PUBLICATION

Loss of αklotho causes reduced motor ability and short lifespan in zebrafish

Authors
Ogura, Y., Kaneko, R., Ujibe, K., Wakamatsu, Y., Hirata, H.
ID
ZDB-PUB-210728-16
Date
2021
Source
Scientific Reports   11: 15090 (Journal)
Registered Authors
Hirata, Hiromi
Keywords
none
MeSH Terms
  • Aging/metabolism
  • Animals
  • Bone and Bones/metabolism
  • Caenorhabditis elegans/metabolism
  • Fibroblast Growth Factors/metabolism
  • Glucuronidase/metabolism*
  • Humans
  • Kidney/metabolism
  • Longevity/physiology*
  • Mice
  • Mice, Knockout
  • Zebrafish/metabolism*
PubMed
34301962 Full text @ Sci. Rep.
Abstract
The klotho gene encodes a transmembrane protein αKlotho that interacts with a fibroblast growth factor (FGF) receptor in renal tubular epithelial cells and functions as a co-receptor for FGF23, which is an osteocytes-derived hormone. This bone-to-kidney signal promotes urinary phosphate excretion. Interestingly, αKlotho knockout mice show an accelerated aging and a shortened life span. Similarly, C. elegans lacking the αklotho homologue showed a short life span. However, the physiological basis of aging-related function of αklotho remain unclear. The αklotho-deficient vertebrate animals other than mice have been awaited as an alternative model of premature aging. We here employed zebrafish in our study and revealed that αklotho mutant zebrafish appeared to be normal at 3 months postfertilization (mpf) but eventually underwent premature death by 9 mpf, while normal zebrafish is known to survive for 42 months. We also assessed the motor ability of zebrafish in a forced swimming assay and found that αklotho mutant zebrafish displayed reduced swimming performance before their survival declined. A recent study also reported a similar finding that αklotho-deficient zebrafish exhibited a short life span and reduced spontaneous movements. Taken together, these results suggest that αKlotho mutant zebrafish show premature aging and are useful to investigate aging in vertebrates.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping