ABCG34 Antibody
Description
Introduction to ABCG34 Antibody
The ABCG34 antibody targets the ATP-binding cassette (ABC) transporter protein ABCG34, a membrane-localized protein involved in the secretion of camalexin, a phytoalexin critical for defense against necrotrophic pathogens . This antibody enables researchers to detect ABCG34 expression, localization, and functional roles in plant-pathogen interactions.
Functional Role of ABCG34 in Plant Defense
ABCG34 mediates the secretion of camalexin, a sulfur-containing antimicrobial compound, to the leaf surface. Key findings include:
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Camalexin Transport:
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Pathogen Sensitivity:
Table 1: Functional Outcomes of ABCG34 Modulation in Arabidopsis
| Plant Line | Camalexin Secretion | Pathogen Resistance (vs. Wild Type) | Sensitivity to Sclareol |
|---|---|---|---|
| Wild Type | Baseline | Baseline | Baseline |
| atabcg34 mutant | ↓ 30–50% | ↓ 50–70% | ↑ Hypersensitive |
| ABCG34 Overexpr. | ↑ 60–80% | ↑ 100–120% | ↓ Tolerant |
Table 2: ABCG34 Localization and Induction
| Parameter | Observation | Method Used |
|---|---|---|
| Tissue Localization | Plasma membrane of epidermal cells | GFP tagging |
| Inducing Factors | Methyl-jasmonate, A. brassicicola infection | GUS reporter assays |
Applications in Scientific Studies
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Localization Studies:
ABCG34 antibodies confirm polar localization at the plasma membrane using confocal microscopy (e.g., GFP-tagged constructs) . -
Functional Assays:
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Genetic Variant Analysis:
Natural Arabidopsis accessions with higher ABCG34 expression show ~15–20% greater disease resistance .
Technical Considerations
Product Specs
Constituents: 50% Glycerol, 0.01M PBS, pH 7.4
Target Background
- AtABCG34 mediates camalexin secretion to the leaf surface, thereby preventing Abrassicicola infection. PMID: 28652324
Q&A
FAQ: ABCG34 Antibody Research in Academic Context
Curated for experimental biologists and plant pathology researchers
Advanced Research Questions
How to resolve contradictions in ABCG34’s contribution to disease resistance across natural Arabidopsis accessions?
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Hypothesis: Genetic background influences compensatory mechanisms (e.g., redundant transporters like ABCG36).
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Method: GWAS on 100+ accessions using:
What controls are critical when analyzing ABCG34’s polar localization in epidermal cells?
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Technical controls:
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Co-stain with plasma membrane marker (e.g., PIP2A-mCherry).
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Use abcg34 mutants to confirm signal specificity.
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Biological controls:
How to design a study evaluating ABCG34’s interaction with other defense pathways?
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Step 1: Transcriptomic profiling of abcg34 mutants under jasmonate/ethylene treatment.
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Step 2: Co-immunoprecipitation (Co-IP) with:
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Camalexin biosynthetic enzymes (e.g., CYP71A13).
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Signaling kinases (e.g., MPK3/6).
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Step 3: Metabolite flux analysis using ¹⁴C-labeled camalexin in mutant/transgenic lines .
Data Conflict Analysis Framework
Scenario: Discrepancy in ABCG34’s role across pathogen species (e.g., strong effect on A. brassicicola vs. weak on B. cinerea).
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Root-cause analysis:
