Evidence map›Paper›PMID 39503509›Full record

ArticlemSystems2024

Ecological drivers of CRISPR immune systems.

Wei Xiao, J L Weissman, Philip L F Johnson

Abstract read
In one paragraph

Article in mSystems, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors.

Wei XiaoDepartment of Biology, University of Maryland, College Park, Maryland, USA.ORCID 0000-0002-6313-3543
J L WeissmanDepartment of Ecology and Evolution, Stony Brook University, Stony Brook, New York, USA.ORCID 0000-0002-4237-4807
Philip L F JohnsonDepartment of Biology, University of Maryland, College Park, Maryland, USA.ORCID 0000-0001-6087-7064

Funding

Developing CRISPR repeats as a means of phylogenetically profiling metagenomic dataR21GM147759 · NIGMS · UNIV OF MARYLAND, COLLEGE PARK · PI JOHNSON, PHILIP LEE FALK · 2022 to 2023
$223k
NIGMS NIH HHS R21 GM147759
6 · The paper itself

Abstract

CRISPR-Cas is the only known adaptive immune system of prokaryotes. It is a powerful defense system against mobile genetic elements such as bacteriophages. While CRISPR-Cas systems can be found throughout the prokaryotic tree of life, they are distributed unevenly across taxa and environments. Since adaptive immunity is more useful in environments where pathogens persist or reoccur, the density and/or diversity of the host/pathogen community may drive the uneven distribution of CRISPR systems. We directly tested hypotheses connecting CRISPR incidence with prokaryotic density/diversity by analyzing 16S rRNA and metagenomic data from publicly available environmental sequencing projects. In terms of density, we found that CRISPR systems are significantly favored in lower abundance (less dense) taxa and disfavored in higher abundance taxa, at least in marine environments. When we extended this work to compare taxonomic diversity between samples, we found CRISPR system incidence strongly correlated with diversity in human oral environments. Together, these observations confirm that, at least in certain types of environments, the prokaryotic ecological context indeed plays a key role in selecting for CRISPR immunity. IMPORTANCE: Microbes must constantly defend themselves against viral pathogens, and a large proportion of prokaryotes do so using the highly effective CRISPR-Cas adaptive immune system. However, many prokaryotes do not. We investigated the ecological factors behind this uneven distribution of CRISPR-Cas immune systems in natural microbial populations. We found strong patterns linking CRISPR-Cas systems to prokaryotic density within ocean environments and to prokaryotic diversity within human oral environments. Our study validates previous within-lab experimental results that suggested these factors might be important and confirms that local environment and ecological context interact to select for CRISPR immunity.

Indexed as

CRISPR-Cas SystemsRNA, Ribosomal, 16SBacteriaHumansMetagenomicsRNA, Ribosomal, 16Sadaptive immunityCRISPRevolutionprokaryotes

Identifiers

PMID39503509
PMCPMC11651112

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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.