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Abstract

Standardized raw fruits of 6 texturally different pickling cucumber (Cucumis sativus L.) genotypes and 1 parthenocarpic slicing genotype were compared for several pericarp features: total radial thickness, % of fruit radius (% pericarp), overall average parenchyma cell size and number within the pericarp radius, as well as gradient in parenchyma cell size along this radius. Texture-related rank positions were devised and assigned genotypes for each pericarp feature. These were compared to rank positions assigned these genotypes for several textural components, based on machine-measured scores. Correlation analysis showed a strong relationship between ranking genotypes for texture and ranking them for average cell number but not for texture and any of the other pericarp features. The slicing genotype deviated from the very uniform pickling genotypes in having a significantly thicker pericarp, greater % pericarp, and greater cell size across the pericarp radius.

Clusters of Vitis labruscana cv. Concord were grown either in full sun or canopy shade, and either not sprayed or sprayed with 3.4 Kg/Ha chlorothalonil every 2 wk from pre-bloom to veraison. Only sun-exposed, sprayed fruit produced skin russeting. Clusters of the very susceptible V. vinifera cv. Rosette were grown in direct sun, sprayed with chlorothalonil 4 times from bloom to veraison, in the presence or absence of purported anti-russeting agents. Heavy russet occurred in all treatments. Russet initiation was similar in the 2 cvs.: epidermal cells first died beneath spray residue in full sun, a phellogen then arose in the hypodermis, followed by periderm. Epidermal death began in `Rosette' within a wk of the bloom spray, but in `Concord' only after 2-3 wk post bloom and 3 sprays. `Concord' russet generally appeared as patches or scabs, whereas `Rosette' russet ranged from freckles, welts, scabs to large smooth burnished areas. In both cvs., unbroken russet consisted of uniform layers of phellum. New, deeper periderm initials arose beneath checks and cracks which formed as fruit enlarged. In `Concord', but not `Rosette', the daughter cells of each such initial were often enclosed in the original cell wall. In all cases of russet, cell walls in the periderm were suberized and sometimes lignified. Cells also contained much phenolic material.

Grapevine yellows is a destructive, worldwide disease of grapevines that is caused by a phytoplasma, a bacterium-like organism that infects and disrupts the vascular system of shoots. The North American form of grapevine yellows (NAGY) has been observed in New York State since the mid-1970s and in Virginia since the mid-1990s. Symptoms duplicate those of vines suffering from an Australian disease complex known as Australian grapevine yellows (AGY). We sought to determine if infected `Chardonnay' vines have common anatomical characteristics across the three regions. At each geographic site in late summer, 2003–04, leaf and internode samples were taken from younger green regions of shoots and from mature basal regions in the fruiting zone. These were processed for histology. The anatomy of each organ type was compared between locations on the shoot, between geographic locations, and between affected and normal shoots. The phloem was the only tissue universally affected in vines with NAGY or AGY symptoms. In stem internodes, both primary phloem and secondary phloem showed many senescent cells, abnormally proliferated giant cells, and hyperplasia. In affected secondary phloem there was disruption of the radial files of cells that normally differentiate from the cambium into mature phloem cell types. Normal bands of secondary phloem fibers (“hard phloem”) in internodes were weak or absent in affected vines. Leaves also had disrupted phloem organization but near-normal xylem organization in vines with symptoms. Leaves of infected vines frequently showed a disruption of sugar transport out of the leaf blades, manifested by a heavy buildup of starch in chloroplasts of mesophyll cells and bundle-sheath cells.

Overwintering buds and internodes of Vitis labruscana `Concord' were taken from minimal- (MP) and balance-pruned (BP) vines in Dec. 1993 and Dec. 1994 from canes whose weight, crop weight, total nodes, and nodes with periderm were known. Winter characters recorded were: node-5's primary bud basal area, total nodes, and developmental stage of cluster primordia; stage of largest cluster in the secondary bud; vascular area of cane internode 5. Fifty node-5 buds were tagged in each treatment and flower and fruit number per cluster later recorded. Regression analysis showed no effect of a shoot's crop, cane weight, node number, or nodes having periderm on any character measured in the overwintering buds or canes for either treatment. Regression analysis did show mean flower number per cluster was linearly related to mean winter stage per cluster in both treatments, with all values falling on one line. Differences between treatments were one of degree of cluster development; BP vines had more-developed winter and spring clusters and more flowers and fruit per shoot. The slope of the regression was identical the last 3 years, although the y intercept varied each year; thus, a given cluster stage in the overwintering bud was capable of producing a variable number of flowers the next season, depending on year. Flower number per shoot appeared positively related to growing-degree-days the previous season.

The objective of this research was to determine the effect of water temperature during spring and fall floods on nonstructural carbohydrate concentration and anatomy/morphology of ‘Stevens’ and ‘Early Black’ cranberry vines. Potted vines of each cultivar were subjected to either a simulated 1-month late water (LW) flood in the spring at either 11 or 21 °C or a simulated 1-week harvest flood in the fall at either 12 or 20 °C. Higher water temperature resulted in decreased total nonstructural carbohydrate concentration (TNSC) during the LW flood in both uprights (i.e., vertical shoots) and roots of ‘Early Black’ and ‘Stevens’. The effect of water temperature was much less during the harvest flood than during the LW flood, but flooding at either temperature during the harvest flood had an impact on TNSC, whereas for LW floods, high water temperature was more influential than low water temperature. Clumping of chloroplasts in the palisade layer and occlusion of vascular tissues was observed in the leaves of both cultivars as a result of LW flooding. Some epidermal erosion and formation of a fungal mat was apparent on the upper epidermis of some flooded leaves. Senescence in some fine roots was visible after harvest flooding, more so in vines flooded at 20 °C than at 12 °C. Stems and major roots showed no influence of flooding on tissue senescence.

