Component

Saccharomyces cerevisiae growth during allicin exposure

Saccharomyces cerevisiae growth during allicin exposure. Interpret through the linked study species, preparation, exposure and measured endpoint.

8 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. Deletion of yeast-ctr1 increased yeast sensitivity to allicin.

    Saccharomyces cerevisiae high-affinity copper transporter / Ctr1 → Saccharomyces cerevisiae growth during allicin exposure source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
    experimental_condition
    Yeast comparator without that deletion at matched allicin exposure deleted · Saccharomyces cerevisiae high-affinity copper transporter / Ctr1 Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    Yeast comparator without that deletion at matched allicin exposure present · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "yeast-ctr1 deletion with allicin", "comparator": "Yeast comparator without that deletion at matched allicin exposure", "endpoint": "Deletion of yeast-ctr1 increased yeast sensitivity to allicin.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "yeast-ctr1", "state": "deleted"}, {"entity_slug": "allicin", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Saccharomyces cerevisiae deletion screen; primary abstract; exact dose and exposure duration unextracted.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Hypersensitivity does not prove direct binding to the deleted protein or distinguish metal uptake from metalloprotein dysfunction.
    plain_language
    Deletion of yeast-ctr1 increased yeast sensitivity to allicin.
    primary_references
    A Mini HIP HOP Assay Uncovers a Central Role for Copper and Zinc in the Antifungal Mode of Action of Allicin. | 2017 | DOI 10.1021/acs.jafc.7b00250 | PMID 28421744 | https://pubmed.ncbi.nlm.nih.gov/28421744/ | https://doi.org/10.1021/acs.jafc.7b00250
    source_locator
    Reviewed reference lines 59-59; exact primary location described in quoted passage where extracted.
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 59–59

    Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Saccharomyces cerevisiae deletion screen; primary abstract; exact dose and exposure duration unextracted. · source_derived_draft · unverified_draft

    **Yeast metal requirements.** In a chemical-genetic screen of Saccharomyces cerevisiae, loss of CTR1, MAC1, or ZAP1 increased sensitivity to allicin; copper or zinc additions rescued the relevant sensitized phenotypes. This supports involvement of metal acquisition or metalloprotein function but does not discriminate those alternatives. It is not direct proof that allicin binds each protein, chelates all intracellular copper, or causes human mineral deficiency. Exact supplementation concentrations and all strain-specific contrasts remain unextracted from the accessible abstract. [Prescott and Panaretou 2017](https://pubmed.ncbi.nlm.nih.gov/28421744/)
    Complete structured claim and evidence

  2. Deletion of yeast-mac1 increased yeast sensitivity to allicin.

    Saccharomyces cerevisiae copper-responsive transcription factor / Mac1 → Saccharomyces cerevisiae growth during allicin exposure source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
    experimental_condition
    Yeast comparator without that deletion at matched allicin exposure present · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    Yeast comparator without that deletion at matched allicin exposure deleted · Saccharomyces cerevisiae copper-responsive transcription factor / Mac1 Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "yeast-mac1 deletion with allicin", "comparator": "Yeast comparator without that deletion at matched allicin exposure", "endpoint": "Deletion of yeast-mac1 increased yeast sensitivity to allicin.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "yeast-mac1", "state": "deleted"}, {"entity_slug": "allicin", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Saccharomyces cerevisiae deletion screen; primary abstract; exact dose and exposure duration unextracted.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Hypersensitivity does not prove direct binding to the deleted protein or distinguish metal uptake from metalloprotein dysfunction.
    plain_language
    Deletion of yeast-mac1 increased yeast sensitivity to allicin.
    primary_references
    A Mini HIP HOP Assay Uncovers a Central Role for Copper and Zinc in the Antifungal Mode of Action of Allicin. | 2017 | DOI 10.1021/acs.jafc.7b00250 | PMID 28421744 | https://pubmed.ncbi.nlm.nih.gov/28421744/ | https://doi.org/10.1021/acs.jafc.7b00250
    source_locator
    Reviewed reference lines 59-59; exact primary location described in quoted passage where extracted.
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 59–59

    Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Saccharomyces cerevisiae deletion screen; primary abstract; exact dose and exposure duration unextracted. · source_derived_draft · unverified_draft

    **Yeast metal requirements.** In a chemical-genetic screen of Saccharomyces cerevisiae, loss of CTR1, MAC1, or ZAP1 increased sensitivity to allicin; copper or zinc additions rescued the relevant sensitized phenotypes. This supports involvement of metal acquisition or metalloprotein function but does not discriminate those alternatives. It is not direct proof that allicin binds each protein, chelates all intracellular copper, or causes human mineral deficiency. Exact supplementation concentrations and all strain-specific contrasts remain unextracted from the accessible abstract. [Prescott and Panaretou 2017](https://pubmed.ncbi.nlm.nih.gov/28421744/)
    Complete structured claim and evidence

  3. Deletion of yeast-zap1 increased yeast sensitivity to allicin.

    Saccharomyces cerevisiae zinc-responsive transcription factor / Zap1 → Saccharomyces cerevisiae growth during allicin exposure source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
    experimental_condition
    Yeast comparator without that deletion at matched allicin exposure deleted · Saccharomyces cerevisiae zinc-responsive transcription factor / Zap1 Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    Yeast comparator without that deletion at matched allicin exposure present · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "yeast-zap1 deletion with allicin", "comparator": "Yeast comparator without that deletion at matched allicin exposure", "endpoint": "Deletion of yeast-zap1 increased yeast sensitivity to allicin.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "yeast-zap1", "state": "deleted"}, {"entity_slug": "allicin", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Saccharomyces cerevisiae deletion screen; primary abstract; exact dose and exposure duration unextracted.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Hypersensitivity does not prove direct binding to the deleted protein or distinguish metal uptake from metalloprotein dysfunction.
    plain_language
    Deletion of yeast-zap1 increased yeast sensitivity to allicin.
    primary_references
    A Mini HIP HOP Assay Uncovers a Central Role for Copper and Zinc in the Antifungal Mode of Action of Allicin. | 2017 | DOI 10.1021/acs.jafc.7b00250 | PMID 28421744 | https://pubmed.ncbi.nlm.nih.gov/28421744/ | https://doi.org/10.1021/acs.jafc.7b00250
    source_locator
    Reviewed reference lines 59-59; exact primary location described in quoted passage where extracted.
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 59–59

    Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Saccharomyces cerevisiae deletion screen; primary abstract; exact dose and exposure duration unextracted. · source_derived_draft · unverified_draft

    **Yeast metal requirements.** In a chemical-genetic screen of Saccharomyces cerevisiae, loss of CTR1, MAC1, or ZAP1 increased sensitivity to allicin; copper or zinc additions rescued the relevant sensitized phenotypes. This supports involvement of metal acquisition or metalloprotein function but does not discriminate those alternatives. It is not direct proof that allicin binds each protein, chelates all intracellular copper, or causes human mineral deficiency. Exact supplementation concentrations and all strain-specific contrasts remain unextracted from the accessible abstract. [Prescott and Panaretou 2017](https://pubmed.ncbi.nlm.nih.gov/28421744/)
    Complete structured claim and evidence

