Genetic and behavioral characterization of a Kmt2d mouse mutant, a new model for Kabuki Syndrome
The recessive mutant mice bate palmas (bapa) ‐ claps in Portuguese arose from N‐ethyl‐N‐nitrosourea mutagenesis. A single nucleotide, T > C, change in exon 13, leading to a Thr1289Ala substitution, was identified in the lysine (K)‐specific methyltransferase 2D gene (Kmt2d) located on chromosome 1...
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Published in | Genes, brain and behavior Vol. 18; no. 8; pp. e12568 - n/a |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
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Oxford, UK
Blackwell Publishing Ltd
01.11.2019
John Wiley & Sons, Inc |
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Abstract | The recessive mutant mice bate palmas (bapa) ‐ claps in Portuguese arose from N‐ethyl‐N‐nitrosourea mutagenesis. A single nucleotide, T > C, change in exon 13, leading to a Thr1289Ala substitution, was identified in the lysine (K)‐specific methyltransferase 2D gene (Kmt2d) located on chromosome 15. Mutations with a loss‐of‐function in the KMT2D gene on chromosome 12 in humans are responsible for Kabuki syndrome (KS). Phenotypic characterization of the bapa mutant was performed using a behavioral test battery to evaluate the parameters related to general activity, the sensory nervous system, the psychomotor system, and the autonomous nervous system, as well as to measure motor function and spatial memory. Relative to BALB/cJ mice, the bapa mutant showed sensory and psychomotor impairments, such as hypotonia denoted by a surface righting reflex impairment and hindquarter fall, and a reduction in the auricular reflex, suggesting hearing impairment. Additionally, the enhanced general activity showed by the increased rearing and grooming frequency, distance traveled and average speed possibly presupposes the presence of hyperactivity of bapa mice compared with the control group. A slight motor coordination dysfunction was showed in bapa mice, which had a longer crossing time on the balance beam compared with BALB/cJ controls. Male bapa mice also showed spatial gait pattern changes, such as a shorter stride length and shorter step length. In conclusion, the bapa mouse may be a valuable animal model to study the mechanisms involved in psychomotor and behavior impairments, such as hypotonia, fine motor coordination and hyperactivity linked to the Kmt2d mutation.
Comparison and filtering steps were performed to select only exclusive homozygous nonsynonymous or splice site variants in the bapa mutant compared with inbred strains as well as those in the Mouse Genomes Project database (REL‐1211) (A); Validation of the candidate single nucleotide variant (SNV) by Sanger sequencing of genomic DNA samples from bapa mutant (−/−) and C57BL/6J, BALB/cJ, A/J mice as well as an unrelated N‐ethyl‐N‐nitrosourea‐mutant controls (+/+) (B); SNV candidate found in exon 13 of Kmt2d gene, which creates a nonsynonym exchange of a threonine residue to an alanine residue in KMT2D protein (C). |
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AbstractList | The recessive mutant mice bate palmas (bapa) ‐ claps in Portuguese arose from N‐ethyl‐N‐nitrosourea mutagenesis. A single nucleotide, T > C, change in exon 13, leading to a Thr1289Ala substitution, was identified in the lysine (K)‐specific methyltransferase 2D gene (Kmt2d) located on chromosome 15. Mutations with a loss‐of‐function in the KMT2D gene on chromosome 12 in humans are responsible for Kabuki syndrome (KS). Phenotypic characterization of the bapa mutant was performed using a behavioral test battery to evaluate the parameters related to general activity, the sensory nervous system, the psychomotor system, and the autonomous nervous system, as well as to measure motor function and spatial memory. Relative to BALB/cJ mice, the bapa mutant showed sensory and psychomotor impairments, such as hypotonia denoted by a surface righting reflex impairment and hindquarter fall, and a reduction in the auricular reflex, suggesting hearing impairment. Additionally, the enhanced general activity showed by the increased rearing and grooming frequency, distance traveled and average speed possibly presupposes the presence of hyperactivity of bapa mice compared with the control group. A slight motor coordination dysfunction was showed in bapa mice, which had a longer crossing time on the balance beam compared with BALB/cJ controls. Male bapa mice also showed spatial gait pattern changes, such as a shorter stride length and shorter step length. In conclusion, the bapa mouse may be a valuable animal model to study the mechanisms involved in psychomotor and behavior impairments, such as hypotonia, fine motor coordination and hyperactivity linked to the Kmt2d mutation.
