α-Klotho KO/Jcl

Animals/Genetically Modified Animals/

α-Klotho KO/Jcl

Ordering name: α-Klotho KO/Jcl
Nomenclature: B6.129-Kltm1Yin/Jcl
Availability: Cryopreserved

Origin

klotho/Jcl is a mutant mouse of alpha-klotho so it is not null mutation actually although the alpha-klotho gene expression chance is extremely low and can be ignored as the functional point of view. In addition, the mutate expression can be back because the alpha-klotho gene expression is recovered by low phosphorus food and etc. Due to the fact that alpha-klotho mouse was created by knocking out the alpha-klotho gene because it is necessary to make null mutation mouse. (Takeshita et al., 2004)
alpha-klotho KO mouse shows the gene mutation expression as the klotho/Jcl stably except slightly better sexual gland maturation because of the C57BL/6 back ground.

Characteristics

This strain grows as normal as its wild type until 3 weeks but stop growing after that.

Phenotype and growth disease

  • Early death (average life span: 60 days)
  • Artery medial calcification and medial thickening
  • Arteriosclerosis with age
  • Bone density suppressing
  • Amygdala purkinje cell exfoliation
  • Obvious obsolescence of ovary, uterus, spermary (There is no first meiosis)
  • Obvious obsolescence of thymus
  • Soft tissue calcification at gastric parietal, skin, trachea, cardiac valve, and etc.
  • Obsolescence of skin
  • Hair bulbs decreasing
  • Subcutaneous fat disappear
  • Hypanakinesia, gait abnormality
  • Growth hormone secretion granule decreasing


  • Alpha-klotho mouse shows up-regulation 1 alpha-hydroxylase, makes high serum 1,25(OH)2D,FGF23 and vitamin D precursor change to active form. These characteristics are disappeared by reducing vitamin D activation up-regulation by shading and supplying vitamin D deficiency diet or mating with 1 alpha-hydroxylase (Cyp27b1)gene knockout mouse. The strain can be kept long term by supplying vitamin D deficiency diet.

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