Genetic quality assurance and genetic monitoring of laboratory mice and rats: FELASA Working Group Report

Benavides, Fernando; Rülicke, Thomas; Prins, J.B.; Bussell, James; Scavizzi, Ferdinando; Cinelli, Paolo; Hérault, Yann; Wedekind, Dirk

doi:10.1177/0023677219867719

Cited by 42 publications

(27 citation statements)

References 56 publications

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“…Regarding commercial vendors, they should raise the awareness and responsibility to at a minimum continue to provide transparency on the realities and limitations of commercial animal production. Commercial animal suppliers produce animals utilizing processes that prioritize the maintenance of high genetic quality and health standards [30,31]. In order to provide animals that are at minimum specific pathogen free, vendors have exclusion criteria that stock are maintained against.…”

Section: Discussionmentioning

confidence: 99%

Temporospatial shifts within commercial laboratory mouse gut microbiota impact experimental reproducibility

et al. 2020

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Background Experimental reproducibility in mouse models is impacted by both genetics and environment. The generation of reproducible data is critical for the biomedical enterprise and has become a major concern for the scientific community and funding agencies alike. Among the factors that impact reproducibility in experimental mouse models is the variable composition of the microbiota in mice supplied by different commercial vendors. Less attention has been paid to how the microbiota of mice supplied by a particular vendor might change over time. Results In the course of conducting a series of experiments in a mouse model of malaria, we observed a profound and lasting change in the severity of malaria in mice infected with Plasmodium yoelii; while for several years mice obtained from a specific production suite of a specific commercial vendor were able to clear the parasites effectively in a relatively short time, mice subsequently shipped from the same unit suffered much more severe disease. Gut microbiota analysis of frozen cecal samples identified a distinct and lasting shift in bacteria populations that coincided with the altered response of the later shipments of mice to infection with malaria parasites. Germ-free mice colonized with cecal microbiota from mice within the same production suite before and after this change followed by Plasmodium infection provided a direct demonstration that the change in gut microbiota profoundly impacted the severity of malaria. Moreover, spatial changes in gut microbiota composition were also shown to alter the acute bacterial burden following Salmonella infection, and tumor burden in a lung tumorigenesis model. Conclusion These changes in gut bacteria may have impacted the experimental reproducibility of diverse research groups and highlight the need for both laboratory animal providers and researchers to collaborate in determining the methods and criteria needed to stabilize the gut microbiota of animal breeding colonies and research cohorts, and to develop a microbiota solution to increase experimental rigor and reproducibility.

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Section: Discussionmentioning

confidence: 99%

Temporospatial shifts within commercial laboratory mouse gut microbiota impact experimental reproducibility

et al. 2020

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“…The temperature was maintained at 23–24°C with humidity levels between 35% and 70%. The breeding procedures were conducted as recommended by the International Committee on Standardized Genetic Nomenclature for Mice and in the guidelines provided by the Jackson Laboratory (Benavides et al, 2020, https://www.jax.org, under “strain‐background‐and‐genetic‐drift”), both stating that in a new colony strict inbreeding for at least 10 generations is necessary to consider the strain an inbreed one. All animals were kept under strict veterinary care with daily health inspections.…”

Section: Methodsmentioning

confidence: 99%

“…In this case, animals were housed in the Animal House of Nencki Institute of Experimental Biology for at least 2 weeks before the onset of the experimental procedures. The breeding procedures were conducted as recommended by the International Committee on Standardized Genetic Nomenclature for Mice and in the guidelines provided by the Jackson Laboratory (Benavides et al, 2020, https://www.jax.org, under “strain‐background‐and‐genetic‐drift”), both stating that in a new colony strict inbreeding for at least 10 generations is necessary to consider the strain an inbreed one.…”

Section: Methodsmentioning

confidence: 99%

Chronic fluoxetine treatment impairs motivation and reward learning by affecting neuronal plasticity in the central amygdala

