Maternal and grandmaternal age influence offspring fitness in<i>Drosophila</i>

Hercus, Miriam J.; Hoffmann, Ary A.

doi:10.1098/rspb.2000.1256

Cited by 167 publications

(165 citation statements)

References 35 publications

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“…It is uncertain that the progress made in saving lives is due to improved health in advanced age and, hence, an important topic for research (Vaupel 2010). Furthermore, there is a need to address not only the problems associated with reproduction at later ages and suggest potential remedies but also suggest possible ways of producing viable, healthy, and fertile progeny at older ages as offspring viability is shown to decline with increasing parental age in Drosophila (Hercus and Hoffmann 2000;Kern et al 2001). Fortunately, a sizable fraction of many signaling pathways regulating aging in short-lived organisms is shown to extend lifespan in mammals as well (Kenyon 2010).…”

Section: Drmentioning

confidence: 99%

Curcumin enhances parental reproductive lifespan and progeny viability in Drosophila melanogaster

Chandrashekara

Popli

Shakarad

2014

AGE

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Organismal lifespan is a complex trait that is governed by both its genetic makeup as well as the environmental conditions. The improved socioeconomic condition of humans has led to many lifestyle changes that in turn have altered the demography that includes postponement of procreation. Late age progeny is shown to suffer from many congenital diseases. Hence, there is a need to identify and evaluate natural molecules that could enhance reproductive health span. We have used the well-established model organism, Drosophila melanogaster, and ascertained the consequence of diet supplementation with curcumin. Flies reared on curcumin-supplemented diet had significantly higher lifespan. The progeny of flies reared on curcumin had a higher viability. The activity of a key mitochondrial enzyme-aconitase was significantly higher in flies reared on curcumin-supplemented diet. The results suggest that curcumin can not only correct a key step in the citric acid cycle and help in the release of additional energy but also permanently correct developmental and morphogenetic processes.

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Section: Drmentioning

confidence: 99%

Curcumin enhances parental reproductive lifespan and progeny viability in Drosophila melanogaster

Chandrashekara

Popli

Shakarad

2014

AGE

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“…Age-related decreases in either maternal fertility or cumulative survival will cause linear increases in neonatal mortality. We can use [13] to determine whether the senescence that is predicted to evolve by the classical theory (1, 4, 44, 45) is necessary for maternal effect senescence to evolve. Let us assume for the moment that age-specific fertility and mortality are independent of age.…”

Section: Significancementioning

confidence: 99%

“…1 shows us short-term conditions in which selection can favor increases in maternal effect selection. Accordingly, [13] can be used to identify these. The derivative of neonatal log mortality with respect to maternal age and recognizing that dln½lðxÞ =dx = −μðxÞ identifies these in terms of the rate of change of fertility over time as dmðxÞ=dx = mðxÞðr + μðxÞÞ.…”

Section: Significancementioning

confidence: 99%

“…Amid the many studies of senescing traits, a clear pattern is emerging that relates maternal age to the health, fitness, and lifespan of their progeny across widely diverse taxa including humans (8), birds (9, 10), mammals (11,12), Drosophila species (13)(14)(15) and other arthropods (16)(17)(18), and plants (19). Although observations suggest that maternal effect senescence may not proceed at the same rate as fertility senescence (12,(20)(21)(22)(23)(24), there is no evolutionary theory yet capable of explaining maternal effect senescence or its distinction from fertility senescence.…”

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confidence: 99%

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Evolution of maternal effect senescence

Moorad

Nussey

2015

Proc. Natl. Acad. Sci. U.S.A.