Comparison and filtering steps were performed to select only exclusive homozygous nonsynonymous or splice site variants in the bapa mutant compared with inbred strains as well as those in the Mouse Genomes Project database (REL‐1211) (A); Validation of the candidate single nucleotide variant (SNV) by Sanger sequencing of genomic DNA samples from bapa mutant (−/−) and C57BL/6J, BALB/cJ, A/J mice as well as an unrelated N‐ethyl‐N‐nitrosourea‐mutant controls (+/+) (B); SNV candidate found in exon 13 of Kmt2d gene, which creates a nonsynonym exchange of a threonine residue to an alanine residue in KMT2D protein (C). The recessive mutant mice bate palmas (bapa) - claps in Portuguese arose from N-ethyl-N-nitrosourea mutagenesis. A single nucleotide, T > C, change in exon 13, leading to a Thr Ala substitution, was identified in the lysine (K)-specific methyltransferase 2D gene (Kmt2d) located on chromosome 15. Mutations with a loss-of-function in the KMT2D gene on chromosome 12 in humans are responsible for Kabuki syndrome (KS). Phenotypic characterization of the bapa mutant was performed using a behavioral test battery to evaluate the parameters related to general activity, the sensory nervous system, the psychomotor system, and the autonomous nervous system, as well as to measure motor function and spatial memory. Relative to BALB/cJ mice, the bapa mutant showed sensory and psychomotor impairments, such as hypotonia denoted by a surface righting reflex impairment and hindquarter fall, and a reduction in the auricular reflex, suggesting hearing impairment. Additionally, the enhanced general activity showed by the increased rearing and grooming frequency, distance traveled and average speed possibly presupposes the presence of hyperactivity of bapa mice compared with the control group. A slight motor coordination dysfunction was showed in bapa mice, which had a longer crossing time on the balance beam compared with BALB/cJ controls. Male bapa mice also showed spatial gait pattern changes, such as a shorter stride length and shorter step length. In conclusion, the bapa mouse may be a valuable animal model to study the mechanisms involved in psychomotor and behavior impairments, such as hypotonia, fine motor coordination and hyperactivity linked to the Kmt2d mutation. The recessive mutant mice bate palmas (bapa) ‐ claps in Portuguese arose from N‐ethyl‐N‐nitrosourea mutagenesis. A single nucleotide, T > C, change in exon 13, leading to a Thr 1289 Ala substitution, was identified in the lysine (K)‐specific methyltransferase 2D gene ( Kmt2d ) located on chromosome 15. Mutations with a loss‐of‐function in the KMT2D gene on chromosome 12 in humans are responsible for Kabuki syndrome (KS). Phenotypic characterization of the bapa mutant was performed using a behavioral test battery to evaluate the parameters related to general activity, the sensory nervous system, the psychomotor system, and the autonomous nervous system, as well as to measure motor function and spatial memory. Relative to BALB/cJ mice, the bapa mutant showed sensory and psychomotor impairments, such as hypotonia denoted by a surface righting reflex impairment and hindquarter fall, and a reduction in the auricular reflex, suggesting hearing impairment. Additionally, the enhanced general activity showed by the increased rearing and grooming frequency, distance traveled and average speed possibly presupposes the presence of hyperactivity of bapa mice compared with the control group. A slight motor coordination dysfunction was showed in bapa mice, which had a longer crossing time on the balance beam compared with BALB/cJ controls. Male bapa mice also showed spatial gait pattern changes, such as a shorter stride length and shorter step length. In conclusion, the bapa mouse may be a valuable animal model to study the mechanisms involved in psychomotor and behavior impairments, such as hypotonia, fine motor coordination and hyperactivity linked to the Kmt2d mutation. The recessive mutant mice bate palmas (bapa) ‐ claps in Portuguese arose from N‐ethyl‐N‐nitrosourea mutagenesis. A single nucleotide, T > C, change in exon 13, leading to a Thr1289Ala substitution, was identified in the lysine (K)‐specific methyltransferase 2D gene (Kmt2d) located on chromosome 15. Mutations with a loss‐of‐function in the KMT2D gene on chromosome 12 in humans are responsible for Kabuki syndrome (KS). Phenotypic characterization of the bapa mutant was performed using a behavioral test battery to evaluate the parameters related to general activity, the sensory nervous system, the psychomotor system, and the autonomous nervous system, as well as to measure motor function and spatial memory. Relative to BALB/cJ mice, the bapa mutant showed sensory and psychomotor impairments, such as hypotonia denoted by a surface righting reflex impairment and hindquarter fall, and a reduction in the auricular reflex, suggesting hearing impairment. Additionally, the enhanced general activity showed by the increased rearing and grooming frequency, distance traveled and average speed possibly presupposes the presence of hyperactivity of bapa mice compared with the control group. A slight motor coordination dysfunction was showed in bapa mice, which had a longer crossing time on the balance beam compared with BALB/cJ controls. Male bapa mice also showed spatial gait pattern changes, such as a shorter stride length and shorter step length. In conclusion, the bapa mouse may be a valuable animal model to study the mechanisms involved in psychomotor and behavior impairments, such as hypotonia, fine motor coordination and hyperactivity linked to the Kmt2d mutation. |
