scholarly journals Irreversibility of a bad start: early exposure to osmotic stress limits growth and adaptive developmental plasticity

Oecologia ◽  
2011 ◽  
Vol 169 (1) ◽  
pp. 15-22 ◽  
Author(s):  
Chi-Shiun Wu ◽  
Ivan Gomez-Mestre ◽  
Yeong-Choy Kam
Author(s):  
Mary Jane West-Eberhard

A book on developmental plasticity needs a chapter on assessment, if only to show that adaptive environmental assessment occurs. Skepticism regarding the ability of nonhuman organisms to assess conditions well enough to make adaptive decisions has a long history in evolutionary biology, and it has been an important barrier to understanding the evolution of adaptive developmental plasticity. It is worth briefly reviewing this history in order to understand certain preconceptions about assessment that still persist. In the nineteenth century, critics of Darwin’s theory of sexual selection (Darwin, 1871) balked at the idea of an “aesthetic sense” in lowly creatures that would enable female choice of mates (representative papers are reprinted and discussed in Bajema, 1984). Later, the barrier persisted for other reasons. Even though naturalists routinely used the condition-appropriate expression of phenotypic traits to support adaptation hypotheses—a practice that assumes adaptive assessment of conditions as it is defined here—theoretically inclined biologists paid little attention to the question of facultatively expressed traits. Part of the difficulty lay in the problem of explaining how adaptive assessment could evolve within the framework of conventional genetics. Theodosius Dobzhansky, one of the twentieth century’s leading evolutionary biologists, acknowledged this unresolved problem in remarks following a lecture by J. S. Kennedy on the phase polyphenisms of migratory locusts (Kennedy, 1961). Dobzhansky referred to the “challenge to a geneticist” of explaining the adaptive switch between the sedentary and the migratory phenotypes of the locusts, which had been shown to be largely independent of genotype. He suggested that an extrachromosomal factor may be involved, a symbiotic microorganism that acts as a “plasmagene” whose multiplication would eventually stimulate phase change. Although Dobzhansky’s proposal was no more preposterous than some of the regulatory devices that have actually been discovered, Kennedy (1961) minced no words in his reply to this suggestion: . . . [W]e need not feel obliged to invoke a second organism to explain [phase polymorphism] unless we are reluctant to concede an important part to the environment as well as to heredity in moulding development. . . .


2019 ◽  
Vol 286 (1905) ◽  
pp. 20191072 ◽  
Author(s):  
Ilan M. Ruhr ◽  
Heather McCourty ◽  
Afaf Bajjig ◽  
Dane A. Crossley ◽  
Holly A. Shiels ◽  
...  

For some species of ectothermic vertebrates, early exposure to hypoxia during embryonic development improves hypoxia-tolerance later in life. However, the cellular mechanisms underlying this phenomenon are largely unknown. Given that hypoxic survival is critically dependent on the maintenance of cardiac function, we tested the hypothesis that developmental hypoxia alters cardiomyocyte physiology in a manner that protects the heart from hypoxic stress. To test this hypothesis, we studied the common snapping turtle, which routinely experiences chronic developmental hypoxia and exploits hypoxic environments in adulthood. We isolated cardiomyocytes from juvenile turtles that embryonically developed in either normoxia (21% O 2 ) or hypoxia (10% O 2 ), and subjected them to simulated anoxia and reoxygenation, while simultaneously measuring intracellular Ca 2+ , pH and reactive oxygen species (ROS) production. Our results suggest developmental hypoxia improves cardiomyocyte anoxia-tolerance of juvenile turtles, which is supported by enhanced myofilament Ca 2+ -sensitivity and a superior ability to suppress ROS production. Maintenance of low ROS levels during anoxia might limit oxidative damage and a greater sensitivity to Ca 2+ could provide a mechanism to maintain contractile force. Our study suggests developmental hypoxia has long-lasting effects on turtle cardiomyocyte function, which might prime their physiology for exploiting hypoxic environments.


Author(s):  
Ainash Childebayeva ◽  
Jaclyn M Goodrich ◽  
Fabiola Leon-Velarde ◽  
Maria Rivera-Chira ◽  
Melisa Kiyamu ◽  
...  

Abstract High-altitude adaptation is a classic example of natural selection operating on the human genome. Physiological and genetic adaptations have been documented in populations with a history of living at high altitude. However, the role of epigenetic gene regulation, including DNA methylation, in high-altitude adaptation is not well understood. We performed an epigenome-wide DNA methylation association study based on whole blood from 113 Peruvian Quechua with differential lifetime exposures to high altitude (>2,500) and recruited based on a migrant study design. We identified two significant differentially methylated positions (DMPs) and 62 differentially methylated regions (DMRs) associated with high-altitude developmental and lifelong exposure statuses. DMPs and DMRs were found in genes associated with hypoxia-inducible factor pathway, red blood cell production, blood pressure, and others. DMPs and DMRs associated with fractional exhaled Nitric Oxide (FeNO) also were identified. We found a significant association between EPAS1 methylation and EPAS1 SNP genotypes, suggesting that local genetic variation influences patterns of methylation. Our findings demonstrate that DNA methylation is associated with early developmental and lifelong high-altitude exposures among Peruvian Quechua as well as altitude-adaptive phenotypes. Together these findings suggest that epigenetic mechanisms might be involved in adaptive developmental plasticity to high altitude. Moreover, we show that local genetic variation is associated with DNA methylation levels, suggesting that methylation associated SNPs could be a potential avenue for research on genetic adaptation to hypoxia in Andeans.


Nature ◽  
2004 ◽  
Vol 431 (7006) ◽  
pp. 261-262 ◽  
Author(s):  
Fabien Aubret ◽  
Richard Shine ◽  
Xavier Bonnet

2017 ◽  
Vol 284 (1849) ◽  
pp. 20162784 ◽  
Author(s):  
Tobias D. Zimmermann ◽  
Sylvia Kaiser ◽  
Michael B. Hennessy ◽  
Norbert Sachser

Environmental conditions during early life can adaptively shape the phenotype for the prevailing environment. Recently, it has been suggested that adolescence represents an additional temporal window for adaptive developmental plasticity, though supporting evidence is scarce. Previous work has shown that male guinea pigs living in large mixed-sex colonies develop a low-aggressive phenotype as part of a queuing strategy that is adaptive for integrating into large unfamiliar colonies. By contrast, males living in pairs during adolescence become highly aggressive towards strangers. Here, we tested whether the high-aggressive phenotype is adaptive under conditions of low population density, namely when directly competing with a single opponent for access to females. For that purpose, we established groups of one pair-housed male (PM), one colony-housed male (CM) and two females. PMs directed more aggression towards the male competitor and more courtship and mating towards females than did CMs. In consequence, PMs attained the dominant position in most cases and sired significantly more offspring. Moreover, they showed distinctly higher testosterone concentrations and elevated cortisol levels, which probably promoted enhanced aggressiveness while mobilizing necessary energy. Taken together, our results provide the clearest evidence to date for adaptive shaping of the phenotype by environmental influences during adolescence.


The Lancet ◽  
2009 ◽  
Vol 373 (9675) ◽  
pp. 1654-1657 ◽  
Author(s):  
Peter D Gluckman ◽  
Mark A Hanson ◽  
Patrick Bateson ◽  
Alan S Beedle ◽  
Catherine M Law ◽  
...  

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