title: Moderately lower temperatures greatly extend the lifespan of Brachionus manjavacas (Rotifera): Thermodynamics or gene regulation?
abstract: Environmental temperature greatly affects lifespan in a wide variety of animals, but the exact mechanisms underlying this effect are still largely unknown. A moderate temperature decrease from 22°C to 16°C extends the lifespan of the monogonont rotifer Brachionus manjavacas by up to 163%. Thermodynamic effects on metabolism contribute to this increase in longevity, but are not the only cause. When rotifers are exposed to 16°C for four days and then transfered to 22°C, they survive until day 13 at nearly identical rates as rotifers maintained at 16°C continuously. This persistence of the higher survival for nine days after transfer to 22°C suggests that low temperature exposure alters the expression of genes that affect the rate of aging. The relative persistence of the gene regulation effect suggests that it may play an even larger role in slowing aging than the thermodynamic effects. The life extending effects of these short-term low temperature treatments are largest when the exposure happens early in the life cycle, demonstrating the importance of early development. There is no advantage to lowering the temperature below 16°C to 11° or 5°C. Rotifers exposed to 16°C also displayed increased resistance to heat, starvation, oxidative and osmotic stress. Reproductive rates at 16°C were lower than those at 22°C, but because they reproduce longer, there is no significant change in the lifetime fecundity of females. To investigate which genes contribute to these effects, the expression of specific temperature sensing genes was knocked down using RNAi. Of 12 genes tested, RNAi knockdown of four eliminated the survival enhancing effects of the four-day cold treatment: TRP7, forkhead box C, Y-box factor, and ribosomal protein S6. This demonstrates that active gene regulation is an important factor in temperature mediated life extension, and that these particular genes play an integral role in these pathways. As a thermoresponsive sensor, TRP7 may be responsible for triggering the signaling cascade contributing to temperature mediated life extension. The TRP genes may also provide especially promising candidates for targeted gene manipulations or pharmacological interventions capable of mimicking the effects of low temperature exposure. These results support recent theories of aging that claim rate of aging is determined by an actively regulated genetic mechanism rather than an accumulation of molecular damage.
authors.affiliation: School of Biology, Georgia Institute of Technology, Atlanta, GA 30332-0230, USA. Electronic address: rachel.johnston@biology.gatech.edu.
authors.forename: Rachel K
authors.initials: RK
authors.lastname: Johnston
authors.affiliation: School of Biology, Georgia Institute of Technology, Atlanta, GA 30332-0230, USA.
authors.forename: Terry W
authors.initials: TW
authors.lastname: Snell
mesh_terms: D000818:Animals; D005260:Female; D005786:Gene Expression Regulation; D055785:Gene Knockdown Techniques; D008136:Longevity; D034622:RNA Interference; D012098:Reproduction; D012403:Rotifera / Q000235:genetics* / Q000502:physiology*; D050053:TRPM Cation Channels / Q000235:genetics; D013696:Temperature
chemical_list: D050053:TRPM Cation Channels
keywords: Aging; Lifespan; RNAi; Rotifera; TRP; Temperature