FB2026_02 , released June 18, 2026
Human Disease Model Report: cancer, intestinal, impact of Pseudomonas aeruginosa infection
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General Information
Name
cancer, intestinal, impact of Pseudomonas aeruginosa infection
FlyBase ID
FBhh0001147
Disease Ontology Term
Parent Disease
OMIM
Overview

Flies infected via feeding with a highly virulent strain of Pseudomonas aeruginosa typically die within 20 days. Infection results in mild intestinal tissue hyperplasia, manifested by a significant increase in the width of the posterior midgut compared to that of uninfected flies and an increase in the number of intestinal stem cells; both phenotypes are reversible upon bacteria clearance.

Infection with P. aeruginosa has been combined with several Drosophila cancer models to assess the impact of bacterial infection upon normal cells of the fly gut vs cells that have been potentiated by expression of a cancer-implicated gene variant. The most extensively characterized is in combination with the activated Ras85DV12 allele, expressed specifically in the gut; a dominant-negative form of Notch (N) and RNAi knockdown of the tumor suppressor gene discs large (dlg1) have also been assessed. Higher levels of intestinal hyperplasia are observed; affected intestines develop excess layers of cells with altered apicobasal polarity reminiscent of dysplasia.

When expressed in the adult hindgut (without bacterial infection), Ras85DV12 results in delamination of hindgut cells and some dissemination of cells away from the hindgut; this phenotype is exacerbated by sustained infection with P. aeruginosa. The enhanced phenotype is reversed upon bacteria clearance.

The role of JNK signaling in these responses has been assessed.

[updated Nov. 2019 by FlyBase; FBrf0222196]

Disease Summary Information
Disease Summary: cancer, intestinal, impact of Pseudomonas aeruginosa infection
OMIM report
Human gene(s) implicated
Symptoms and phenotype

In human, Pseudomonas aeruginosa has become an important cause of gram-negative infection, especially in patients with compromised host defense mechanisms. It is the most common pathogen isolated from patients who have been hospitalized longer than 1 week. Pseudomonas infections can be life-threatening. (https://emedicine.medscape.com/article/226748-overview)

Genetics
Cellular phenotype and pathology
Molecular information
External links
    Disease synonyms
    Search term: colorectal cancer
    Ortholog Information
    Human gene(s) in FlyBase
      Other mammalian ortholog(s) used
        D. melanogaster Gene Information (1)
        Gene Snapshot
        Ras oncogene at 85D (Ras85D) encodes a protein that acts downstream of several cell signals, most notably from Receptor Tyrosine Kinases, to regulate tissue growth and development. When abnormally activated it can direct developmental defects and tissue hyperplasia, mimicking aspects of human disease including Rasopathies and cancer, respectively. [Date last reviewed: 2019-03-14]
        Cellular component (GO)
        Gene Groups / Pathways
        Comments on ortholog(s)

        High-scoring ortholog of human genes KRAS, HRAS, and NRAS (many to many; multiple paralogs and orthologs in both species). Dmel\Ras85D shares 78-86% identity and 86-92% similarity with KRAS, HRAS, and NRAS; for these three human genes, Ras85D is the highest-scoring ortholog in Drosophila.

        Orthologs and Alignments from DRSC
        DIOPT - DRSC Integrative Ortholog Prediction Tool - Click the link below to search for orthologs in Humans
        Other Genes Used: Viral, Bacterial, Synthetic (0)
          Summary of Physical Interactions (29 groups)
          protein-protein
          Interacting group
          Assay
          References
          anti tag coimmunoprecipitation, peptide massfingerprinting
          anti tag coimmunoprecipitation, peptide massfingerprinting
          pull down, anti tag western blot
          anti tag coimmunoprecipitation, peptide massfingerprinting
          anti tag coimmunoprecipitation, peptide massfingerprinting
          anti tag coimmunoprecipitation, autoradiography, two hybrid
          anti tag coimmunoprecipitation, peptide massfingerprinting
          anti tag coimmunoprecipitation, peptide massfingerprinting
          anti tag coimmunoprecipitation, peptide massfingerprinting
          anti tag coimmunoprecipitation, anti tag western blot
          anti tag coimmunoprecipitation, peptide massfingerprinting
          anti tag coimmunoprecipitation, peptide massfingerprinting
          gtpase assay, autoradiography
          anti tag coimmunoprecipitation, peptide massfingerprinting
          pull down, western blot, two hybrid
          anti tag coimmunoprecipitation, peptide massfingerprinting
          two hybrid, anti tag coimmunoprecipitation, anti tag western blot, pull down
          pull down, anti tag western blot
          anti tag coimmunoprecipitation, peptide massfingerprinting
          anti tag coimmunoprecipitation, peptide massfingerprinting
          anti tag coimmunoprecipitation, peptide massfingerprinting
          anti tag coimmunoprecipitation, peptide massfingerprinting
          anti tag coimmunoprecipitation, peptide massfingerprinting
          anti tag coimmunoprecipitation, peptide massfingerprinting
          anti tag coimmunoprecipitation, peptide massfingerprinting
          anti tag coimmunoprecipitation, anti tag western blot
          pull down, covalent binding, western blot, anti tag coimmunoprecipitation, Identification by mass spectrometry
          Alleles Reported to Model Human Disease (Disease Ontology) (26 alleles)
          Models Based on Experimental Evidence ( 17 )
          Allele
          Disease
          Evidence
          References
          model of  cancer
          Modifiers Based on Experimental Evidence ( 19 )
          Allele
          Disease
          Interaction
          References
          model of  cancer
          is exacerbated by ITPUAS.F
          model of  cancer
          is ameliorated by InRGL00139
          is ameliorated by InRJF01183
          is ameliorated by InRJF01482
          is ameliorated by NetBΔ
          is ameliorated by NetBKK103672
          is ameliorated by unc-5MI04273
          is ameliorated by TimpUAS.cPa
          is ameliorated by bskDN.UAS
          is ameliorated by bskHMS00777
          is ameliorated by JraNIG.2275R
          is exacerbated by hepAct.UAS
          is exacerbated by imdUAS.cGa
          ameliorates  cancer
          model of  kidney cancer
          is ameliorated by Pka-C1B3
          is ameliorated by mTorΔP
          model of  cancer
          is exacerbated by exe1
          is exacerbated by Ptp61FΔ
          is exacerbated by M6W186stop
          is exacerbated by p53UAS.cUa
          is ameliorated by Ptip3804
          is ameliorated by Ilp8MI00727
          is exacerbated by Clbn1Q
          exacerbates  carcinoma
          model of  carcinoma
          is exacerbated by NkapGD11807
          Alleles Representing Disease-Implicated Variants
          Genetic Tools, Stocks and Reagents
          Sources of Stocks
          Contact lab of origin for a reagent not available from a public stock center.
          Bloomington Stock Center Disease Page
          Related mammalian, viral, bacterial, or synthetic transgenes
          Allele
          Transgene
          Publicly Available Stocks
          Selected Drosophila transgenes
          Allele
          Transgene
          Publicly Available Stocks
          RNAi constructs available
          Allele
          Transgene
          Publicly Available Stocks
          Selected Drosophila classical alleles
          Allele
          Allele class
          Mutagen
          Publicly Available Stocks
          loss of function allele
          loss of function allele
          P-element activity
          amorphic allele - genetic evidence
          References (5)