Btbr t tf j

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BTBR T+tf/J is a mouse strain that is commonly used in research. It serves as a genetic model for various studies, but a detailed description of its core functions would require more information than can be provided concisely and without interpretation.

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5 protocols using btbr t tf j

Mouse Strains for PTR Studies

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The PTR studies in mice were performed as described previously,^{34 (link)} using multiple strains from Jackson Labs (Bar Harbor, ME, USA): KK/HIJ, LG/J, AKR/J, FVB/NJ, C3H/HeJ, DBA/2J, NOD/ShiLtJ, 129X1/SvJ, 129S1/SvImJ, A/J, BTBR/T+ tf/J, Balb/cByJ, C57Bl/6J. UbiC-GFP male mice, on a C57BL/6 background, were bred to FVB/NJ females in the Bloodworks NW Research Institute Vivarium (Seattle, WA, USA) and offspring were used as transfusion recipients at 24–28 weeks of age.^{34 (link)}

Nemkov T., Sun K., Reisz J.A., Song A., Yoshida T., Dunham A., Wither M.J., Francis R.O., Roach R.C., Dzieciatkowska M., Rogers S.C., Doctor A., Kriebardis A., Antonelou M., Papassideri I., Young C.T., Thomas T.A., Hansen K.C., Spitalnik S.L., Xia Y., Zimring J.C., Hod E.A, & D’Alessandro A. (2018). Hypoxia modulates the purine salvage pathway and decreases red blood cell and supernatant levels of hypoxanthine during refrigerated storage. Haematologica, 103(2), 361-372.

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Cav1-Null and BTBR Acallosal Mouse Models

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All animal procedures were performed in accordance with the Harvard University animal care committee’s regulations. Cav1-null mice on a congenic C57/Bl6 background (B6.Cg-Cav1^tm1Mls/J) were obtained from The Jackson Laboratory, strain number 007083 (RRID:IMSR_JAX:007083). The original targeted null mutation was generated by Michael Lisanti at The Albert Einstein College of Medicine. A 2.2-kb region of the gene including exons 1 and 2 and a portion of the promoter region was replaced with a neomycin resistance cassette via homologous recombination (Razani et al., 2001 (link)).
BTBR acallosal mice on a congenic background (BTBR T⁺tf/J) were obtained from The Jackson Laboratory, strain number 002282 (RRID:IMSR_JAX:002282; Wahlsten et al., 2003 (link)). LP/J mice have been shown to be an appropriate callosal control population for BTBR mice. LP/J mice (LP/J) were obtained from The Jackson Laboratory, strain number 000676 (RRID:IMSR_JAX:000676).
C57/Bl6 wild-type (WT) mice were obtained from The Jackson Laboratory (RRID:IMSR_JAX:000664), and were used to breed with Cav1-null mice, and for birthdating and electroporation experiments. FEZF2 mutants were generated by Hirata et al. (2004 (link); GenBank accession number: AB042399).

MacDonald J.L., Fame R.M., Gillis-Buck E.M, & Macklis J.D. (2018). Caveolin1 Identifies a Specific Subpopulation of Cerebral Cortex Callosal Projection Neurons (CPN) Including Dual Projecting Cortical Callosal/Frontal Projection Neurons (CPN/FPN). eNeuro, 5(1), ENEURO.0234-17.2017.

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Genetic Diversity of Mouse Strains

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129S1/SvImJ, A/J, AKR/J, BALB/cByJ, BTBRT⁺tf/J, BUB/BnJ, C3H/HeJ, C57BL/10J, C57BL/6J, C57BLKS/J, C57BR/cdJ, C57L/J, CAST/EiJ, CBA/J, DBA/2J, FVB/NJ, KK/HlJ, LP/J, MRL/MpJ, NOD.B10Sn-H2^b/J (a congenic strain with the NOD genetic background but with a histocompatibility locus from a diabetes-resistant strain), NON/ShiLtJ, NZO/HlLtJ, NZW/LacJ, P/J, PL/J, PWD/PhJ, RIIIS/J, SJL/J, SM/J, SWR/J, and WSB/J were obtained from The Jackson Laboratory (Bar Harbor, ME). Three of the strains were not evaluated at all time points because of lymphoma development (AKR/J), lack of sufficient mice for analysis (CAST/EiJ), or self-mutilations resulting in euthanasia for humane purposes (SJL/J). (9 , 10 (link)) Taken together the strains selected were genetically diverse, which was estimated by SNP genotyping of over 100 strains into 7 distinct genetic groups, so that there were 3–7 strains representing each of the groups.(11 (link))

Linn S.C., Mustonen A.M., Silva K.A., Kennedy V.E., Sundberg B.A., Bechtold L.S., Alghamdi S., Hoehndorf R., Schofield P.N, & Sundberg J.P. (2018). Nail Abnormalities Identified in an Aging Study of 30 Inbred Mouse Strains. Experimental dermatology, 28(4), 383-390.

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Genetic Mapping of Obese Mouse Strains

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C57BL/6J (abbreviated B6 or B) and BTBR T⁺tf/J (abbreviated BTBR or R) mice were purchased from the Jackson Laboratory (Bar Harbor, ME) and bred at the University of Wisconsin–Madison. The Lep^ob mutation was introgressed into all strains using heterozygous parents to generate homozygous Lep^ob/ob offspring. F₂ mice, all Lep^ob/ob, were the offspring of F₁ parents derived from a cross between BTBR females and B6 males (Supporting Information, Figure S1). F₂ mice and a small number of parental and F₁ controls were genotyped with the 5K GeneChip (Affymetrix).

Broman K.W., Keller M.P., Broman A.T., Kendziorski C., Yandell B.S., Sen Ś, & Attie A.D. (2015). Identification and Correction of Sample Mix-Ups in Expression Genetic Data: A Case Study. G3: Genes|Genomes|Genetics, 5(10), 2177-2186.

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Postmortem Cerebellum Analysis of Autism Individuals

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The frozen cerebellum from male and female BTBR T+tf/J and C57BL/6J mice (8 weeks of age, n = 5 per gender/strain) were obtained from the Jackson Laboratory (Bar Harbor, ME, USA). The frozen blocks of post-mortem cerebellum from autism individuals (n = 15) and unaffected control individuals (n = 15) were obtained from the National Institute of Child Health and Development Brain Tissue Bank for Developmental Disorders at the University of Maryland, and from the Autism Tissue Program at the Harvard Brain Tissue Resource Center, Bellmont, MA, USA. All donors had a confirmed diagnosis of autism based on Diagnostic and Statistical Manual of Mental Disorders and Diagnostic Interview Revised. Autism and control groups were matched, as closely as possible, for post-mortem interval, age, gender, race, and cause of death. The demographic data of case-control tissue samples are detailed in James et al.[23] (link). The analysis of postmortem brain specimens is not defined as human research by the United State Department of Health and Health Services (DHHS) and Food and Drug Administration (FDA) regulations.

Shpyleva S., Ivanovsky S., de Conti A., Melnyk S., Tryndyak V., Beland F.A., James S.J, & Pogribny I.P. (2014). Cerebellar Oxidative DNA Damage and Altered DNA Methylation in the BTBR T+tf/J Mouse Model of Autism and Similarities with Human Post Mortem Cerebellum. PLoS ONE, 9(11), e113712.

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