CYTOLOGICAL EXPRESSION OF EARLY RESPONSE TO INFECTION BY HETERODERA-GLYCINES ICHINOHE IN RESISTANT PI-437654 SOYBEAN

Citation
R. Mahalingam et Ht. Skorupska, CYTOLOGICAL EXPRESSION OF EARLY RESPONSE TO INFECTION BY HETERODERA-GLYCINES ICHINOHE IN RESISTANT PI-437654 SOYBEAN, Genome, 39(5), 1996, pp. 986-998
Citations number
37
Categorie Soggetti
Genetics & Heredity
Journal title
GenomeACNP
ISSN journal
08312796
Volume
39
Issue
5
Year of publication
1996
Pages
986 - 998
Database
ISI
SICI code
0831-2796(1996)39:5<986:CEOERT>2.0.ZU;2-8
Abstract
The soybean PI 437654 is resistant to all known races of the soybean c yst nematode (SCN) in the U.S.A. and became a new source of resistance genes in cultivar development. Race 3, a wide-ranging nematode pathot ype, was used to examine root cells of PI 437654 and susceptible 'Esse x', 2, 3, and 5 days after inoculation (DAI). In initial response to S CN, both genotypes formed syncytia by cell wall dissolutions. Hypertro phy of syncytium component cells and hyperplasia of cells near syncyti a were observed. At 2 DAI, incompatible response of PI 437654 to SCN w as exhibited: limited cell hypertrophy, inhibition of syncytium growth , initiation of necrosis, and wall appositions. At 3 DAI, cellular eve nts appeared to be a sum of the operative mechanisms for SCN resistanc e: irregular wall thickening, pronounced wall appositions, necrosis, a nd nuclear breakdown followed by cytoplasmic collapse. The cells surro unding the syncytia showed necrosis, wall apposition, and accumulation of electron-dense bodies. By 5 DAI, syncytia and neighboring cells we re totally devoid of ground plasma and the degeneration process was co mpleted. The normal route for early syncytium development in 'Essex' ( increased number of organelles, intense vacuolization, accumulation of dense deposits in vacuoles, and wall ingrowths) suggests the involvem ent of portions of the developmental pathway of differentiating tissue s in organogenesis. Early onset of SCN resistance 2 DAI in PI 437654 s uggests rapid activation of genes in a cascade reaction leading to cel l death.