Cited by 66Neuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsInflammasome and immune disorders

Behavioral and transcriptomic analysis of Trem2-null mice: not all knockout mice are created equal

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Kang, Silvia S, Kurti, Aishe, Baker, Kelsey E, Liu, Chia-Chen, Colonna, Marco, Ulrich, Jason D, Holtzman, David M, Bu, Guojun +1 more·2018·Human Molecular Genetics

Abstract

It is clear that innate immune system status is altered in numerous neurodegenerative diseases. Human genetic studies have demonstrated that triggering receptor expressed in myeloid cells 2 (TREM2) coding variants have a strong association with Alzheimer's disease (AD) and other neurodegenerative diseases. To more thoroughly understand the impact of TREM2 in vivo, we studied the behavioral and cognitive functions of wild-type (WT) and Trem2-/- (KO) mice during basal conditions and brain function in the context of innate immune stimulation with peripherally administered lipopolysaccharide (LPS). Early markers of neuroinflammation preceded Aif1 and Trem2 upregulation that occurred at later stages (24-48 h post-LPS). We performed a transcriptomic study of these cohorts and found numerous transcripts and pathways that were altered in Trem2-/- mice both at baseline and 48 h after LPS challenge. Importantly, our transcriptome analysis revealed that our Trem2-/- mouse line (Velocigene allele) results in exaggerated Treml1 upregulation. In contrast, aberrantly high Treml1 expression was absent in the Trem2 knockout line generated by the Colonna lab and the Jackson Labs CRISPR/Cas9 Trem2 knockout line. Notably, removal of the floxed neomycin selection cassette ameliorated aberrant Treml1 expression, validating the artifactual nature of Treml1 expression in the original Trem2-/- Velocigene line. Clearly further studies are needed to decipher whether the Treml1 transcriptional artifact is functionally meaningful, but our data indicate that caution is warranted when interpreting functional studies with this particular line. Additionally, our results indicate that other Velocigene alleles or targeting strategies with strong heterologous promoters need to carefully consider downstream genes.

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Crossref · 10.1093/hmg/ddx366

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  • Several Trem2 KO mice show various - sometimes contradictory - phenotypes due to alterations of expression in other genes beyond Trem2 (e.g. Trem1L) in some models.

    “several Trem2 KO mice show various – sometimes contradictory – phenotypes due to alterations of expression in other genes beyond Trem2 (e.g. Trem1L) in some models [107]”

    From TREM2/PLCγ2 signalling in immune cells: function, structural insight, and potential therapeutic modulation (2021) · cites this paper as [107]

    The Results section ('Trem2 deletion alters Treml1 expression depending on targeting construct'; page unavailable) shows that Trem2 knockout strategies differ in their effects on Treml1 and other gene expression. But the Discussion says it is uncertain whether Treml1 compensates for or masks TREM2 deficiency; the paper does not establish that altered expression causes the differing or contradictory phenotypes claimed. (LLM, conf=0.88)

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Authors
Kang, S. S., Kurti, A., Baker, K. E., Liu, C.-C., Colonna, M., Ulrich, J. D., Holtzman, D. M., Bu, G., & Fryer, J. D.
Affiliations
  • Mayo Clinic (US)
  • Washington University in St. Louis (US)
Corresponding author
Fryer, John D
Venue
Human Molecular Genetics
Published
2017-10-11
Volume
27
Issue
2
Pages
211-223
ISSN
  • 0964-6906 (ISSN-L)
  • 1460-2083
OpenAlex
W2762857072
Cited by
62
References
64
Citations by year
2026: 2 · 2025: 8 · 2024: 6 · 2023: 4 · 2022: 3 · 2021: 6 · 2020: 19 · 2019: 4 · 2018: 9 · 2017: 1
FWCI
5.04
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Human Molecular Genetics (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Digital Commons@Becker (Washington University School of Medicine) (submittedVersion, cc-by)
  • Rare & Special e-Zone (The Hong Kong University of Science and Technology) (submittedVersion)
Funders
  • NIH (NS094137, AG047327, AG049992, MH103632, AG027924, AG035355, and NS074969)
  • Mayo Foundation
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
Keywords
TREM2, TREM2 knockout mice, neuroinflammation, lipopolysaccharide challenge, innate immunity, Alzheimer's disease, neurodegenerative diseases, transcriptome, heterologous promoters
MeSH terms
Animals, Behavior, Animal, Brain, Cognition, Disease Models, Animal, Immunity, Innate, Membrane Glycoproteins, Mice, Inbred C57BL, Receptors, Immunologic, Up-Regulation, Microglia, Mice, Knockout, Gene Expression Profiling, Mice, Transcriptome

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