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논문 기본 정보

자료유형
학술저널
저자정보
Young Ho Kim (Seoul National University) Kyung Soo Kim (University of Arkansas) Robert D. Riggs (University of Arkansas)
저널정보
한국식물병리학회 The Plant Pathology Journal The Plant Pathology Journal Vol.28 No.4
발행연도
2012.12
수록면
401 - 408 (8page)

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초록· 키워드

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Initial subcellular responses in susceptible (PI 274420) and resistant (cv. Hartwig) soybeans infected with the soybean cyst nematode (SCN) were examined 2 and 4 days after inoculation (DAI). Subcellular features common to both soybeans at 2 DAI included hypertrophied initial syncytial cells (ISCs) and syncytium-component cells (SCs) with a dense cytoplasm containing proliferated rough and smooth endoplasmic reticulum (RER and SER), a hypertrophied nucleolus, and reduced vacuoles, suggesting that the nematode-infected cells were dedifferentiated. In the resistant soybean, a striking initial subcellular difference from the susceptible soybean was the dilation of the RER, indicating ER dysfunction and leading to cell death. This disturbed nematode feeding, as evidenced by disrupted feeding tubes. In PI 274420, the ISC cytoplasm was depleted, with the exception of ER membranes, at 4 DAI, while the SC cytoplasm was dense with proliferation of starch-containing plastids around multiple nuclei that might be derived from the congregation of nuclei in the neighboring SCs and in part by nuclear division without cytokinesis. In cv. Hartwig, syncytia were necrotized with secondary cell wall thickening outside the plasma membrane and an extremely dense cytoplasm containing a nucleus with an electron-lucent nucleolus, accompanied by the proliferation of closely stacked parallel RER and ribosomes. These results suggest that syncytia develop continuously in PI 274420 to produce and store nutritional substances in SCs, providing for the nematode through ISC until maturation, but in cv. Hartwig, syncytia degenerate early due to excessive metabolism, blocking nematode feeding and cytoplasmic connections with adjacent intact cells.

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Materials and Methods
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UCI(KEPA) : I410-ECN-0101-2014-481-000638891