RESUMEN
Only two hydromedusan species, Turritopsis dohrnii and T. sp., have exhibited experimental multiple-repeat life cycle reversion in the laboratory, which can be artificially induced by various means such as incubation with CsCl, heat shock, and mechanical damage with needles. In the present study, we constructed a genome assembly of T. dohrnii using Pacific Biosciences long-reads and Illumina short-reads, for which the genome DNA was extracted from 1,500 young medusae originated from a single clone. The total length of the draft genome sequence of T. dohrnii was 435.9 Mb (N50 length 747.2 kb). We identified 23,314 high-confidence genes and found the characteristics of RNA expression amongst developmental stages. Our genome assembly and transcriptome data provide a key model system resource that will be useful for understanding cyclical rejuvenation.
Asunto(s)
Genoma , Transcriptoma , Perfilación de la Expresión Génica , Análisis de Secuencia de ADN , ADN , Anotación de Secuencia MolecularRESUMEN
Mammalian hibernators endure severe and prolonged hypothermia that is lethal to non-hibernators, including humans and mice. The mechanisms responsible for the cold resistance remain poorly understood. Here, we found that hepatocytes from a mammalian hibernator, the Syrian hamster, exhibited remarkable resistance to prolonged cold culture, whereas murine hepatocytes underwent cold-induced cell death that fulfills the hallmarks of ferroptosis such as necrotic morphology, lipid peroxidation and prevention by an iron chelator. Unexpectedly, hepatocytes from Syrian hamsters exerted resistance to cold- and drug-induced ferroptosis in a diet-dependent manner, with the aid of their superior ability to retain dietary α-tocopherol (αT), a vitamin E analog, in the liver and blood compared with those of mice. The liver phospholipid composition is less susceptible to peroxidation in Syrian hamsters than in mice. Altogether, the cold resistance of the hibernator's liver is established by the ability to utilize αT effectively to prevent lipid peroxidation and ferroptosis.