JAX
Mouse Strain Datasheet - 000506
B6C3Fe a/a-Qkqk-v/J
Also Known As: quaking, quaking viable
Mice homozygous for the quaking spontaneous mutation (Qk) have marked rapid tremor which disappears when they are at rest but increases during locomotion. The tremor in homozygous mutant mice begins at about 10 days and is fully developed by 3 weeks. Mature mice may have seizures in which a motionless posture is maintained for many seconds. Females are viable and fertile, males are sterile due to defective spermatic differentiation. The entire CNS of quaking mutant mice is severely deficient in myelin and there is a less severe myelin deficiency in the PNS.
Genetic overview
| Genetic Background | Generation |
|---|---|
|
|
Qkqk-v
| Allele Type | Gene Symbol | Gene Name |
|---|---|---|
| Spontaneous | Qk | quaking |
a
| Allele Type | Gene Symbol | Gene Name |
|---|---|---|
| Spontaneous | a | nonagouti |
Research Applications
- Neurobiology Research
- Apoptosis Research
- Cell Biology Research
- Reproductive Biology Research
- Sensorineural Research
Detailed Description
Mice homozygous for the quaking spontaneous mutation (Qk) have marked rapid tremor which disappears when they are at rest but increases during locomotion. The tremor in homozygous mutant mice begins at about 10 days and is fully developed by 3 weeks. Mature mice may have seizures in which a motionless posture is maintained for many seconds. Females are viable and fertile, males are sterile due to defective spermatic differentiation. The entire CNS of quaking mutant mice is severely deficient in myelin and there is a less severe myelin deficiency in the PNS.
Development
The quaking (Qkqk) mutation arose spontaneously in 1961 in the DBA/2J strain. It was crossed twice to C3H then transferred to the C57BL/6JEi background via backcross-intercross mating until N10 then sibling bred. At N11F10 it was bred to C57BL/6J-T2J, and a repulsion stock was generated. In 1976 a Qkqk homozygote was outcrossed to a B6C3HF1 male, removing the T2J mutation, and the Qkqk mutation was maintained via cross-intercross using Qkqk homozygous females and B6C3F1 males for the cross since homozygous males are sterile. At N8F4 a change was made to use B6C3Fe-a/a F1 for the outcross. In 1987 homozygous females at N15F1 were bred with B6C3F3-a/a F1 males to generate embryos for cryopreservation.
Control Suggestions
Selected References
- SIDMAN RL; DICKIE MM; APPEL SH. 1964. MUTANT MICE (QUAKING AND JIMPY) WITH DEFICIENT MYELINATION IN THE CENTRAL NERVOUS SYSTEM. Science 144:309-11. PubMed: 14169723MGI: J:13141
Qkqk-v
Allele Symbol: Qkqk-v
| Allele Name | quaking viable |
|---|---|
| Allele Type | Spontaneous |
| Allele Synonym(s) | Qkqk; qk; qkv |
| Gene Symbol and Name | Qk, quaking |
| Gene Synonym(s) | 1110003F05Rik; 1110003F05Rik; Hqk; QK; QK1; QK3; QkI; Qki; RIKEN cDNA 1110003F05 gene; hqkI; l(17)-1Wis; l(17)-1Wis; l17Wis1; l17Wis1; lethal, Chr 17, U Wisconsin 1 |
| Strain of Origin | DBA/2J |
| Chromosome | 17 |
| General Note | The quaking mutation arose spontaneously in the DBA/2J strain. Homozygotes have marked rapid tremor which disappears when they are at rest but increases during locomotion. It begins at about 10 days and is fully developed by 3 weeks. Mature mice may have seizures in which a motionless posture is maintained for many seconds. Females are viable and fertile, males sterile.Homozygotes are severely deficient in myelin, the material which ensheathes and insulates the axons of the central (CNS) and peripheral (PNS) nervous systems (see Mbp). The entire CNS is very deficient in myelin at all ages (J:13141), and there is a less severe myelin deficiency in the PNS nervous system (J:5177). Myelin sheaths are present in the CNS, but they are thinner than normal, some consisting of only one to four myelin lamellae. The sheaths are usually loosely wound, with patches of oligodendroglial cell cytoplasm between the lamellae, and there are abnormal inclusions and vacuoles in the processes and perikarya of oligodendrocytes. Development of the myelin sheaths appears to be arrested in a stage characteristic of very young animals (J:5189)(J:5271)(J:5218). There is variable hyperplasia of oligodendrocytes, greatest in the tracts with the greatest degree of myelination (J:5615). Axons have normal morphology but there is abnormally high proteolysis in the axons of the optic nerve (J:6971). There is evidence that the myelination defect in the CNS is due to defective oligodendrocytes (J:6216).Handling-induced convulsive seizures in qk/qk mice can be inhibited by administration of N-methyl-D-aspartate (NMDA) antagonists. Modulatory mechanisms