  4. Added copper-ii reversed the relevant metal-defence-mutant hypersensitivity to allicin in yeast.

    Copper(II) ion → Saccharomyces cerevisiae growth during allicin exposure source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
    experimental_condition
    Same sensitized yeast with allicin without added metal added in relevant mutant background · Copper(II) ion Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    Same sensitized yeast with allicin without added metal present · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "Metal addition to the corresponding sensitized allicin-exposed yeast", "comparator": "Same sensitized yeast with allicin without added metal", "endpoint": "Added copper-ii reversed the relevant metal-defence-mutant hypersensitivity to allicin in yeast.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "copper-ii", "state": "added in relevant mutant background"}, {"entity_slug": "allicin", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Saccharomyces cerevisiae sensitized-mutant rescue; accessible abstract; exact individual strain-dose mapping not fully extracted.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Abstract reports copper/zinc rescue but does not provide all strain-specific values. No human mineral-deficiency or supplementation claim.
    plain_language
    Added copper-ii reversed the relevant metal-defence-mutant hypersensitivity to allicin in yeast.
    primary_references
    A Mini HIP HOP Assay Uncovers a Central Role for Copper and Zinc in the Antifungal Mode of Action of Allicin. | 2017 | DOI 10.1021/acs.jafc.7b00250 | PMID 28421744 | https://pubmed.ncbi.nlm.nih.gov/28421744/ | https://doi.org/10.1021/acs.jafc.7b00250
    source_locator
    Reviewed reference lines 59-59; exact primary location described in quoted passage where extracted.

    Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 59–59

    Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Saccharomyces cerevisiae sensitized-mutant rescue; accessible abstract; exact individual strain-dose mapping not fully extracted. · source_derived_draft · unverified_draft

    **Yeast metal requirements.** In a chemical-genetic screen of Saccharomyces cerevisiae, loss of CTR1, MAC1, or ZAP1 increased sensitivity to allicin; copper or zinc additions rescued the relevant sensitized phenotypes. This supports involvement of metal acquisition or metalloprotein function but does not discriminate those alternatives. It is not direct proof that allicin binds each protein, chelates all intracellular copper, or causes human mineral deficiency. Exact supplementation concentrations and all strain-specific contrasts remain unextracted from the accessible abstract. [Prescott and Panaretou 2017](https://pubmed.ncbi.nlm.nih.gov/28421744/)
    Complete structured claim and evidence

  5. Added zinc-ion reversed the relevant metal-defence-mutant hypersensitivity to allicin in yeast.

    Zinc(II) ion → Saccharomyces cerevisiae growth during allicin exposure source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary indexed abstract reviewed; full methods, exact concentrations or species-specific attribution remain unextracted unless explicitly stated in the abstract or separately verified publisher text.
    experimental_condition
    Same sensitized yeast with allicin without added metal added in relevant mutant background · Zinc(II) ion Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    Same sensitized yeast with allicin without added metal present · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "Metal addition to the corresponding sensitized allicin-exposed yeast", "comparator": "Same sensitized yeast with allicin without added metal", "endpoint": "Added zinc-ion reversed the relevant metal-defence-mutant hypersensitivity to allicin in yeast.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "zinc-ion", "state": "added in relevant mutant background"}, {"entity_slug": "allicin", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Saccharomyces cerevisiae sensitized-mutant rescue; accessible abstract; exact individual strain-dose mapping not fully extracted.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Abstract reports copper/zinc rescue but does not provide all strain-specific values. No human mineral-deficiency or supplementation claim.
    plain_language
    Added zinc-ion reversed the relevant metal-defence-mutant hypersensitivity to allicin in yeast.
    primary_references
    A Mini HIP HOP Assay Uncovers a Central Role for Copper and Zinc in the Antifungal Mode of Action of Allicin. | 2017 | DOI 10.1021/acs.jafc.7b00250 | PMID 28421744 | https://pubmed.ncbi.nlm.nih.gov/28421744/ | https://doi.org/10.1021/acs.jafc.7b00250
    source_locator
    Reviewed reference lines 59-59; exact primary location described in quoted passage where extracted.

    Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 59–59

    Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Saccharomyces cerevisiae sensitized-mutant rescue; accessible abstract; exact individual strain-dose mapping not fully extracted. · source_derived_draft · unverified_draft

    **Yeast metal requirements.** In a chemical-genetic screen of Saccharomyces cerevisiae, loss of CTR1, MAC1, or ZAP1 increased sensitivity to allicin; copper or zinc additions rescued the relevant sensitized phenotypes. This supports involvement of metal acquisition or metalloprotein function but does not discriminate those alternatives. It is not direct proof that allicin binds each protein, chelates all intracellular copper, or causes human mineral deficiency. Exact supplementation concentrations and all strain-specific contrasts remain unextracted from the accessible abstract. [Prescott and Panaretou 2017](https://pubmed.ncbi.nlm.nih.gov/28421744/)
    Complete structured claim and evidence

  6. Loss of yeast-glr1 increased susceptibility in the allicin arm of the yeast chemical-genetic comparison.

    Saccharomyces cerevisiae glutathione reductase / Glr1 → Saccharomyces cerevisiae growth during allicin exposure source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
    experimental_condition
    Wild-type yeast at the same allicin exposure deleted · Saccharomyces cerevisiae glutathione reductase / Glr1 Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    Wild-type yeast at the same allicin exposure present · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "yeast-glr1 deletion with allicin", "comparator": "Wild-type yeast at the same allicin exposure", "endpoint": "Loss of yeast-glr1 increased susceptibility in the allicin arm of the yeast chemical-genetic comparison.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "yeast-glr1", "state": "deleted"}, {"entity_slug": "allicin", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Saccharomyces cerevisiae; separate gene deletions and allicin exposures compared with an analogue; Figure 3.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Keep dose and compound distinctions: analogue effects cannot substitute for allicin. Not a human nutrient-deficiency phenotype.
    plain_language
    Loss of yeast-glr1 increased susceptibility in the allicin arm of the yeast chemical-genetic comparison.
    primary_references
    The Sulfilimine Analogue of Allicin, <i>S</i>-Allyl-<i>S</i>-(<i>S</i>-allyl)-<i>N</i>-Cyanosulfilimine, Is Antimicrobial and Reacts with Glutathione. | 2020 | DOI 10.3390/antiox9111086 | PMID 33158268 | https://pubmed.ncbi.nlm.nih.gov/33158268/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC7694261/ | https://doi.org/10.3390/antiox9111086
    source_locator
    Reviewed reference lines 49-49; exact primary location described in quoted passage where extracted.
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 49–49

    Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Saccharomyces cerevisiae; separate gene deletions and allicin exposures compared with an analogue; Figure 3. · source_derived_draft · unverified_draft

    **Redox-defense impairment.** A study comparing allicin with a sulfilimine analogue included allicin-exposed Saccharomyces cerevisiae mutants. The GLR1, ZWF1, and YAP1 perturbations connect susceptibility to glutathione recycling, NADPH supply, and stress regulation; effects depended on concentration and compound. The analogue was more potent in some low-concentration comparisons, and its results must not be copied onto allicin. TRX2 loss had a much smaller effect in this system. Human B2 deficiency, G6PD deficiency, or selenium status cannot be assigned the yeast phenotype without direct evidence. [Horn 2020](https://pmc.ncbi.nlm.nih.gov/articles/PMC7694261/)
    Complete structured claim and evidence

  7. Loss of yeast-yap1 increased susceptibility in the allicin arm of the yeast chemical-genetic comparison.

    Saccharomyces cerevisiae oxidative-stress transcription factor / Yap1 → Saccharomyces cerevisiae growth during allicin exposure source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
    experimental_condition
    Wild-type yeast at the same allicin exposure deleted · Saccharomyces cerevisiae oxidative-stress transcription factor / Yap1 Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    Wild-type yeast at the same allicin exposure present · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "yeast-yap1 deletion with allicin", "comparator": "Wild-type yeast at the same allicin exposure", "endpoint": "Loss of yeast-yap1 increased susceptibility in the allicin arm of the yeast chemical-genetic comparison.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "yeast-yap1", "state": "deleted"}, {"entity_slug": "allicin", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Saccharomyces cerevisiae; separate gene deletions and allicin exposures compared with an analogue; Figure 3.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Keep dose and compound distinctions: analogue effects cannot substitute for allicin. Not a human nutrient-deficiency phenotype.
    plain_language
    Loss of yeast-yap1 increased susceptibility in the allicin arm of the yeast chemical-genetic comparison.
    primary_references
    The Sulfilimine Analogue of Allicin, <i>S</i>-Allyl-<i>S</i>-(<i>S</i>-allyl)-<i>N</i>-Cyanosulfilimine, Is Antimicrobial and Reacts with Glutathione. | 2020 | DOI 10.3390/antiox9111086 | PMID 33158268 | https://pubmed.ncbi.nlm.nih.gov/33158268/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC7694261/ | https://doi.org/10.3390/antiox9111086
    source_locator
    Reviewed reference lines 49-49; exact primary location described in quoted passage where extracted.
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 49–49

    Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Saccharomyces cerevisiae; separate gene deletions and allicin exposures compared with an analogue; Figure 3. · source_derived_draft · unverified_draft

    **Redox-defense impairment.** A study comparing allicin with a sulfilimine analogue included allicin-exposed Saccharomyces cerevisiae mutants. The GLR1, ZWF1, and YAP1 perturbations connect susceptibility to glutathione recycling, NADPH supply, and stress regulation; effects depended on concentration and compound. The analogue was more potent in some low-concentration comparisons, and its results must not be copied onto allicin. TRX2 loss had a much smaller effect in this system. Human B2 deficiency, G6PD deficiency, or selenium status cannot be assigned the yeast phenotype without direct evidence. [Horn 2020](https://pmc.ncbi.nlm.nih.gov/articles/PMC7694261/)
    Complete structured claim and evidence

  8. Loss of yeast-zwf1 increased susceptibility in the allicin arm of the yeast chemical-genetic comparison.

    Saccharomyces cerevisiae glucose-6-phosphate dehydrogenase / Zwf1 → Saccharomyces cerevisiae growth during allicin exposure source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
    experimental_condition
    Wild-type yeast at the same allicin exposure present · Allicin Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    Wild-type yeast at the same allicin exposure deleted · Saccharomyces cerevisiae glucose-6-phosphate dehydrogenase / Zwf1 Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "yeast-zwf1 deletion with allicin", "comparator": "Wild-type yeast at the same allicin exposure", "endpoint": "Loss of yeast-zwf1 increased susceptibility in the allicin arm of the yeast chemical-genetic comparison.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "yeast-zwf1", "state": "deleted"}, {"entity_slug": "allicin", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Saccharomyces cerevisiae; separate gene deletions and allicin exposures compared with an analogue; Figure 3.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Keep dose and compound distinctions: analogue effects cannot substitute for allicin. Not a human nutrient-deficiency phenotype.
    plain_language
    Loss of yeast-zwf1 increased susceptibility in the allicin arm of the yeast chemical-genetic comparison.
    primary_references
    The Sulfilimine Analogue of Allicin, <i>S</i>-Allyl-<i>S</i>-(<i>S</i>-allyl)-<i>N</i>-Cyanosulfilimine, Is Antimicrobial and Reacts with Glutathione. | 2020 | DOI 10.3390/antiox9111086 | PMID 33158268 | https://pubmed.ncbi.nlm.nih.gov/33158268/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC7694261/ | https://doi.org/10.3390/antiox9111086
    source_locator
    Reviewed reference lines 49-49; exact primary location described in quoted passage where extracted.
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 49–49

    Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Saccharomyces cerevisiae; separate gene deletions and allicin exposures compared with an analogue; Figure 3. · source_derived_draft · unverified_draft

    **Redox-defense impairment.** A study comparing allicin with a sulfilimine analogue included allicin-exposed Saccharomyces cerevisiae mutants. The GLR1, ZWF1, and YAP1 perturbations connect susceptibility to glutathione recycling, NADPH supply, and stress regulation; effects depended on concentration and compound. The analogue was more potent in some low-concentration comparisons, and its results must not be copied onto allicin. TRX2 loss had a much smaller effect in this system. Human B2 deficiency, G6PD deficiency, or selenium status cannot be assigned the yeast phenotype without direct evidence. [Horn 2020](https://pmc.ncbi.nlm.nih.gov/articles/PMC7694261/)
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.