One strategy to reduce postharvest losses of fruits to pathogens is to introduce organisms with biological control capabilities. Our objective was to determine the effectiveness of two yeast isolates in inhibiting lesion development caused by Botrytis cinerea (Bc) on freshly harvested apples differing in maturity. `Golden Delicious' apples were harvested on 29 Aug., 23 Sept., and 10 Oct. 1995. Apples receiving the seven treatments [control, wound, Cryptococcus humicola (Ch), Sporobolomyces roseus (Sr), Bc, Ch + Bc, Sr + Bc] were placed in plastic boxes with damp paper towels. Each day for 7 days, ethylene production and lesion diameter at the wound were recorded. Ethylene production was not affected by treatment, and increased with later harvest date. Lesion diameter on apples treated with Bc was smaller on the first harvest than on the second and third harvests. Sr provided partial control on the second and third harvests, and Ch completely inhibited lesion development except for day 7 of the third harvest.
Jeffrey A. Anderson, Alexander B. Filonow and Helen S. Vishniac
Jeff Anderson, Alexander B. Filonow and Helen S. Vishniac
Strategies to reduce postharvest losses of fruit to pathogens include low-temperature storage, fungicides, and use of organisms with biological control capabilities. Our objective was to determine the effectiveness of two yeast isolates in inhibiting lesion development caused by Botrytis cinerea (Bc) on freshly harvested apples of different maturity. `Golden Delicious' apples were harvested on 29 Aug., 23 Sept., and 10 Oct. 1995. Apples comprising the seven treatments [control, wound, Cryptococcus humicola (Ch), Sporobolomyces roseus (Sr), Bc, Bc + Ch, Bc + Sr] were placed in plastic boxes with damp paper towels. Each day for 7 days, ethylene and CO2 production and lesion diameter at the wound were recorded. Ethylene and CO2 production were not affected by treatment. Lesion diameter on apples treated with Bc was smaller on the first harvest, compared with the second and third harvests. Sr provided partial control on the second and third harvests, and Ch completely inhibited lesion development on all harvests.
Galen Peiser, Gloria López-Gálvez, Marita Cantwell and Mikal E. Saltveit
Russet spotting is a physiological disorder of lettuce (Lactuca sativa L.) caused by exposure to hormonal levels (<1 μL·L-1) of ethylene in air at ≈5 °C. Enhanced phenolic metabolism and the accumulation of phenolic compounds accompany the appearance of brown, oval lesions on the leaf midrib. Phenylalanine ammonia-lyase (PAL) is the first committed enzyme in the phenylpropanoid pathway. Three inhibitors of PAL activity [2-aminoindan-2-phosphonic acid (AIP), α-aminooxyacetic acid (AOA), and α-aminooxi-β-phenylpropionic acid (AOPP)] greatly reduced the accumulation of phenolic compounds and browning of lesions. At a concentration of 50 μm, AIP inhibited the formation of chlorogenic and dicaffeoyl tartaric acids in cut midribs of iceberg lettuce by 92% and 98%, respectively. AIP competitively inhibited PAL activity from a lettuce midrib homogenate with an apparent Ki of 22 nm. While the formation of phenolic compounds was strongly inhibited by AIP, the number of lesions associated with russet spotting was not affected. Only the color of the lesions was affected by AIP. In control midribs the russet spotting lesions were brown while those in the AIP-treated midribs were initially olive green and after 3 to 7 days these lesions turned the characteristic brown color. No tyrosine ammonia-lyase activity was detected in a homogenate of lettuce midrib tissue. These results indicate that the early development of russet spotting lesions is independent of the increase in PAL activity and phenolic compounds rather than an effect of these increases as previously suggested. However, accumulation of phenolic compounds does contribute to the subsequent browning symptoms indicative of russet spotting.
Joshua K. Craver, Chad T. Miller, Kimberly A. Williams and Daniel L. Boyle
“lesion” is used when referring to these abnormal growths. The objective of this research was to further characterize lesion nomenclature and development on four plant species: ornamental sweetpotato ‘Blackie’, tomato ‘Maxifort’, interspecific hybrid
Abbasali Ravanlou and Mohammad Babadoost
were inoculated. Inoculated plants were placed in a greenhouse at 24 to 28 °C with 14-h photoperiod. During 3 weeks from inoculation, development of the symptoms, including water-soaked and necrotic lesions were recorded. The pathogen was isolated from
Richard O. Nyankanga, Ocen Modesto Olanya, Hans C. Wien, Ramzy El-Bedewy, John Karinga and Peter S. Ojiambo
premature death of the potato plant and tuber rot in the field and storage. Tubers become infected when sporangia produced on leaf and stem lesions are washed into the soil ( Lacey, 1967 ). In vitro tuber blight development may occur through occasional tuber
Jiaqi Yan, Megan M. Dewdney, Pamela D. Roberts and Mark A. Ritenour
treatment had no significant inhibition on CBS development ( Agostini et al., 2006 ; Lucon et al., 2010 ). Infected fruit may develop lesions after packing and shipping that could eventually exceed USDA grade standards, causing economic losses from
Melinda A. Miller-Butler, Barbara J. Smith, Kenneth J. Curry and Eugene K. Blythe
epidemics ( Forcelini and Peres, 2018 ; LaMondia, 1995 ; Smith and Black, 1993a , 1993b ). Ideal anthracnose disease control relies on the development and planting of disease-resistant cultivars. Many years are required to develop anthracnose
Norman Lalancette, Daniel L. Ward and Joseph C. Goffreda
the causal agent ( Daines and Trout, 1977 ; Ries and Royse, 1978 ). Recent molecular-based research examining the rDNA internal transcribed spacer sequences of fungal thallus from rusty spot lesions has confirmed the pathogen to be P. leucotricha
Qianni Dong, Xinwang Wang, David H. Byrne and Kevin Ong
, 2000 ). The typical symptoms of this disease include dark rounded spots with a feathery edge on the adaxial side of the leaves while the abaxial epidermis remains unaffected. The disease can lead to the development of chlorosis around the lesion and