for the NMDA receptor complex may differ in qk/qk mice from wild-type (J:1930). a2-adrenoceptor (A2A) antagonists also inhibit these seizures, while A2A agonists potentiate them. qk/qk mice have increased brain binding sites for A2A agonists (J:1169).In the PNS, thinly myelinated and unmyelinated fibers have been described in the sciatic nerve and in the intracranial portion of the trigeminal nerve (J:5189)(J:5271). The sheaths may be structurally abnormal with regions of uncompacted myelin lamellae similar to those of the CNS (J:5778). Orthotopic transplantation of pieces of sciatic nerve between quaking and normal mice has shown that the genetic defect is expressed in Schwann cells (J:14892). Qk causes defective myelinogenesis in both oligodendrocytes and Schwann cells (J:6411).There is an extensive literature on biochemical defects related to the deficiency of myelin in quaking mice (J:26986), a consistent finding of which is a severe deficiency of the myelin lipids, sphingomyelin, cerebrosides, and sulfatides, particularly those containing long-chain fatty acids. The normal increase in these fatty acids which occurs between 15 and 20 days does not occur in qk/qk mice, so that adult mutants tend to resemble very young controls (J:5171). Brain proteolipids in adult quaking mice retain the relative proportions found in 10-day controls (J:5408). The myelin-associated glycoproteins of different molecular weight in the brains of quaking mice 15 days of age and older are expressed in abnormal proportions (J:7990). Synthesis of myelin basic protein and proteolipids is normal in quaking brains but their incorporation into myelin is defective (J:6151). mRNAs for myelin basic protein, for example, occur in oligodendrocyte cell bodies, but not in the cell processes that actually form the myelin sheath, in qk/qk brain (J:1931). Quaking mice may have abnormal levels of copper and zinc in the brain, but the evidence on this point is conflicting (J:7214).The sterility of male qk/qk mice is due to defective spermatid differentiation, the details of which have been described (J:5241). It has been further demonstrated that male sterility in these mice is the result of the loss of Pacrg expression (J:90667). |
| Molecular Note | The quaking phenotype has been attributed to a 1.85 Mb deletion on chromosome 17. The proximal breakpoint was located in the promoter region of the Qk gene and affects transcript levels of that gene. The distal breakpoint lies between exons 5 and 6 of the parkin gene. Both the parkin gene and another co-regulated gene, Pacrg, are inactivated. Although parkin is not expressed in these mutants, the described phenotype appears due to to the defect in Qk expression. |
a
Allele Symbol: a
| Allele Name | nonagouti |
|---|---|
| Allele Type | Spontaneous |
| Allele Synonym(s) | |
| Gene Symbol and Name | a, nonagouti |
| Gene Synonym(s) | AGSW; AGTI; AGTIL; ASP; As; As; SHEP9; agouti; agouti signal protein; agouti suppressor |
| Strain of Origin | old mutant of the mouse fancy |
| Chromosome | 2 |
| Molecular Note | Characterization of this allele shows an insertion of DNA comprised of a 5.5kb virus-like element, VL30, into the first intron of the agouti gene. The VL30 element itself contains an additional 5.5 kb sequence, flanked by 526 bp of direct repeats. The host integration site is the same as for at-2Gso and Aw-38J and includes a duplication of four nucleotides of host DNA and a deletion of 2 bp from the end of each repeat. Northern analysis of mRNA from skin of homozygotes shows a smaller agouti message and levels 8 fold lower than found in wild-type. |
Disease Terms
Research Areas By Genotype
This mouse can be used to support research in many areas including:
- Neurobiology Research
- Parkinson's Disease
- Park2 (parkin) mutants
- Parkinson's Disease
Genotype: Qkqk-v related
- Apoptosis Research
- Cell Biology Research
- Cell Cycle Regulation
- Protein Processing
- degradation
- Neurobiology Research
- Epilepsy
- Hearing Defects
- Myelination Defects
- Neurodegeneration
- Parkinson's Disease
- Tremor Defects
- Reproductive Biology Research
- Developmental Defects Affecting Gonads
- males only
- Fertility Defects
- males only
- Developmental Defects Affecting Gonads
- Sensorineural Research
- Hearing Defects
Mammalian Phenotype Terms by Genotype
Genotype: Qkqk-v/Qkqk-v
B6C3Fe a/a-Qkqk-v/J
hearing/vestibular/ear phenotype
- reduced linear vestibular evoked potential
- prolonged latency for all peaks and larger amplitudes for P1/N1 (MGI Ref ID J:116914)
nervous system phenotype
- Purkinje cell degeneration
- aging mutants exhibit Purkinje cell axonal swellings, indicating neurodegeneration (MGI Ref ID J:102038)
