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  • Author or Editor: C. Rom x
  • Journal of the American Society for Horticultural Science x
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Abstract

Young peach trees 1) trained to a single shoot or 2) allowed to branch, were pruned by removing 50% of current growth at either or both of 2 summer dates. Another group of trees had 0%, 25%, 50%, and 75% shoot growth removed by pruning in midseason. Net photosynthesis (Pn) and transpiration (Tr) were increased within 3 days after pruning at either date. Plants pruned twice at 30-day intervals had a 2nd cycle of increased Pn and Tr, with rates returning to levels of unpruned controls within 24 days. Distribution of water soluble carbohydrates in various plant tissues was not altered by pruning. Pruning at 60 days reduced root starch, whereas pruning again at 90 days increased total root carbohydrate content. Pruning early in the season increased lateral shoot formation, and terminal bud formation was delayed by pruning. Plant dry weight was reduced by all pruning treatments, with delayed pruning and increasing pruning severity resulting in greatest reductions. Distribution of dry weight was not altered substantially by pruning, and a balance of growth was maintained between different plant parts.

Open Access

Abstract

Leaves of spurs and/or shoots of small fruiting ‘Starkrimson Delicious’ apple trees were exposed to light or shade treatments from 60 days after petal fall until fruit maturity. Shading spurs reduced spur leaf photosynthesis (Pn) and transpiration (Tr), but shading shoots had no effect on spur leaf Pn. There was no difference between fruiting and nonfruiting spur Pn and Tr. Shading shoots reduced fruit growth and delayed maturity, but shading spurs had no effect on either. Fruiting reduced—but did not eliminate—spur flowering the following year. Light conditions late in the season had no effect on flowering or spur leaf development the following spring.

Open Access

Abstract

Trees of Malus domestica (Borkh.) ‘Miller Sturdeespur’ were hand thinned to achieve light, medium, and heavy fruit loads. A heavy European red mite (ERM), Panonychus ulmi (Koch), infestation was encouraged by mite seeding and predator elimination in half the trees for each fruit load. The effect of these treatments were determined on fruit number, number and percentage of drops, fruit size, color, soluble solids, titratable acidity, pH, firmness, and percentage of foliar concentration for 5 macronutrients. Mite feeding increased the percentage of drop and reduced red pigmentation, soluble solids, and leaf phosphorus and calcium. Deleterious effects of mite feeding increased with increasing fruit load. With light fruit loads, heavy mite feeding had a negligible effect on fruit quality.

Open Access

When sweetpotato chlorotic stunt crinivirus (SPCSV) and sweetpotato feathery mottle potyvirus (SPFMV) infect sweetpotato [Ipomoea batatas (L.) Lam.], they interact synergistically and cause sweetpotato virus disease (SPVD), a major constraint to food productivity in east Africa. The genetic basis of resistance to these diseases was investigated in 15 sweetpotato diallel families (1352 genotypes) in Uganda, and in two families of the same diallel at the International Potato Center (CIP), Lima, Peru. Graft inoculation with SPCSV and SPFMV resulted in severe SPVD symptoms in all the families in Uganda. The distribution of SPVD scores was skewed toward highly susceptible categories (SPVD scores 4 and 5), eliminating almost all the resistant genotypes (scores 1 and 2). Likewise, when two promising diallel families (`Tanzania' × `Bikilamaliya' and `Tanzania' × `Wagabolige') were graft inoculated with SPCSV and SPFMV at CIP, severe SPVD was observed in most of the progenies. Individual inoculation of these two families with SPCSV or SPFMV, and Mendelian segregation analysis for resistant vs. susceptible categories led us to hypothesize that resistance to SPCSV and SPFMV was conditioned by two separate recessive genes inherited in a hexasomic or tetradisomic manner. Subsequent molecular marker studies yielded two genetic markers associated with resistance to SPCSV and SPFMV. The AFLP and RAPD markers linked to SPCSV and SPFMV resistance explained 70% and 72% of the variation in resistance, respectively. We propose naming these genes as spcsv1 and spfmv1. Our results also suggest that, in the presence of both of these viruses, additional genes mediate oligogenic or multigenic horizontal (quantitative) effects in the progenies studied for resistance to SPVD.

Free access