|Characteristics||This mutant is a leptin receptor-defficient medaka. This knockout mutant had a point mutation of cysteine for stop codon at the 357th amino acid just before the leptin-binding domain. The evidence for loss of function of leptin-mediated signaling in the mutant is based on a lack of response to feeding in the expression of key appetite-related neuropeptides in the diencephalon.|
|Special affairs [Address]||
■ The RECIPIENT shall refer the following publication in any PUBLICATIONS.
(Name of the Publication: Chisada S et al. Leptin receptor-deficient (knockout) medaka, Oryzias latipes, show chronical up-regulated levels of orexigenic neuropeptides, elevated food intake and stage specific effects on growth and fat allocation. Gen Comp Endocrinol. 195: 9-20, 2014)
■ The RECIPIENT shall give proper credit to the DEVELOPER in any publications reporting results of research using any derivatives developed from the BIOLOGICAL MATERIALS (hereinafter referred to as “the DERIVATIVES”), and shall procure other institutionsto which the DERIVATIVES are provided (including when provided through the NBRP) to do the same.
|Category||Mutants created by TILLING|
|Organization||National Institute for Basic Biology|
|Live in NIBB||○|
|Frozen sperm in NIBB||○|
|Deposited by||Fisheries Research Agency|
MT996_figure_LepRKOmedaka Food intake
Quantitative analysis of food intake using Artemia nauplii as prey.
A, post-juvenile fish (BWWT = 37.5±4.4 mg, BWLepRKO = 38.9±8.6 mg). B, adult fish (BWWT = 421.3±59.1 mg, BWLepRKO = 449.4±77.5 mg). *p <0.05 compared with WT medaka. Chisada et al. (2014) gives detail information on the quantitative method and post-hatched growth curves of WT and mutant medaka.