Abstract
Lactofen belongs to the diphenylether class of herbicides, which targets protoporphyrinogen oxidase, which in turn causes singlet oxygen generation. In tolerant plants like soybean (Glycine max), the chemical nonetheless causes necrotic patches called "bronzing" in contact areas. Here it is shown that such bronzing is accompanied by cell death, which was quantified from digital microscopic images using Assess Software. Cellular autofluorescence accompanied cell death, and a homolog of the cell death marker gene, Hsr203j, was induced by lactofen in treated soybean tissues. Thus, this form of chemically induced cell death shares some hallmarks of certain types of programmed cell death. In addition to the cell death phenotype, lactofen caused enhanced expressions of chalcone synthase and chalcone reductase genes, mainly in the exposed and immediately adjacent (proximal) cells. Furthermore, isoflavone synthase genes, which are wound inducible in soybean, were up-regulated by lactofen in both proximal and distal cell zones in minimally wounded cotyledons and further enhanced in wounded tissues. Moreover, if the wall glucan elicitor from Phytophthora sojae was present during lactofen treatment, the induction of isoflavone synthase was even more rapid. These results are consistent with the fact that lactofen triggers massive isoflavone accumulations and activates the capacity for glyceollin elicitation competency. In addition, lactofen induces late expression of a selective set of pathogenesis-related (PR) protein genes, including PR-1a, PR-5, and PR-10, mainly in treated proximal tissues. These various results are discussed in the context of singlet oxygen-induced responses and lactofen's potential as a disease resistance-inducing agent.
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Claims 10
Claim · model-written summary
Lactofen bronzing in soybean was accompanied by cell death.
Not reportedTaxon
Verbatim
e0“such bronzing is accompanied by cell death”
Claim · model-written summary
Cellular autofluorescence accompanied soybean cell death after lactofen treatment.
Not reportedTaxon
Verbatim
e0“Cellular autofluorescence accompanied cell death”
Claim · model-written summary
Lactofen induced a homolog of Hsr203j in soybean tissue.
- Taxon
- soybean
Glycine maxe0 - Treatment
- lactofene0
- Gene
- Hsr203je0
- Outcome
- cell death marker genee0
- Direction
- inducede0
Not reportedComparator
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“a homolog of the cell death marker gene, Hsr203j, was induced by lactofen in treated soybean tissues”
Claim · model-written summary
Lactofen enhanced chalcone synthase and chalcone reductase gene expression, mainly in exposed and proximal soybean cells.
- Organ / stage
- exposed and immediately adjacent (proximal) cellse0
- Treatment
- lactofene0
- Gene
- chalcone synthase and chalcone reductase genese0
- Outcome
- expressions of chalcone synthase and chalcone reductase genese0
- Direction
- enhancede0
Not reportedTaxonComparator
Verbatim
e0“lactofen caused enhanced expressions of chalcone synthase and chalcone reductase genes, mainly in the exposed and immediately adjacent (proximal) cells”
Claim · model-written summary
Lactofen up-regulated isoflavone synthase genes in proximal and distal soybean cotyledon zones.
- Taxon
- soybeanGlycine maxe0
- Organ / stage
- minimally wounded cotyledonse0
- Treatment
- lactofene0
- Gene
- isoflavone synthase genese0
- Outcome
- isoflavone synthase genese0
- Direction
- up-regulatede0
Not reportedComparator
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“isoflavone synthase genes, which are wound inducible in soybean, were up-regulated by lactofen in both proximal and distal cell zones in minimally wounded cotyledons”
Claim · model-written summary
Wounding further enhanced lactofen-induced isoflavone synthase expression in soybean tissue.
Not reportedTaxonGeneOutcome
Verbatim
e0“were up-regulated by lactofen in both proximal and distal cell zones in minimally wounded cotyledons and further enhanced in wounded tissues”
Claim · model-written summary
Adding Phytophthora sojae wall glucan elicitor during lactofen treatment accelerated isoflavone synthase induction.
- Treatment
- wall glucan elicitor from Phytophthora sojaee0
- Interactor
- Phytophthora sojaePhytophthora sojaee0pathogen
- Gene
- isoflavone synthasee0
- Outcome
- induction of isoflavone synthasee0
- Direction
- even more rapide0
Not reportedTaxonComparator
Verbatim
e0“if the wall glucan elicitor from Phytophthora sojae was present during lactofen treatment, the induction of isoflavone synthase was even more rapid”
Claim · model-written summary
Lactofen triggered massive isoflavone accumulation in soybean.
Not reportedTaxonComparator
Verbatim
e0“lactofen triggers massive isoflavone accumulations”
Claim · model-written summary
Lactofen activated soybean glyceollin elicitation competency.
Not reportedTaxonComparator
Verbatim
e0“lactofen triggers massive isoflavone accumulations and activates the capacity for glyceollin elicitation competency”
Claim · model-written summary
Lactofen induced late expression of PR-1a, PR-5 and PR-10, mainly in treated proximal soybean tissues.
- Organ / stage
- treated proximal tissuese0
- Treatment
- lactofene0
- Gene
- PR-1a, PR-5, and PR-10e0
- Outcome
- expression of a selective set of pathogenesis-related (PR) protein genese0
- Direction
- inducese0
Not reportedTaxonComparator
Verbatim
e0“lactofen induces late expression of a selective set of pathogenesis-related (PR) protein genes, including PR-1a, PR-5, and PR-10, mainly in treated proximal tissues”
The same questions in other papers
Phytophthora sojae · molecular: expression · Glycine max (soybean)Positive and negative results
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- no effect
- positive
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See all 10 papers →resistance inducer · molecular: expression · Glycine max (soybean)Positive and negative results
7 papers in the same direction as this paper · 1 in the opposite direction
- no effect
- positive
- positive
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See all 9 papers →Claims are grouped by organism, treatment and what was measured or targeted. A paper counts as positive when any of its claims in the group is positive.