Evidence map›Paper›PMID 40148565›Full record

ArticleNature microbiology2025

Inducible transposon mutagenesis identifies bacterial fitness determinants during infection in mice.

David W Basta, Ian W Campbell, Emily J Sullivan, Julia A Hotinger, Karthik Hullahalli, Mehek Garg, Matthew K Waldor

Abstract read
In one paragraph

Article in Nature microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Catabolism of serine enantiomers represses enterohemorrhagicProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Revealing fitness and virulence determinants of hypervirulentFrontiers in cellular and infection microbiology · 2025
    Article
  12. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

David W Basta *Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. dbasta@bwh.harvard.edu.ORCID http://orcid.org/0000-0003-4176-6566
Ian W Campbell *Division of Infectious Diseases, Brigham and Women's Hospital, Boston, MA, USA.ORCID http://orcid.org/0000-0003-3019-2560
Emily J SullivanDivision of Infectious Diseases, Brigham and Women's Hospital, Boston, MA, USA.ORCID http://orcid.org/0000-0001-9558-3883
Julia A HotingerDivision of Infectious Diseases, Brigham and Women's Hospital, Boston, MA, USA.
Karthik HullahalliDivision of Infectious Diseases, Brigham and Women's Hospital, Boston, MA, USA.ORCID http://orcid.org/0000-0003-3064-2090
Mehek GargDivision of Infectious Diseases, Brigham and Women's Hospital, Boston, MA, USA.
Matthew K WaldorDivision of Infectious Diseases, Brigham and Women's Hospital, Boston, MA, USA. mwaldor@bwh.harvard.edu.ORCID http://orcid.org/0000-0003-1843-7000

Funding

STRUCTURE-FUNCTION RELATIONSHIPS IN THE ALIMENTARY TRACTP30DK034854 · NIDDK · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI JONATHAN C KAGAN · 1986 to 2026
$32.4M
Vibrio cholerae intestinal colonization and vaccine developmentR01AI042347 · NIAID · TUFTS UNIVERSITY BOSTON · PI WALDOR, MATTHEW K · 1998 to 2025
$7.3M
Hepatic survival and population dynamics of extraintestinal pathogenic Escherichia coliF31AI156949 · NIAID · HARVARD MEDICAL SCHOOL · PI HULLAHALLI, KARTHIK · 2021 to 2023
$111k
NIAID NIH HHS R01 AI042347U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID) F31AI156949U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID) R01AI042347U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (National Institute of Diabetes & Digestive & Kidney Diseases) P30DK034854U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (National Institute of Diabetes & Digestive & Kidney Diseases) T32DK007477-37
6 · The paper itself

Abstract

Transposon insertion sequencing (Tn-seq) is a powerful method for genome-scale forward genetics in bacteria. However, inefficient transposon delivery or stochastic loss of mutants due to population bottlenecks can limit its effectiveness. Here we have developed 'InducTn-seq', where an arabinose-inducible Tn5 transposase enables temporal control of mini-Tn5 transposition. InducTn-seq generated up to 1.2 million transposon mutants from a single colony of enterotoxigenic Escherichia coli, Salmonella typhimurium, Shigella flexneri and Citrobacter rodentium. This mutant diversity enabled more sensitive detection of subtle fitness defects and measurement of quantitative fitness effects for essential and non-essential genes. Applying InducTn-seq to C. rodentium in a mouse model of infectious colitis bypassed a highly restrictive host bottleneck, generating a diverse population of >5 × 10

Indexed as

Citrobacter rodentiumDNA Transposable ElementsGenetic FitnessMutagenesis, InsertionalAnimalsColitisDisease Models, AnimalEnterobacteriaceae InfectionsMiceSalmonella typhimuriumShigella flexneriTransposasesDNA Transposable ElementsTransposases

Identifiers

PMID40148565
PMCPMC12055562

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.