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Aging (Albany NY). 2014 Jun;6(6):468-80.

The age related markers lipofuscin and apoptosis show different genetic architecture by QTL mapping in short-lived Nothobranchius fish.

Author information

1
Biology of Ageing, Leibniz Institute for Age Research - Fritz Lipmann Institute, 07745 Jena, Germany.
2
Genome Analysis, Leibniz Institute for Age Research - Fritz Lipmann Institute, 07745 Jena, Germany.
3
Institute of Clinical Molecular Biology, Christian-Albrechts-University, 24105 Kiel, Germany.
4
Hufeland Klinikum Mühlhausen, Institut für Infektiologie und Pathobiologie, 99974 Mühlhausen, Germany.
5
Biology of Ageing, Leibniz Institute for Age Research - Fritz Lipmann Institute, 07745 Jena, Germany. Neurobiology Laboratory, Scuola Normale Superiore, 56124 Pisa, Italy.

Abstract

Annual fish of the genus Nothobranchius show large variations in lifespan and expression of age-related phenotypes between closely related populations. We studied N. kadleci and its sister species N. furzeri GRZ strain, and found that N.kadleci is longer-lived than the N. furzeri. Lipofuscin and apoptosis measured in the liver increased with age in N. kadleci with different profiles: lipofuscin increased linearly, while apoptosis declined in the oldest animals. More lipofuscin (P<0.001) and apoptosis (P<0.001) was observed in N. furzeri than in N. kadleci at 16w age. Lipofuscin and apoptotic cells were then quantified in hybrids from the mating of N. furzeri to N. kadleci. F₁individuals showed heterosis for lipofuscin but additive effects for apoptosis. These two age-related phenotypes were not correlated in F₂ hybrids. Quantitative trait loci analysis of 287 F₂ fish using 237 markers identified two QTL accounting for 10% of lipofuscin variance (P<0.001) with overdominance effect. Apoptotic cells revealed three significant- and two suggestive QTL explaining 19% of variance (P<0.001), showing additive and dominance effects, and two interacting loci. Our results show that lipofuscin and apoptosis are markers of different age-dependent biological processes controlled by different genetic mechanisms.

PMID:
25093339
PMCID:
PMC4100809
DOI:
10.18632/aging.100660
[Indexed for MEDLINE]
Free PMC Article

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