production. In discs from AVG-treated fruit, ethephon induced α-farnesene synthesis. Cycloheximide, actinomycin D, and silver ion counteracted the stimulation effect of ethephon. When added to discs from preclimacteric fruit peel or AVG-treated fruit peel, hydroxymethylglutarc acid, mevalonic acid lactone, and farnesyl pyrophosphate induced α-farnesene synthesis, which was not affected by cycloheximide or actinomycin D.
At harvest, internal ethylene was >0.5 mL·L–1 and α-farnesene concentrations were below detectable levels in `Golden Supreme', `Delicious', and `Granny Smith' apples. After 30 days of storage at 20 °C, control fruit produced high levels of internal ethylene and α-farnesene. Lovastatin at 100 to 1000 mL·L–1 did not affect ethylene synthesis, but significantly inhibited α-farnesene production. In `Golden Delicious', ethephon treatment increased ethylene synthesis in lovastatin-treated fruit but did not stimulate α-farnesene production. In lovastatin-treated fruit peel of `Delicious' and `Granny Smith', mevalonate (MAL) and farnesyl pyrophosphate (FPP) induced α-farnesene production, but hydroxymethylglutaric acid (HMG) did not. The induction of α-farnesene synthesis by MAL and FPP was concentration-dependent. Precursor feeding did not affect ethylene production in fruit peel. When high level of α-farnesene was detected in fruit peel (5 mm thick), it was not found in outer (adjacent to peel) and inner cortex (mid of flesh) tissues. Adding HMG, MAL, and FPP induced α-farnesene biosynthesis in both cortex tissues. When lovastatin was added to the feeding solution, MAL and FPP induced α-farnesene production but HMG did not.
The cuticle is a complex organ. As the first line of defense for apple fruit, its main function is to protect cells from desiccation. It begins developing within several weeks of anthesis and continues responding to environmental conditions until the underlying tissue becomes necrotic. The physicochemical properties of the cuticle differ with cultivar and stage of development but are thought to be composed of carbohydrate fibers extending from the cell wall or the aqueous apoplast. If the latter is true, these fibers could allow contact or exchange with the environment through the lipoidal cuticle matrix. This visual report is the result of an examination of the substructure of the apple cuticle using scanning electron microscopy. These high-resolution micrographs suggest a transcuticular continuum exist in the form of tubular fibers.
Abstract
Deblossomed 8-year-old Malus domestica L. ‘Goldspur Golden Delicious’ trees on seedling rootstock exhibited less extension growth than trees that had carried a crop during either the current year or the previous year. Trees in the “on” year consistently had more extension growth than trees in the “off” year. Fruitful branches of ‘Golden Delicious’ and spur-type ‘Golden Delicious’ generally had more new growth than branches without fruit from the same tree.
CPPU was applied to whole spur `Delicious' apple (Malus domestica Borkh.) trees in central Washington at 0,6.25,12.5,25, or 50 mg·liter-1 at full bloom (FB) or FB plus 2 weeks. At both application times, the flesh firmness of treated fruit linearly increased with increasing concentration. CPPU applied at 0,5,10,15, or 20 mg·liter-1 to spur `Delicious' trees in Massachusetts at king bloom resulted in a linear increase in flesh firmness at harvest and following 28 weeks in air storage at 0C. CPPU did not affect the incidence of senescent breakdown, decay, or cork spot. Fruit length: diameter (L/D) ratios generally increased at all doses. Fruit weight was not influenced at either location. All CPPU concentrations reduced return bloom on `Delicious' apples in Massachusetts in 1989. Of the 10, 20, or 40 mg·liter-1 treatments for `Empire' apples, only CPPU at 40 mg·liter-1 reduced return bloom. CPPU applied to `Empire' apples in Massachusetts did not effect fruit set, soluble solids concentration, L/D, or firmness; however, fruit weight increased linearly with concentration. CPPU applied at 100 mg·liter-1 retarded preharvest fruit drop of `Early McIntosh' in Massachusetts for ≈7 days but was not as effective as NAA at 20 mg·liter-1. In a larger semicommercial trial, `Delicious' fruit treated with CPPU at 5,10, or 15 mg·liter-1 at FB, petal fall (PF), or PF plus 1 week, respectively, were harvested and graded over a commercial packing line. Malformities caused by CPPU at the highest doses reduced packout, although all CPPU application rates reduced the percent fruit culled due to poor color. CPPU increased packed fruit size, since the size of fruit (64 mm in diameter) in the >150-fruit/box size decreased, while the size of fruit (72 mm in diameter) in the 100- and 130-fruit/box sizes increased. Treated fruit stored for 7 months at 1C were firmer than nontreated controls. Chemical names used: N-(2-chloro-4-pyridyl)- N' -phenylurea (CPPU); 1 naphthalene-acetic acid (NAA).
