scholarly journals The biology of developmental plasticity and the Predictive Adaptive Response hypothesis

2014 ◽  
Vol 592 (11) ◽  
pp. 2357-2368 ◽  
Author(s):  
Patrick Bateson ◽  
Peter Gluckman ◽  
Mark Hanson
2017 ◽  
Author(s):  
Amy J. Osborne ◽  
Peter K. Dearden

AbstractThe Developmental Origins of Health and Disease (DOHaD) hypothesis predicts that early-life environmental exposures can be detrimental to later-life health, and that mismatch between the pre- and postnatal environment may contribute to the growing non-communicable disease (NCD) epidemic. Within this is an increasingly recognised role for epigenetic mechanisms; epigenetic modifications can be influenced by, e.g., nutrition, and can alter gene expression in mothers and offspring. Currently, there are no whole-genome transcriptional studies of response to nutritional alteration. Thus, we sought to explore how nutrition affects the expression of genes involved in epigenetic processes in Drosophila melanogaster. We manipulated Drosophila food macronutrient composition at the F0 generation, mismatched F1 offspring back to a standard diet, and analysed the transcriptome of the F0 – F3 generations by RNA-sequencing. At F0, the altered (high protein, low carbohydrate, HPLC) diet increased expression of genes involved in epigenetic processes, with coordinated downregulation of genes involved in immunity, neurotransmission and neurodevelopment, oxidative stress and metabolism. Upon reversion to standard nutrition, mismatched F1 and F2 generations displayed multigenerational inheritance of altered gene expression. By the F3 generation, gene expression had reverted to F0 (matched) levels. These nutritionally-induced gene expression changes demonstrate that dietary alteration can upregulate epigenetic genes, which may influence the expression of genes with broad biological functions. Further, the multigenerational inheritance of the gene expression changes in F1 and F2 mismatched generations suggests a predictive adaptive response (PAR) to maternal nutrition. Our findings may help to understand the interaction between maternal diet and future offspring health, and have direct implications for the current NCD epidemic.


2010 ◽  
Vol 24 (1) ◽  
pp. 178-185 ◽  
Author(s):  
Godefroy Devevey ◽  
Pierre Bize ◽  
Sara Fournier ◽  
Emilie Person ◽  
Philippe Christe

Author(s):  
Hamish G. Spencer ◽  
Anthony B. Pleasants ◽  
Peter D. Gluckman ◽  
Graeme C. Wake

Abstract Predictive adaptive responses (PARs) are a form of developmental plasticity in which the developmental response to an environmental cue experienced early in life is delayed and yet, at the same time, the induced phenotype anticipates (i.e., is completely developed before) exposure to the eventual environmental state predicted by the cue, in which the phenotype is adaptive. We model this sequence of events to discover, under various assumptions concerning the cost of development, what lengths of delay, developmental time, and anticipation are optimal. We find that in many scenarios modeled, development of the induced phenotype should be completed at the exact same time that the environmental exposure relevant to the induced phenotype begins: that is, in contrast to our observed cases of PARs, there should be no anticipation. Moreover, unless slow development is costly, development should commence immediately after the cue: there should be no delay. Thus, PARs, which normally have non-zero delays and/or anticipation, are highly unusual. Importantly, the exceptions to these predictions of zero delays and anticipation occurred when developmental time was fixed and delaying development was increasingly costly. We suggest, therefore, that PARs will only evolve under three kinds of circumstances: (i) there are strong timing constraints on the cue and the environmental status, (ii) delaying development is costly, and development time is either fixed or slow development is costly, or (iii) when the period between the cue and the eventual environmental change is variable and the cost of not completing development before the change is high. These predictions are empirically testable.


2019 ◽  
Vol 10 (5) ◽  
pp. 587-594
Author(s):  
Abdel Halim Harrath ◽  
Abdulkarem Alrezaki ◽  
Saleh H. Alwasel ◽  
Abdelhabib Semlali

AbstractWe sought to examine whether rat maternal food restriction (MFR) affects the expression of steroidogenesis-related genes Cyp19, Cyp17a1, Insl3 and Gdf-9 in the ovaries of offspring from the first (FRG1) and second (FRG2) generations at pre-pubertal age (week 4) and during adulthood (week 8). At week 4, MFR significantly increased the expression of RNAs for all analyzed genes in both FRG1 and FRG2 females, which may indicate that MFR affects the onset of the reproductive lifespan, by inducing early pubertal onset. At week 8, the Cyp19 gene was still upregulated in MRF-subjected animals (Cyp19: P=0.0049 and P=0.0508 in FRG1 and FRG2, respectively), but MFR induced a significant decrease in Cyp17 and Gdf-9 gene expression in the offspring of both FRG1 and FRG2 females when compared with the controls (Cyp17: P=0.0018 and P=0.0016, respectively; Gdf-9: P=0.0047 and P=0.0023, respectively). This suggests that females at week 8, which should normally be in their optimal reproductive capacity, experience premature ovarian aging. At week 4, the activation of Cyp19 and Cyp17 was higher in the FRG1 ovaries than in the FRG2 ovaries, whereas the extent of Insl3 and Gdf-9 activation was lower in the FRG1 ovaries. This may indicate that FRG2 females were more vulnerable to MFR than their mothers (FRG1) and grandmothers, which is consistent with the ‘predictive adaptive response’ hypothesis. Our findings reveal that MFR may induce intergenerational ovarian changes as an adaptive response to ensure reproductive success before death.


2021 ◽  
Author(s):  
Severi Luoto ◽  
Peter K. Jonason

We thank Sharpe and colleagues for the opportunity to discuss our article titled “The dark side of the rainbow: Homosexuals and bisexuals have higher Dark Triad traits than heterosexuals” in more detail. Here, we address the methodological concerns raised by Sharpe et al. and conclude by discussing our critics’ problematic suggestion that there is something pathologically “wrong” with homosexual and bisexual people. As scientists, we avoid moralizing on such topics, instead openly reporting the results of our research, even hypothesizing that elevated Dark Triad traits in nonheterosexual individuals might constitute an adaptive response or a predictive adaptive response to environmental harshness, whether such harshness may be experienced prenatally, in adolescence, or in adulthood. We further wish to reject and distance ourselves from the prejudiced view of homosexuality voiced by Sharpe et al. Their suggestion to avoid the term “homosexuality” is in itself prejudiced and in stark opposition to the liberation and empowerment of people with same-sex sexual attractions. We encourage other sex researchers to continue using the term “homosexual” as a purely descriptive scientific term which carries no moral implications, and the relevant communities and organizations to accept its continued use in science alongside other sexual orientation categories.


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