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Increased maternal age at reproduction is often associated with decreased offspring performance in numerous species of plants and animals (including humans). Current evolutionary theory considers such maternal effect senescence as part of a unified process of reproductive senescence, which is under identical age-specific selective pressures to fertility. We offer a novel theoretical perspective by combining William Hamilton's evolutionary model for aging with a quantitative genetic model of indirect genetic effects. We demonstrate that fertility and maternal effect senescence are likely to experience different patterns of age-specific selection and thus can evolve to take divergent forms. Applied to neonatal survival, we find that selection for maternal effects is the product of age-specific fertility and Hamilton's age-specific force of selection for fertility. Population genetic models show that senescence for these maternal effects can evolve in the absence of reproductive or actuarial senescence; this implies that maternal effect aging is a fundamentally distinct demographic manifestation of the evolution of aging. However, brief periods of increasingly beneficial maternal effects can evolve when fertility increases with age faster than cumulative survival declines. This is most likely to occur early in life. Our integration of theory provides a general framework with which to model, measure, and compare the evolutionary determinants of the social manifestations of aging. Extension of our maternal effects model to other ecological and social contexts could provide important insights into the drivers of the astonishing diversity of lifespans and aging patterns observed among species.S enescence is the age-related deterioration of organismal function and fitness. Evolutionary theory explains its pervasiveness as the result of age-related declines in the strength of natural selection to preserve survival and reproduction (1). Genes deleterious to survival or fertility in late life can persist or even come to fixation as a result of this weakening of selection in old age (2-4). To date, most theoretical and empirical research into the evolution of senescence has focused on age-specific survival and fertility (vital rates), as these rates are most proximate to fitness. Both age-related declines in survival (actuarial senescence) and fertility (reproductive senescence) can evolve independently from initially nonsenescent life histories (1).These vital rates are a product of complex interactions among different physiological systems, phenotypic traits, and their environment. One important source of environmental contributions involves social interactions. The influence of other individuals in the environment on a particular phenotype can itself be heritable, and the importance of these so-called "indirect genetic effects" (IGEs) is now established within evolutionary biology (5-7). IGEs are known to readily alter the evolutionary predictions of standard quantitative genetic models incorporating only direct genetic ...

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“…Beckerman et al 2002Beckerman et al , 2006, they can last more than one generation (e.g. Fox & Savalli 1998;Hercus & Hoffmann 2000) and their expression can be contingent depending on specific environmental circumstances (e.g. Räsänen et al 2005;Beckerman et al 2006;Plaistow et al 2006).…”

Section: The Current Status Of the Maternal Effects Hypothesismentioning

confidence: 99%

Maternal effects mechanism of population cycling: a formidable competitor to the traditional predator–prey view

Inchausti

Ginzburg

2009

Phil. Trans. R. Soc. B

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In the language of mathematics, one needs minimally two interacting variables (two dimensions) to describe repeatable periodic behaviour, and in the language of density dependence, one needs delayed, not immediate, density dependence to produce cyclicity. Neither language specifies the causal mechanism. There are two major potential mechanisms: exogenous mechanisms involving species interactions as in predator-prey or host-parasite, and endogenous mechanisms such as maternal effects where population growth results from the cross-generational transmission of individual quality. The species interactions view stemming from a major observation of Elton and a simultaneous independent theory by Lotka and Volterra is currently dominant. Most ecologists, when faced with cyclic phenomena, automatically look for an interacting species one step below or above in a food chain in order to find an explanation. Maternal effects hypothesis, verbally suggested in the 1950s, had only found its theoretical implementation in the 1990s. In a relatively short time, the degree of acceptance of this view grew to the level of a 'minority opinion' as evidenced by the widely used textbook of Begon et al. This short review attempts to describe the arguments for and against this internal two-dimensional approach.

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Maternal and grandmaternal age influence offspring fitness inDrosophila

Cited by 167 publications

References 35 publications

Curcumin enhances parental reproductive lifespan and progeny viability in Drosophila melanogaster

Curcumin enhances parental reproductive lifespan and progeny viability in Drosophila melanogaster

Evolution of maternal effect senescence

Maternal effects mechanism of population cycling: a formidable competitor to the traditional predator–prey view

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