Biology subjects

Sekajova, Z.

Publications and source records attributed to Sekajova, Z..

3 recordsLinked to original sources

bioRxiv2023

Evolution during uncorrelated environmental fluctuations: bet-hedging or phenotypic plasticity?

Evolution in fluctuating environments is predicted to disfavor specialization and instead select for alternative strategies, such as phenotypic plasticity or possibly bet-hedging, depending on the accuracy of environmental cues and type of fluctuations. While these two alternatives are often contrasted in theoretical studies, their evolution are seldom studied together in empirical work. We used experimental evolution in the nematode worm Caenorhabditis remanei to simultaneously study the evolution of plasticity and bet-hedging in environments differing only in their temperature variability. We exposed worms for 30 generations to either fluctuating or slowly increasing temperature, these two environments had the same average temperature over evolutionary time. After experimental evolution, we scored size at sexual maturity and fitness in full siblings reared in two different temperatures, optimal 20{degrees}C and mildly stressful 25{degrees}C. Experimental evolution in the fluctuating environment resulted in the evolution of increased body size plasticity but not increased bet-hedging, compared to evolution in the slowly changing environment. Plasticity followed the temperature size rule as size decreased with increasing temperature and this plastic response was adaptive. In addition, we documented substantial standing genetic variation in body size, which represents a potential for further evolutionary change.

evolutionary biology↗

bioRxiv2020

Compensatory growth in C. elegans is regulated by a thermosensitive TRP channel and increases reproductive fitness

O_LIAnimals are often not growing at the maximum rate, but can compensate for a bad start of life by subsequently increasing growth rate. While this compensatory growth is widespread, its direct fitness consequences are seldom investigated and its genetic basis is unknown. C_LIO_LIWe investigated the genetic regulation, as well as fitness and lifespan consequences of compensatory growth in response to temperature, using C. elegans knockout of the thermo-sensitive TRP ion channel TRPA-1, involved in temperature recognition. We exposed juvenile worms to cold, favourable (intermediate) or warm temperatures in order to delay or speed up development. C_LIO_LIWild-type worms initially exposed to cold temperature experienced slower growth but after being switched to a more favourable temperature, they expressed compensatory growth and caught up in size. Those initially reared at warmer temperatures than favourable experienced slower growth and attained smaller adult size after being switched to the most favourable temperature. C_LIO_LICompensatory growth also altered the reproductive schedule. While rate-sensitive individual fitness decreased by cold juvenile temperatures, as a direct effect of the substantial developmental delay, once worms returned to more favourable temperature, they shifted their reproductive schedule towards early reproduction. Therefore, when focusing on the post-treatment period, the reproductive rate increased even though lifetime reproductive success was unaffected. Surprisingly, compensatory growth did not reduce adult lifespan. In contrast to the findings for wild-type worms, juvenile temperature did not induce compensatory or slowed-down growth in the trpa-1 knockout mutants. C_LIO_LIWe thus show that the trpa-1 is involved in the network regulating temperature-induced compensatory growth in C. elegans and that this compensatory growth can influence the reproductive rate. C_LI

evolutionary biology↗

bioRxiv2018

Reduced insulin/IGF-1 signalling in adult parents increases offspring fitness

Classical theory maintains that ageing evolves via energy trade-offs between reproduction and survival leading to accumulation of unrepaired cellular damage with age. In contrast, the emerging new theory postulates that ageing evolves because of deleterious late-life hyper-function of reproduction-promoting genes leading to excessive biosynthesis in late-life. The hyper-function theory uniquely predicts that optimizing nutrient-sensing molecular signalling in adulthood can simultaneously postpone ageing and increase Darwinian fitness. Here we show that reducing evolutionarily conserved insulin/IGF-1 nutrient-sensing signalling via daf-2 RNA interference (RNAi) fulfils this prediction in Caenorhabditis elegans nematodes. Long-lived daf-2 RNAi parents showed normal fecundity as self-fertilizing hermaphrodites and improved late-life reproduction when mated to males. Remarkably, the offspring of daf-2 RNAi parents had higher Darwinian fitness across three different genotypes. Thus, reduced nutrient-sensing signalling in adulthood improves both parental longevity and offspring fitness supporting the emerging view that sub-optimal gene expression in late-life lies at the heart of ageing. Impact StatementUnderstanding mechanisms underpinning ageing is fundamental to improving quality of life in an increasingly long-lived society. Recent breakthroughs have challenged the long-standing paradigm that the energy trade-off between reproduction and somatic maintenance causes organismal senescence via slow accumulation of unrepaired cellular damage with age. The emerging new theory of ageing provides a conceptually novel framework by proposing that ageing is a direct consequence of physiological processes optimized for early-life function, such as growth and early-life reproduction, that are running too high (i.e. at hyperfunction) in late adulthood. Contrary to the classic view based on damage accumulation, the hyperfunction theory proposes that suboptimal gene expression in late-life causes ageing via excessive biosynthesis. Thus, the hyperfunction theory uniquely predicts that longevity and Darwinian fitness can be simultaneously increased by reducing unnecessarily high levels of nutrient-sensing signalling in adulthood. Here we show that reducing evolutionarily conserved nutrient-sensing signalling pathway fulfils this prediction in Caenorhabditis elegans nematodes. We found that downregulation of the insulin/IGF-1 signalling in adult C. elegans nematodes not only improves longevity but, most intriguingly, increases fitness of the resulting offspring in the next generation. We found support for increase in offspring fitness across different genetic backgrounds. Our findings contradict the theoretical conjecture that energy trade-offs between growth, reproduction and longevity is the universal cause of senescence and provide strong experimental support for the emerging hyperfunction theory of ageing.

genetics↗