Development of valid temperature-based models of physiological processes such as seed germination, bud development, vegetative growth, fruit development, or fruit maturation, requires a parameter to link temperature with plant metabolism. The Thermal Kinetic Window (TKW) concept uses the temperature characteristics of an enzyme kinetic parameter, the Michaelis constant (Km) as indicators of metabolic efficiency. Recently, Burke3 has shown that the temperature dependence of the rate and magnitude of the reappearance of photosystem II (PSII) variable fluorescence following illumination corresponded with the optimal temperature described by the TKW for several plant species. The present study investigated the use of the temperature sensitivity of PSII fluorescence in the identification of temperature optima of apple cultivars and rootstocks. 3Burke, J.J. 1990. Plant Physiol. 93:652-656.
Effects of α-farnesene biosynthesis precursors on α-farnesene and ethylene production were studied using Lovastatin-treated or nontreated `Delicious' and `Granny Smith' apples [Malus sylvestris (L.) Mill. var. domestica (Borkh.) Mansf.]. In nontreated fruit, α-farnesene was detected only in fruit peel (≈3 mm) and not in the more proximal cortical tissue. α-Farnesene was not detectable in preclimacteric fruit peel at harvest. Mevalonic acid lactone (MAL) or farnesyl pyrophosphate (FPP) induced α-farnesene production when fed to preclimacteric peel tissue, but hydroxymethylglutaric acid (HMG) did not. Fruit stored at 0 °C for 30 days (climacteric fruit) produced α-farnesene, and addition of HMG, MAL, or FPP further increased α-farnesene production. When treated at harvest with Lovastatin at 1.25 mmol·L-1 and stored at 0 °C for 30 days, fruit produced ethylene but did not produce α-farnesene. Whereas MAL and FPP induced α-farnesene production in peel sections from these fruit, HMG did not. Induction of α-farnesene by precursor feeding was concentration-dependent and had no effect on ethylene production. Cortical tissue sections from climacteric fruit did not produce α-farnesene unless HMG, MAL, or FPP were fed during incubation. Including Lovastatin at 0.63 mmol·L-1 in the feeding solution eliminated HMG induced α-farnesene production, but did not affect MAL or FPP-induced α-farnesene production. Neither precursor feeding nor Lovastatin treatment affected ethylene production in cortical tissues. Chemical name used: [1S-[1a (R°), 3α, 7β, 8β (2S°, 4S°), 8αβ]]-1,2,3,7,8,8α-hexahydro-3,7-dimethyl-8-[2-(tetrahydro-4-hydroxy-6-oxo-2H-pyran-2-yl)ethyl]-1-naphthalnyl 2-methylbutanoate (Lovastatin).
Lovastatin is a specific hydroxymethylglutaryl coenzyme-A reductase inhibitor in animals and as such, is a potent cholesterol lowering pharmaceutical for human use. Because it has also been shown to inhibit α-farnesene in certain plants, we investigated its effects on ethylene and α-farnesene biosynthesis, volatile production, and fruit color during ripening in `Golden Supreme' apples [Malus sylvestris (L.) Mill. var. domestica (Borkh.) Mansf.]. Immediately after harvest, fruit were dipped in Lovastatin solution for 2 min, allowed to dry, and stored in the dark at 20 °C for 30 days. Internal ethylene at harvest was low (< 0.1 mL·L-1) and α-farnesene was undetectable. Both internal ethylene and α-farnesene increased in nontreated fruit during 30 days storage. Prestorage Lovastatin treatment did not affect ethylene synthesis, but at 1.25 or 2.5 mmol·L-1 nearly eliminated α-farnesene production. At 0.25 mmol·L-1, Lovastatin delayed the increase in α-farnesene production about 12 days and reduced total α-farnesene production by the end of storage compared with controls. When applied to nontreated preclimacteric fruit, ethephon at 1.4 mmol·L-1 increased both internal ethylene concentration and α-farnesene production. In Lovastatin-treated preclimacteric fruit, however, ethephon increased internal ethylene concentration without promoting α-farnesene synthesis. In another trial, after 30 days storage at 0 °C, fruit were treated with 1.25 mmol·L-1 Lovastatin and stored at 20 °C with air circulation for 20 days. These fruit accumulated similar amounts of ethylene as nontreated controls, but α-farnesene production decreased rapidly and was not detectable after 5 days. Treating with ethephon at 1.4 mmol·L-1 increased α-farnesene production in control fruit but not in Lovastatin-treated fruit. Lovastatin treatment did not affect the change in fruit color. Chemical names used: [1S-[1α (R °), 3α, 7β, 8β (2S °, 4S °), 8ab]]-1,2,3,7,8,8α-hexahydro-3,7-dimethyl-8-[2-(tetrahydro-4-hydroxy-6-oxo-2H-pyran-2-yl)ethyl]-1-naphthaienyl 2-methylbutanoate (Lovastatin); 2-chloroethylphosphonic acid (ethephon).