Puścian

Winiarski

Łęski

et al. 2021

British J Pharmacology

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Background and Purpose: The therapeutic effects of fluoxetine are believed to be due to increasing neuronal plasticity and reversing some learning deficits. Nevertheless, a growing amount of evidence shows adverse effects of this drug on cognition and some forms of neuronal plasticity.Experimental Approach: To study the effects of chronic fluoxetine treatment, we combine an automated assessment of motivation and learning in mice with an investigation of neuronal plasticity in the central amygdala and basolateral amygdala. We use immunohistochemistry to visualize neuronal types and perineuronal nets, along with DI staining to assess dendritic spine morphology. Gel zymography is used to test fluoxetine's impact on matrix metalloproteinase-9, an enzyme involved in synaptic plasticity.Key Results: We show that chronic fluoxetine treatment in non-stressed mice increases perineuronal nets-dependent plasticity in the basolateral amygdala, while impairing MMP-9-dependent plasticity in the central amygdala. Further, we illustrate how the latter contributes to anhedonia and deficits of reward learning. Behavioural impairments are accompanied by alterations in morphology of dendritic spines in the central amygdala towards an immature state, most likely reflecting animals' inability to adapt. We strengthen the link between the adverse effects of fluoxetine and its influence on MMP-9 by showing that behaviour of MMP-9 knockout animals remains unaffected by the drug. Conclusion and Implications: Chronic fluoxetine treatment differentially affects various forms of neuronal plasticity, possibly explaining its opposing effects on brain and behaviour. These findings are of immediate clinical relevance since reported side effects of fluoxetine pose a potential threat to patients.

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“…This study was carried out in strict accordance with FELASA guidelines [ 32 ] and with European (European Union Directive 86/609/EEC) regulation. The protocol was approved by the Direção Geral de Alimentação e Veterinária (DGAV 021328).…”

Section: Methodsmentioning

confidence: 99%

ROBO2 signaling in lung development regulates SOX2/SOX9 balance, branching morphogenesis and is dysregulated in nitrofen-induced congenital diaphragmatic hernia

2020

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Background Characterized by abnormal lung growth or maturation, congenital diaphragmatic hernia (CDH) affects 1:3000 live births. Cellular studies report proximal (SOX2+) and distal (SOX9+) progenitor cells as key modulators of branching morphogenesis and epithelial differentiation, whereas transcriptome studies demonstrate ROBO/SLIT as potential therapeutic targets for diaphragm defect repair in CDH. In this study, we tested the hypothesis that (a) experimental-CDH could changes the expression profile of ROBO1, ROBO2, SOX2 and SOX9; and (b) ROBO1 or ROBO2 receptors are regulators of branching morphogenesis and SOX2/SOX9 balance. Methods The expression profile for receptors and epithelial progenitor markers were assessed by Western blot and immunohistochemistry in a nitrofen-induced CDH rat model. Immunohistochemistry signals by pulmonary structure were also quantified from embryonic-to-saccular stages in normal and hypoplastic lungs. Ex vivo lung explant cultures were harvested at E13.5, cultures during 4 days and treated with increasing doses of recombinant rat ROBO1 or human ROBO2 Fc Chimera proteins for ROBO1 and ROBO2 inhibition, respectively. The lung explants were analyzed morphometrically and ROBO1, ROBO2, SOX2, SOX9, BMP4, and β-Catenin were quantified by Western blot. Results Experimental-CDH induces distinct expression profiles by pulmonary structure and developmental stage for both receptors (ROBO1 and ROBO2) and epithelial progenitor markers (SOX2 and SOX9) that provide evidence of the impairment of proximodistal patterning in experimental-CDH. Ex vivo functional studies showed unchanged branching morphogenesis after ROBO1 inhibition; increased fetal lung growth after ROBO2 inhibition in a mechanism-dependent on SOX2 depletion and overexpression of SOX9, non-phospho β-Catenin, and BMP4. Conclusions These studies provided evidence of receptors and epithelial progenitor cells which are severely affected by CDH-induction from embryonic-to-saccular stages and established the ROBO2 inhibition as promoter of branching morphogenesis through SOX2/SOX9 balance.

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Genetic quality assurance and genetic monitoring of laboratory mice and rats: FELASA Working Group Report

Cited by 42 publications

References 56 publications

Temporospatial shifts within commercial laboratory mouse gut microbiota impact experimental reproducibility

Temporospatial shifts within commercial laboratory mouse gut microbiota impact experimental reproducibility

Chronic fluoxetine treatment impairs motivation and reward learning by affecting neuronal plasticity in the central amygdala

ROBO2 signaling in lung development regulates SOX2/SOX9 balance, branching morphogenesis and is dysregulated in nitrofen-induced congenital diaphragmatic hernia

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