Author | Massironi, Silvia M. G. Mori, Claudia M. C. Garcia‐Gomes, Mariana de Souza A. Zanatto, Dennis A. Antiorio, Ana T. F. B. Bernardi, Maria M. Alexandre‐Ribeiro, Sandra R. Oliveira, Nicassia de Souza Menck, Carlos F. M. Yamamoto, Pedro K. Souza, Tiago A. |
Author_xml | – sequence: 1 givenname: Pedro K. surname: Yamamoto fullname: Yamamoto, Pedro K. organization: University of São Paulo (USP) – sequence: 2 givenname: Tiago A. surname: Souza fullname: Souza, Tiago A. organization: University of São Paulo (USP) – sequence: 3 givenname: Ana T. F. B. surname: Antiorio fullname: Antiorio, Ana T. F. B. organization: University of São Paulo (USP) – sequence: 4 givenname: Dennis A. surname: Zanatto fullname: Zanatto, Dennis A. organization: University of São Paulo (USP) – sequence: 5 givenname: Mariana de Souza A. surname: Garcia‐Gomes fullname: Garcia‐Gomes, Mariana de Souza A. organization: University of São Paulo (USP) – sequence: 6 givenname: Sandra R. surname: Alexandre‐Ribeiro fullname: Alexandre‐Ribeiro, Sandra R. organization: University of São Paulo (USP) – sequence: 7 givenname: Nicassia de Souza surname: Oliveira fullname: Oliveira, Nicassia de Souza organization: University of São Paulo (USP) – sequence: 8 givenname: Carlos F. M. surname: Menck fullname: Menck, Carlos F. M. organization: University of São Paulo (USP) – sequence: 9 givenname: Maria M. surname: Bernardi fullname: Bernardi, Maria M. organization: Graduate Program in Environmental and Experimental Pathology, Paulista University – sequence: 10 givenname: Silvia M. G. surname: Massironi fullname: Massironi, Silvia M. G. organization: University of São Paulo (USP) – sequence: 11 givenname: Claudia M. C. orcidid: 0000-0002-9393-240X surname: Mori fullname: Mori, Claudia M. C. email: claumori@gmail.com organization: University of São Paulo (USP) |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30891914$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1002_jnr_25050 crossref_primary_10_1016_j_heliyon_2023_e13629 crossref_primary_10_21769_BioProtoc_3568 crossref_primary_10_1111_joa_13459 crossref_primary_10_1242_dmm_049735 crossref_primary_10_1016_j_yebeh_2020_106945 crossref_primary_10_1096_fj_202100823R crossref_primary_10_3390_genes12040468 crossref_primary_10_1016_j_bbr_2023_114329 crossref_primary_10_1002_wsbm_1552 crossref_primary_10_1016_j_bbr_2023_114562 crossref_primary_10_3389_fcell_2022_979512 |
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Keywords | mouse genetics ENU-mutagenesis mouse phenotype psychomotor impairment Kmt2d gene mutant behavior |
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Notes | Funding information Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq), Grant/Award Number: 14411/2017‐1; Coordenação de Aperfeiçoamento de Pessoal de Nível Superior ‐ Brasil (CAPES), Grant/Award Number: Finance Code 001; Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP), Grant/Award Numbers: 2012/25387‐2, 2016/23659‐6, 2017/21103‐3 |
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Snippet | The recessive mutant mice bate palmas (bapa) ‐ claps in Portuguese arose from N‐ethyl‐N‐nitrosourea mutagenesis. A single nucleotide, T > C, change in exon 13,... The recessive mutant mice bate palmas (bapa) - claps in Portuguese arose from N-ethyl-N-nitrosourea mutagenesis. A single nucleotide, T > C, change in exon 13,... The recessive mutant mice bate palmas (bapa) ‐ claps in Portuguese arose from N‐ethyl‐N‐nitrosourea mutagenesis. A single nucleotide, T > C, change in exon 13,... |
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SubjectTerms | Abnormalities, Multiple - genetics Abnormalities, Multiple - physiopathology Animal models Animals Balance Behavior, Animal Chromosome 12 Chromosome 15 Congenital defects Coordination Disease Models, Animal ENU‐mutagenesis Face - abnormalities Face - physiopathology Gait Grooming Hearing Hearing loss Hematologic Diseases - genetics Hematologic Diseases - physiopathology Histone-Lysine N-Methyltransferase - genetics Hyperactivity Kmt2d gene Loss of Function Mutation Lysine Male Methyltransferase Mice Mice, Inbred BALB C Motor ability Motor task performance mouse genetics mouse phenotype Movement Muscle Hypotonia - genetics Mutagenesis mutant behavior Mutation Myeloid-Lymphoid Leukemia Protein - genetics Nervous system psychomotor impairment Reflex Righting reflex Spatial memory Vestibular Diseases - genetics Vestibular Diseases - physiopathology |
Title | Genetic and behavioral characterization of a Kmt2d mouse mutant, a new model for Kabuki Syndrome |
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