Genetic polymorphisms among C57BL/6 mouse inbred strains

Zurita, Esther; Chagoyen, Mónica; Cantero, Marta; Alonso, Rosario; González‐Neira, Anna; López-Jiménez, Alejandro; López-Moreno, José Antonio; Landel, Carlisle P.; Benı́tez, Javier; Pazos, Florencio; Montoliu, Lluı́s

doi:10.1007/s11248-010-9403-8

Cited by 165 publications

(159 citation statements)

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“…C57BL/6 substrains are often considered interchangeable, and a lack of reference to which specific substrain was used is common in experimental methodologies. However, there is growing awareness of the significant genetic and phenotypic differences between even closely related mouse strains and substrains (19,(26)(27)(28), and the present study demonstrates the complete absence in a C57BL/6 substrain of what is generally considered a ubiquitous plasticity mechanism in both mice and rats (14,16,20,29). This finding underscores the importance of reporting mouse background substrains and of using appropriate littermate controls.…”

Section: Discussionsupporting

confidence: 65%

“…The most prominent genetic difference between the two substrains is the absence of α-synuclein in 6JOla mice; however, we have shown that this protein is not required for the homeostatic component of OD plasticity. The numerous other genetic differences between the two substrains include other absent or mutated genes and a multitude of copy number variations (26,27,30). The analysis of these differences may allow identification of a unique molecular mechanism of homeostatic plasticity as more is discovered about the signaling pathways involved.…”

Section: Discussionmentioning

confidence: 99%

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Homeostatic plasticity mechanisms are required for juvenile, but not adult, ocular dominance plasticity

Ranson

Cheetham²,

Fox³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

122

136

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Ocular dominance (OD) plasticity in the visual cortex is a classic model system for understanding developmental plasticity, but the visual cortex also shows plasticity in adulthood. Whether the plasticity mechanisms are similar or different at the two ages is not clear. Several plasticity mechanisms operate during development, including homeostatic plasticity, which acts to maintain the total excitatory drive to a neuron. In agreement with this idea, we found that an often-studied substrain of C57BL/6 mice, C57BL/ 6JOlaHsd (6JOla), lacks both the homeostatic component of OD plasticity as assessed by intrinsic signal imaging and synaptic scaling of mEPSC amplitudes after a short period of dark exposure during the critical period, whereas another substrain, C57BL/6J (6J), exhibits both plasticity processes. However, in adult mice, OD plasticity was identical in the 6JOla and 6J substrains, suggesting that adult plasticity occurs by a different mechanism. Consistent with this interpretation, adult OD plasticity was normal in TNFα knockout mice, which are known to lack juvenile synaptic scaling and the homeostatic component of OD plasticity, but was absent in adult α-calcium/calmodulin-dependent protein kinase II;T286A (αCaMKII T286A ) mice, which have a point mutation that prevents autophosphorylation of αCaMKII. We conclude that increased responsiveness to open-eye stimulation after monocular deprivation during the critical period is a homeostatic process that depends mechanistically on synaptic scaling during the critical period, whereas in adult mice it is mediated by a different mechanism that requires αCaMKII autophosphorylation. Thus, our study reveals a transition between homeostatic and long-term potentiation-like plasticity mechanisms with increasing age.

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Section: Discussionsupporting

confidence: 65%

Section: Discussionmentioning

confidence: 99%

Homeostatic plasticity mechanisms are required for juvenile, but not adult, ocular dominance plasticity

Ranson

Cheetham²,

Fox³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

122

136

View full text Add to dashboard Cite

show abstract

“…Since its establishment, the C57BL/6 inbred strain has led to the origin of several substrains, which differ genetically and phenotypically with respect to the reference C57BL/6J [8]. To verify the genetic makeup of the Prnp ZH3/ZH3 mouse line, we analyzed 12 SNPs known to be informative among different C57BL/6 substrains.…”

Section: Methodsmentioning

confidence: 99%

Extended characterization of the novel co-isogenic C57BL/6J Prnp^−/− mouse line

Sorce

Paolucci

Aguzzi

2017

Amyloid

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“…Mice may differ in physiologic parameters [7] or in response to triggers. Polymorphisms exist for substrains of the same inbred strains [8]. Genetic background also influences pathways that regulate thrombosis and hemostasis: differences were observed in global bleeding and thrombosis assays [9], coagulation and fibrinolytic factors [10], and susceptibility to treatment [11].…”

mentioning

confidence: 99%

Influence of genetic background on bleeding phenotype in the tail‐tip bleeding model and recommendations for standardization: communication from the SSC of the ISTH