In 2002 in New York State, we collected king fruit of `Gala' and `Red Delicious' on fruiting spurs from 0 to 66 days after full bloom (DAB). In 2003 in Washington State, we collected king fruit of these cultivars from 14 to 62 DAB. At each collection we determined radial cell number across the fruit cortex and developmental stage of the embryo and endosperm in seeds. Fruit diameter was slightly greater in Washington fruit than in New York fruit until about 40 DAB; thereafter, New York `Delicious' outgrew Washington `Delicious', while `Gala' in the two climates (and two different years) grew identically. The New York fruits had a much earlier rise in fruit growth rate and maintained a slightly higher rate throughout the period. The cortex thickness of Washington fruit was greater than that of New York fruit for both cultivars. Most rapid cell division in the cortex occurred between 10 and 28 DAB and, by 40 DAB, most cell proliferation had ceased. The Washington fruit formed more cells across the radius than did New York fruit. Cortex thickness increased with respect to increase in cortex cell number about 30% to 40% faster in Washington fruit than in New York fruit. Developmental stages of embryos and endosperm followed a sigmoid time pattern for both cultivars in both states. By 60 DAB, embryos and endosperm reached their maximum stage of development. In both cultivars and states, cell divisions were nearly completed by the time the embryo and endosperm approached stage 3: for embryos this is the heart-shaped stage, for endosperm it is near completion of cell wall formation. The completion of wall formation in the endosperm, the near completion of cortex cell division, and the generation of the cotyledons and apical meristems in the embryo are highly correlated processes. We saw no evidence that endosperm development precedes embryo development.

For 4 years, six-flowered clusters on 20, unthinned, open-pollinated `Empire'/MM106 trees were labeled at bloom and fruit drop monitored at the king (K) and lateral positions L1 (basal) to L5 (distal) (100 to 120 clusters/year). Depending on year, fruit dropped in 1, 2, or 3 major periods by 8 weeks postbloom (PB), with total percent dropped between 65% and 75%. K fruit dropped least, L4 and L5 most. Trends were that K fruit at October harvest were largest and heaviest (significantly so in some years) and L5 fruit smallest. In nine trees, hand-thinned to single-fruited spurs at 12 days PB, where the fruit at the retained position was known, there was no statistical difference in fruit weight, fruit size, or seed count between cluster positions at final harvest, although L5 fruit tended to be smallest. Numbers of spurs labeled varied from 45 to 72. Percent fruit retained at each position at October harvest was K = 89%, L1 or L2 = 87%, L3 = 83%, L4 = 83%, and L5 = 85%. Presumably, in unthinned trees the limited resources are preferentially taken by the K fruit, which especially seems to reduce set and size of its nearest lateral fruit. However, in thinned trees under lighter cropping stresses, a fruit retained at any of the positions within a cluster has a similar potential for achieving the size and weight typically seen in king fruit.

Winter buds of `Concord' and `Niagara' grapevines were dissected and their embryonic clusters scored to developmental stage. Stage was regressed against flower and fruit number per cluster the following year to see if flowering or fruiting potential could be gauged from bud morphology. `Concord' vines were either minimal-pruned (MP) or balance-pruned (BP) and non-irrigated or provided supplemental irrigation. `Niagara' vines were BP vines which were non-irrigated, irrigated, or nitrogen fertigated. Winter buds of MP `Concord' were significantly less developed than buds of BP vines, and flower and fruit number per cluster also significantly less. Irrigation did not affect bud construction or flower or fruit number per cluster in either pruning regime. Winter buds of `Niagara' had similar cluster stages in all treatments and there were similar flower and fruit number per cluster the following season. Within cultivar and year, there was a positive linear relationship between mean flower number or fruit number per cluster and mean stage of cluster differentiation within buds the previous dormant period. In `Concord', a given winter cluster stage allowed production of significantly more flowers and fruit in 1992 than it did in 1993. A bud's flowering potential thus varies from year to year and depends on factors not solely related to bud morphology.

The perisperm–endosperm (PE) envelope surrounding the embryo of cucumber (Cucumis sativus) acts as a barrier to apoplastic permeability and radicle emergence. The envelope consists of a single cell layer of endosperm whose outer surface is covered by noncellular lipid and callose-rich layers. We compared the structure and histochemistry of the radicle tip and chalazal regions of the envelope, because these regions differ in permeability. Seeds were treated with coumarin 151, a nonionic, fluorescent tracer with systemic activity. Treated seeds were imbibed and on seedcoat removal, the root tip area of the membrane-covered embryo accumulated the fluorescent tracer, but the tracer could not penetrate the envelope that bordered the cotyledons and chalazal region. The cone-shaped remnant of tissue opposite the micropylar region of the envelope was identified as nucellar tissue, the “nucellar beak.” The cuticular membrane and callose layer of the PE envelope were interrupted in the nucellar beak as well as in the chalazal region. Their role in permeability is apparently substituted by the presence of thick-walled suberized cells in the beak and chalaza. A canal was observed in the center of the nucellar beak that likely provided a conduit for the tracer to diffuse from the environment to the embryo. This canal was the remnant of pollen tube entry through the nucellus and was plugged with several cells, presumably residue of the suspensor. These cells degenerated just before cucumber seed germination. This remnant of the pollen tube canal presumably offers less mechanical resistance in the nucellar beak that might help facilitate radicle protrusion during germination. Cells of the outermost and basal regions of the nucellar beak as well as the walls of endosperm cells contained pectic material. Significant pectin methylesterase activity was found in the lateral and cap regions of the PE envelope long before seed germination. Lack of callose in the envelope at the radicle tip suggests that callose does not act as a barrier to radicle emergence during cucumber seed germination.

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.