Evidence map›Paper›PMID 12655397›Full record

ArticleMolecular genetics and genomics : MGG2003

The Aspergillus parasiticus protein AFLJ interacts with the aflatoxin pathway-specific regulator AFLR.

P-K Chang

Abstract read
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In one paragraph

Article in Molecular genetics and genomics : MGG, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

71 citing papers in PubMed.

  1. Functional characterization of HMG_9 and CMicrobial cell factories · 2026
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  2. Identification and Characterization of a Red-Light Sensor FphA inInternational journal of molecular sciences · 2026
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  4. Review
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  6. Aspergillus Mycotoxins: The Major Food Contaminants.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  7. Synergistic inhibition ofFrontiers in veterinary science · 2025
    Article
  8. Article
  9. Comparative Genome Analysis of Japanese Field-IsolatedJournal of fungi (Basel, Switzerland) · 2024
    Article
  10. Article
  11. Article
  12. Review
  13. An environmental isolate ofFrontiers in microbiology · 2024
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Genetic Regulation of Mycotoxin Biosynthesis.Journal of fungi (Basel, Switzerland) · 2022
    Review
  20. Article

11 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

P-K ChangSouthern Regional Research Center, Agricultural Research Service, U.S. Department of Agriculture, 1100 Robert E. Lee Boulevard, New Orleans, LA 70124, USA. pkchang@srrc.ars.usda.gov

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Aspergillus parasiticus aflJgene, which is located in the aflatoxin biosynthetic gene cluster and is transcribed divergently from the aflatoxin pathway regulatory gene aflR, encodes a 438-amino acid protein. Transformation with aflJplus aflR, but not aflJalone, increased the accumulation of aflatoxin precursors substantially in an O-methylsterigmatocystin-accumulating A. parasiticus strain. Disruption of aflJ resulted in non-pigmented mutants that lost the ability to synthesize aflatoxin intermediates. Transcript profiling by real time RT-PCR indicated that the lack of aflJtranscripts in the aflJ knockout mutants is associated with a significant decrease in the transcript levels of the genes for early (pksAand nor1), middle (ver1) and later (omtA) steps in the aflatoxin biosynthetic pathway, with the degree of reduction ranging from 5- to 20-fold. Deletion of aflJ, however, did not have any effect on the aflRtranscript level, and vice versa. Two-hybrid assays showed that AFLJ did not interact with aflatoxin biosynthetic enzymes, including NOR1, VER1, OMTA and ORDA. But AFLJ interacted with full-length AFLR, and the DNA-binding domain of AFLR was found not to be essential for this interaction. Simultaneous substitution of Arg427, Arg429, and Arg431 in the C-terminal region of AFLR with Leu residues abolished its ability to interact with AFLJ. Replacement of Asp436, which was previously shown to be crucial for AFLR's activation activity, with His, in contrast, had little effect on the interaction. On the other hand, deletions in most regions of AFLJ appeared to destroy its function, despite the fact that random amino acid substitution(s) in its C-terminal region did not drastically affect its capacity to interact with AFLR. The results show that aflJis involved in the expression of aflatoxin structural genes and support the hypothesis that aflJis a coactivator gene.

Indexed as

Genes, FungalTranscription FactorsAflatoxinsAmino Acid SequenceAmino Acid SubstitutionAspergillusBase SequenceBinding SitesDNA-Binding ProteinsDNA, FungalFungal ProteinsGene DeletionGene Expression ProfilingGenes, RegulatorMolecular Sequence DataMultigene FamilyAflatoxinsAFLR protein, AspergillusDNA-Binding ProteinsDNA, FungalFungal ProteinsRecombinant Fusion ProteinsTranscription Factors

Identifiers

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.