Schiviz

Magirr

Leidenmühler

et al. 2014

Journal of Thrombosis and Haemostasis

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The murine tail-tip bleeding model is widely used to measure bleeding time, blood loss, and survival after treatment [1][2][3][4]. Because of the considerable variation in data from these studies and thus the need for large sample sizes per group, and the lack of comparability of results from different laboratories, research groups have tried to standardize the model. In 2010, the SSC of the ISTH proposed standardized methods for determining tail bleeding time in mice. The SSC report standardized the tail clipping by endorsing the use of a warming chamber to evenly warm the anesthetized mouse, and assessing the influence of anesthesia and systolic blood pressure on blood loss [5].We sought to test the ability of the standardized method to detect differences in bleeding phenotypes of wild-type mouse strains, which may show different bleeding phenotypes [6]. The relevance of the genetic background of inbred mouse strains or transgenic mice on phenotype has been described in various research fields. Mice may differ in physiologic parameters [7] or in response to triggers. Polymorphisms exist for substrains of the same inbred strains [8]. Genetic background also influences pathways that regulate thrombosis and hemostasis: differences were observed in global bleeding and thrombosis assays [9], coagulation and fibrinolytic factors [10], and susceptibility to treatment [11].To investigate the ability of the tail-tip bleeding assay to detect the influence of genetic background on bleeding phenotype, we used hemophilic mice on different backgrounds, i.e. coagulation factor VIII (exon 17) knockout (FVIII À/À ) [12] mice on a BALB/c, C57BL/6, or mixed background, along with different substrains of wild-type C57BL/6 or BALB/c mice ( Table 1). The mice were anesthetized with 100 mg kg -1 ketamine and 10 mg kg -1 xylazine and placed in a warming chamber. Two millimeters of the tail tip were clipped with a guillotine [4], the tails were immersed in warm saline (2 mL, 35 AE 2°C), and blood was collected over a period of 60 min; anesthesia was maintained as required by subcutaneous supplementation with one-third of the starting dose. Blood loss was determined gravimetrically. At the end of this observation period, the mice were removed from the chamber and humanely killed by cervical dislocation. Pairwise tests of equality of variance were performed with a bootstrap approach; the level of statistical significance was set to P = 0.05.C.FVIII À/À mice showed markedly lower median blood loss (365.7 mg) than B6.FVIII À/À (965.2 mg) and B6; FVIII À/À (890.4 mg) mice. For all three strains, median blood loss was lower in females than in males, with the largest sex difference (634 mg vs. 954 mg for females vs. males) and the highest interindividual variation being observed in B6;FVIII À/À mice (Fig. 1). In 129S1/SvmJ mice and the four substrains of BALB/c mice, median blood loss (23.5 mg and 10.0-19.0 mg, respectively) and interanimal variability were low. In contrast, median blood loss in C57BL/6 substrains varied from 36.0 mg (C57BL/...

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Genetic polymorphisms among C57BL/6 mouse inbred strains

Cited by 165 publications

References 10 publications

Homeostatic plasticity mechanisms are required for juvenile, but not adult, ocular dominance plasticity

Homeostatic plasticity mechanisms are required for juvenile, but not adult, ocular dominance plasticity

Extended characterization of the novel co-isogenic C57BL/6J Prnp^−/− mouse line

Influence of genetic background on bleeding phenotype in the tail‐tip bleeding model and recommendations for standardization: communication from the SSC of the ISTH

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Genetic polymorphisms among C57BL/6 mouse inbred strains

Cited by 165 publications

References 10 publications

Homeostatic plasticity mechanisms are required for juvenile, but not adult, ocular dominance plasticity

Homeostatic plasticity mechanisms are required for juvenile, but not adult, ocular dominance plasticity

Extended characterization of the novel co-isogenic C57BL/6J Prnp−/− mouse line

Influence of genetic background on bleeding phenotype in the tail‐tip bleeding model and recommendations for standardization: communication from the SSC of the ISTH

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Extended characterization of the novel co-isogenic C57BL/6J Prnp^−/− mouse line