It is well understood that an older maternal age at birth results in offspring that are less robust, meaning a shorter life expectancy, lesser degrees of reproductive success, and so forth. The question asked here is how this effect can have persisted in the face of evolutionary competition: why do we not see organisms that can produce equally viable offspring at later ages? This is one slice of the broader evolutionary question of why aging happens at all, and why it is near universal in the animal kingdom. The present consensus on the evolution of aging, insofar as there is a consensus, is the antagonistic pleiotropy hypothesis. Selection pressure is stronger in younger individuals, leading to mechanisms and biological systems that are beneficial in youth but harmful in later life. This, of course, is entirely adequate to explain the observation that older mothers have less robust offspring; it is one narrow manifestation of aging.
In many species, survival and reproduction decrease with advancing age, a process known as "senescence." The evolution of senescence is a long-standing problem in life history theory and has been studied extensively in the laboratory, with mathematical models, and in the field. The evolution of senescence is explained by the age-specific patterns of the strength of selection, measured as selection gradients. Age-specific selection gradients on mortality and fertility decrease with age. Thus, traits expressed early in life have a larger impact on fitness than those expressed later. As a result, selection will favor traits that lead to negative effects on survival and fertility at older ages if there are even small beneficial effects in youth.
"Maternal effect senescence" is defined as the reduced success or quality of offspring with advancing age of the mother. Advanced maternal age has known negative effects on offspring health, lifespan, and fertility in humans and other species. In many taxa, including rotifers, Daphnia, Drosophila, and soil mites, offspring from older mothers have shorter lives, lower reproductive success, or both. Field studies of several species of mammals and birds have shown that offspring with older parents exhibit lower survival and recruitment and increased rates of senescence. In humans, advanced maternal age is associated with reduced lifespan and health. In Caenorhabditis elegans, Daphnia, and rotifers, advanced maternal age also increases offspring size, alters development time, and increases variability in gene expression.
Maternal effect senescence remains an interesting problem in life history evolution. Producing high-quality offspring that live long and prosper should, all else being equal, provide a selective advantage. Thus, the reduced quality of the offspring of old mothers demands an evolutionary explanation. We developed a more general multistate model that can incorporate maternal age effects on age-specific survival and fertility throughout the life cycle and with which we can easily calculate selection gradients on any of those rates as joint functions of age and maternal age.
We fit these models to data from individual-based culture experiments on the aquatic invertebrate, Brachionus manjavacas (Rotifera). By comparing models with and without maternal effects, we found that maternal effect senescence significantly reduces fitness for B. manjavacas and that this decrease arises primarily through reduced fertility, particularly at maternal ages corresponding to peak reproductive output. We also used the models to estimate selection gradients, which measure the strength of selection, in both high growth rate (laboratory) and two simulated low growth rate environments. In all environments, selection gradients on survival and fertility decrease with increasing age. They also decrease with increasing maternal age for late maternal ages, implying that maternal effect senescence can evolve through the same process as in the theory of the evolution of age-related senescence.
Link: https://doi.org/10.1...pnas.1919988117
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