Quantifying the local adaptive landscape of a nascent bacterial community
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Abstract
The fitness effects of all possible mutations available to an organism largely shape the dynamics of evolutionary adaptation. Yet, whether and how this adaptive landscape changes over evolutionary times, especially upon ecological diversification and changes in community composition, remains poorly understood. We sought to fill this gap by analyzing a stable community of two closely related ecotypes (“L” and “S”) shortly after they emerged within the E. coli Long-Term Evolution Experiment (LTEE). We engineered genome-wide barcoded transposon libraries to measure the invasion fitness effects of all possible gene knockouts in the coexisting strains as well as their ancestor, for many different, ecologically relevant conditions. We find consistent statistical patterns of fitness effect variation across both genetic background and community composition, despite the idiosyncratic behavior of individual knockouts. Additionally, fitness effects are correlated with evolutionary outcomes for a number of conditions, possibly revealing shifting patterns of adaptation. Together, our results reveal how ecological and epistatic effects combine to shape the adaptive landscape in a nascent ecological community.
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SHIP1 is a regulator of the NLRP3 inflammasome in human microglia, as both CRISPR/Cas9-mediated knockdown of INPP5D and acute inhibition of SHIP1 led to activation of the inflammasome.
“In line with SHIP1’s role as a brake on inflammation, we recently identified SHIP1 as a regulator of the NLRP3 inflammasome in human microglia, as both the CRISPR/Cas9-mediated knockdown of INPP5D and acute inhibition of SHIP1 led to the activation of the inflammasome11.”
From INPP5D/SHIP1 regulates endo-lysosomal function and cargo-selective phagocytosis in human microglia (2025) · cites this paper as [11]
The Results section, “Measuring knockout fitness effects” (page unavailable), discusses bacterial knockout fitness across genetic backgrounds, not human microglia. Searches for SHIP1, INPP5D, NLRP3, and the claimed CRISPR/Cas9 knockdown and acute-inhibition experiments found no passage in our copy addressing the claim. (LLM, conf=0.78)
Experimental — accuracy not yet measuredAD risk SNPs at the INPP5D locus are intronic and it is unclear how they influence INPP5D levels.
“AD risk SNPs at the INPP5D locus are intronic and it is unclear how they influence INPP5D levels11,12.”
From INPP5D/SHIP1 regulates endo-lysosomal function and cargo-selective phagocytosis in human microglia (2025) · cites this paper as [11]
The Results section discusses knockout fitness effects in a bacterial community, and the Methods section discusses bacterial genomic position; neither addresses Alzheimer’s disease risk variants. Searches for INPP5D, intronic variants, and their effects on INPP5D levels found no relevant passage in our copy. (LLM, conf=0.78)
Experimental — accuracy not yet measuredINPP5D loss-of-function in iMGs reduces autophagic flux.
“we previously reported a reduction in autophagic flux upon INPP5D loss-of-function in iMGs11”
From INPP5D/SHIP1 regulates endo-lysosomal function and cargo-selective phagocytosis in human microglia (2025) · cites this paper as [11]
The Results section, “Measuring knockout fitness effects” (page unavailable), discusses bacterial gene knockouts such as pykF, not INPP5D in iMGs. Searches for the claim and for microglia, autophagy, and autophagic flux found no passage addressing the attributed finding in our copy. (LLM, conf=0.78)
Experimental — accuracy not yet measuredWhile overall protein levels of SHIP1 are elevated in brain tissue from individuals with AD, the levels of full length SHIP1 containing the phosphatase domain are reduced.
“In accord, while overall protein levels of SHIP1 are elevated in brain tissue from individuals with AD, the levels of full length SHIP1 containing the phosphatase domain are reduced11.”
From INPP5D/SHIP1 regulates endo-lysosomal function and cargo-selective phagocytosis in human microglia (2025) · cites this paper as [11]
The Results passages concern bacterial knockout fitness and gene expression, not SHIP1 or Alzheimer’s disease. Searches for SHIP1, its phosphatase domain, and the claimed changes in brain protein levels found no relevant passage in our copy. (LLM, conf=0.79)
Experimental — accuracy not yet measuredThe NLRP3 inflammasome is activated in INPP5D HET microglia and in microglia following acute inhibition of SHIP1.
“We previously reported that the NLRP3 inflammasome is activated in INPP5D HET microglia and in microglia following acute inhibition of SHIP111,15.”
From INPP5D/SHIP1 regulates endo-lysosomal function and cargo-selective phagocytosis in human microglia (2025) · cites this paper as [11]
The Results passages concern bacterial knockout fitness and adaptation, not microglia or inflammasome activation. Searches for NLRP3, INPP5D, SHIP1 inhibition, and microglia found no passage in our copy addressing the claim; this is absence of support, not a contrary finding. The indexed passages provide section labels but no page numbers. (LLM, conf=0.79)
Experimental — accuracy not yet measured
3AC robustly induces secretion of IL-1β and IL-18 upon activation of the NLRP3 inflammasome.
“3AC, which we previously showed to robustly induce the secretion of IL-1β and IL-18 upon activation of the NLRP3 inflammasome11”
From INPP5D/SHIP1 regulates endo-lysosomal function and cargo-selective phagocytosis in human microglia (2025) · cites this paper as [11]
The Results section discusses bacterial knockout fitness and correlations across genetic backgrounds, not inflammasome activation. Searches for 3AC, IL-1β, IL-18, and NLRP3 found no passage in our copy addressing the claimed secretion effect; no page numbers were available. (LLM, conf=0.78)
Experimental — accuracy not yet measured
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- Authors
- Ascensao, J. A., Wetmore, K. M., Good, B. H., Arkin, A. P., & Hallatschek, O.
- Affiliations
- University of California, Berkeley (US)
- Lawrence Berkeley National Laboratory (US)
- Stanford University (US)
- Leipzig University (DE)
- Corresponding author
- Hallatschek, Oskar
- Venue
- Nature Communications
- Published
- 2023-01-16
- Volume
- 14
- Issue
- 1
- Pages
- 248-248
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC9842643
- OpenAlex
- W4316511358
- Cited by
- 447
- References
- 76
- Citations by year
- 2026: 74 · 2025: 172 · 2024: 145 · 2023: 53 · 2022: 2 · 2019: 1
- FWCI
- 73.88
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- OSTI OAI (U.S. Department of Energy Office of Scientific and Technical Information) (submittedVersion)
- Funders
- U.S. Department of Energy (DE-AC02-05CH11231)
- National Science Foundation (1555330)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Evolution and Genetic Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Bacterial Genetics and Biotechnology
- Physical Sciences › Environmental Science › Ecology › Microbial Community Ecology and Physiology
- Keywords
- fitness landscape, Escherichia coli, long-term evolution experiment, gene knockout, transposon mutagenesis, invasion fitness, epistasis, ecological diversification, community composition, fitness effects, adaptive evolution
- MeSH terms
- Adaptation, Physiological, Escherichia coli, Mutation, Genetic Fitness, Ecotype
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