• Korean Journal of Medicinal Crop Science
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• v.6 no.4
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• pp.277-285
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• 1998

Antifungal activity on major seedborne diasease of crops was screened by the treatment of the extracts from 50 medicinal plants in vitro and in vivo. The extracts of garlic and taxus, Rheum undulatum, Achiranthes japonica, Glycyrrhiza uralensis, Oenothera lamar kiana treated with the blotting filter paper and water agar methods inhibited the growth of Pyricularia oryzae, Alternaria sesamicola, Colletotrichum gloeosporioides, and Alternaria brassicicola among the tested plants. Antifungal activities on infected seeds by soaking methods were shown even at the dilution of the extracts by 10 times. The activity was the highest in soaking seeds at $25^{\circ}C$ for 24 hours. The effect of plant extract on seed germination was not significant as compared with untreated seed. However, early growth of seedling was increased by the treatment of extracts. The extract of taxus slightly inhibited the seed germination of radish and chinese cabbage but those of Achirunthes japonica, Glycyrrhiza uralensis and Oenthfera lamarkiana showed severe damage on the seed germination and early growth of seedling.

• Korean journal of applied entomology
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• v.26 no.4 s.73
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• pp.221-228
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• 1987

The optimum temperature range for conidial germination of Pyriculacia oryzae on a slide glass was $26{\sim}30^{\circ}C$, at which at least four hours of leaf wetness period was required to germinate. Conidial germination was significantly reduced under dry conditions (relative humidity<85%) at $34^{\circ}C$ but not at lower temperature (18, 22, 26, $30^{\circ}C$). Number of lesions developed were greater at $26^{\circ}C$ than at other temperature tested. The average leaf wetness period required for production of a lesion per plant was 22 hours at $18^{\circ}C$, 16 hours at $22^{\circ}C$, 10 hours at $26^{\circ}C$, and 8 hours at $30^{\circ}C$. Less than one lesion per plant occurred at $34^{\circ}C$ even under 24 hours of leaf wetness period. The time period between inoculation and lesion appearance was $7{\sim}8$ days at $18^{\circ}C$, $4{\sim}5$ days at $22^{\circ}C$ and $26^{\circ}C$, and $3{\sim}4$ days at $30^{\circ}C$. The time period required for lesion appearance after inoculation was not affected by leaf wetness period and relative humidity. Lesion length increased most rapidly at $30^{\circ}C$ during the first four days after lesion appearance. Thereater, the rate of increase in lesion length was geratest at $26^{\circ}C$. The average increment of lesion length per day when relative humidity was greater than 90% was 0.7mm at $18^{\circ}C\;and\;22^{\circ}C$, 1mm at $26^{\circ}C$, and 0.8mm at $30^{\circ}C$. When relative humidity was less than 85%, the increments of lesion length per day were approximately $50{\sim}60%$ of those under humid conditions (relative humidity>90%) at all temperature regimes except $30^{\circ}C$. Relative humidity did not significantly affected lesion length at $30^{\circ}C$.

• Korean Journal of Breeding Science
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• v.51 no.4
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• pp.395-403
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• 2019

Rice blast caused by the fungus Magnaporthe grisea (anamorphic: Pyricularia oryzae) is an important disease in rice and development of resistant varieties to blast is one of the most important goals in rice breeding programs. A japonica rice variety, Palgong, has shown resistance to the Korean blast pathogen since it was developed in 1996. Nine blast resistance quantitative trait loci (QTLs) in Palgong alleles were identified on chromosomes 2, 4, 7, and 11. Four QTLs of qBn2.3, qBn4.2, qBn11.1, and qBn11.2 explained 28-56.7% of total phenotypic variation, while five QTLs of qBn2.2, qBn2.4, qBn4.1, qBn7.1, and qBn7.2 explained 9.7-18.8%. In a previous study, one to four resistance genes were located on the loci qBn2.2, qBn2.3, qBn4.2, qBn11.1, and qBn11.2, however, resistance genes were not located on the loci qBn2.4, qBn4.1, and qBn7.1. A major QTL, qBn11.2, explaining 56.7% of total phenotypic variation was related to the durable resistance of Palgong. Additionally, rice stripe virus resistance of Palgong was assumed to be based on the Stvb-i gene, which is located on a major QTL qBn11.2.