- abnormal myelination
- decrease in myelination, however more axons are surrounded by thin myelin sheaths than seen in Qke5 homozygotes (MGI Ref ID J:102038)
- microsomes prepared from brains of 18 day old homozygotes show a reduction in fatty acid chain elongation activity with arachidoyl CoA, behenoyl CoA, and palmitoyl CoA substrates (MGI Ref ID J:160743)
- seizures
- onset of seizures begins at 6-8 weeks of age; seizures occur less frequently than in homozygous Qke5 mice (MGI Ref ID J:102038)
behavior/neurological phenotype
- seizures
- onset of seizures begins at 6-8 weeks of age; seizures occur less frequently than in homozygous Qke5 mice (MGI Ref ID J:102038)
reproductive system phenotype
- abnormal sperm flagellum morphology
- (MGI Ref ID J:88151)
- abnormal sperm head morphology
- (MGI Ref ID J:88151)
- abnormal spermatogenesis
- the testis contain many spermatogenic cells, but few spermatozoa and the spermatozoa collected from the cauda epididymis all have abnormal heads and/or tails and less than 0.5% are barely motile, and although in vitro fertilization is not successful, intracytoplasmic sperm injection and round spermatid injection are successful in production of offspring from homozygous malesacytoplasmic sperm injection and round spermatid injection are successful in production of offspring from homozygous males (MGI Ref ID J:88151)
- abnormal spermiogenesis
- (MGI Ref ID J:88151)
- necrospermia
- (MGI Ref ID J:88151)
- oligozoospermia
- (MGI Ref ID J:88151)
cellular phenotype
- abnormal sperm flagellum morphology
- (MGI Ref ID J:88151)
- abnormal sperm head morphology
- (MGI Ref ID J:88151)
- necrospermia
- (MGI Ref ID J:88151)
- oligozoospermia
- (MGI Ref ID J:88151)
The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain
Genotype: Qkqk-v/Qkqk-v
involves: DBA/2J
behavior/neurological phenotype
- abnormal gait
- walk slowly with a trembling gait (MGI Ref ID J:133042)
- abnormal locomotor behavior
- decrease in the frequency of wire mesh climbing in males (MGI Ref ID J:133042)
- abnormal response to novel object
- decrease in the frequency of exploratory sniffing (at wire mesh or a novel object) and leans against the novel object in males (MGI Ref ID J:133042)
- abnormal stationary movement
- decrease in the frequency of leaning against the wall or a novel object and single forepaw lifts in males (MGI Ref ID J:133042)
- hypoactivity
- (MGI Ref ID J:133042)
- increased grooming behavior
- increase in the frequency of hair fluffing in males (MGI Ref ID J:133042)
Genotype: Qkqk-v/Qkqk-v
involves: C3H/Di * DBA/2J
nervous system phenotype
- abnormal myelination
- cells in white matter and grey matter tracts appear normal (MGI Ref ID J:13141)
- cranial and spinal nerves (except optic nerve) are myelinated (MGI Ref ID J:13141)
- loss of myelination begins at the junction of peripheral and central nervous systems (MGI Ref ID J:13141)
- region from olfactory bulb to sacral spinal cord is deficient in myelin at all ages studied (12 days to 4 months) (MGI Ref ID J:13141)
- some fragments of myelin are seen in almost all fiber tracts (MGI Ref ID J:13141)
- tonic seizures
behavior/neurological phenotype
- paraparesis
- some animals exhibit hindlimb weakness at 3 months of age (MGI Ref ID J:13141)
- tonic seizures
- tremors
- in some animals, tremors diminish at 3 months (MGI Ref ID J:13141)
- physical contact with the mouse reduces or stops tremors (MGI Ref ID J:13141)
- tremors are first observed at 10-12 days of age and reach full expression by 3 weeks (MGI Ref ID J:13141)
- tremors are most evident in the caudal part of the trunk and proximal portions of hind extremities (MGI Ref ID J:13141)
- visually, the rate of tremors are 2 to 3 per second (MGI Ref ID J:13141)
reproductive system phenotype
- reduced male fertility
- male homozygotes rarely sire offspring (MGI Ref ID J:13141)
References
- SIDMAN RL; DICKIE MM; APPEL SH. 1964. MUTANT MICE (QUAKING AND JIMPY) WITH DEFICIENT MYELINATION IN THE CENTRAL NERVOUS SYSTEM. Science 144:309-11. PubMed: 14169723MGI: J:13141
Additional References
- Mitrovic N; Caboche J; Carre JB; Besson MJ; Maurin Y. 1991. The quaking mouse: an epileptic mutant with alterations affecting the modulatory mechanisms of the NMDA receptor complex. Brain Res 566(1-2):248-54. PubMed: 1839963MGI: J:1930
- Yanagimachi R; Wakayama T; Kishikawa H; Fimia GM; Monaco L; Sassone-Corsi P. 2004. Production of fertile offspring from genetically infertile male mice. Proc Natl Acad Sci U S A 101(6):1691-5. PubMed: 14757819MGI: J:88151
Additional - a related
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