A tiny aquatic animal is offering scientists a new explanation for one of biology’s most persistent mysteries: how a mother’s age can influence the characteristics of her descendants. Research on the rotifer Brachionus manjavacas suggests that maternal age effects may be transmitted not through the gradual accumulation of DNA mutations or cellular damage, but through reversible epigenetic changes that regulate gene activity. The findings, from a research team at the Marine Biological Laboratory, indicate that the biological consequences of being born to an older mother can change rapidly between generations and may depend strongly on an organism’s genetic background. The work could help explain why maternal age effects appear throughout the animal kingdom, from microscopic invertebrates to humans, while remaining difficult to trace to a single underlying mechanism.
Maternal age effects describe changes in an offspring’s physical traits, behavior, survival, reproduction or health that are associated with the age of its mother. These effects are widespread and are often harmful when mothers reproduce late in life. Offspring of older mothers may have shorter lifespans, lower reproductive success or reduced developmental performance. In humans and other mammals, maternal age is associated with several developmental and health outcomes, although the biological pathways are complex and influenced by many environmental and genetic factors. In rotifers, which are only a fraction of a millimeter long and reproduce rapidly, researchers can observe multiple generations in a relatively short time. Their simple body plan, short lifespan and controlled laboratory reproduction make them useful for investigating how information about a mother’s age reaches her offspring.
Kristin Gribble, an associate scientist in the Marine Biological Laboratory’s Bay Paul Center, and colleagues are using rotifers to examine whether maternal age effects are caused by permanent changes to DNA or by molecular mechanisms that alter the way existing genes function. DNA mutations change the genetic sequence itself and are generally stable once they occur. Epigenetic mechanisms work differently. They can influence whether genes are active or silent without changing the underlying DNA code. These regulatory systems include chemical modifications to DNA and changes to histone proteins, the molecular structures around which DNA is wrapped. By adjusting how tightly DNA is packaged, histone modifications can make particular genes more or less accessible to the cellular machinery that transcribes them into RNA.
The team’s experiments produced a result that challenges a common assumption about aging and inheritance. If maternal age effects were driven primarily by the gradual accumulation of damage inside aging mothers, their impact might be expected to become stronger across successive generations. Instead, research by postdoctoral scientist Alyssa Liguori found that the pattern did not consistently intensify in two different genotypes of the same rotifer species. In some cases, the effects could be reversed within a single generation. That rapid change is difficult to reconcile with a model based only on accumulated cellular damage or new DNA mutations, because such alterations would not normally disappear so quickly. The observations instead point toward a flexible regulatory process capable of being reset, modified or transmitted differently depending on genetic context.
The findings do not yet prove that histone modifications are the mechanism responsible, but they provide a strong direction for further investigation. Histones act as molecular spools that organize the long DNA molecules inside cells. Chemical groups added to or removed from histones can alter the structure of chromatin, the combined complex of DNA and proteins. When chromatin becomes more open, genes may be easier to transcribe; when it becomes more condensed, gene activity may be reduced. If maternal aging changes histone marks in eggs or in reproductive tissues, those changes could influence the development and physiology of offspring without altering their DNA sequences. The researchers are now examining whether particular histone modifications correlate with the lifespan, reproduction and other traits associated with maternal age.
Another possible route involves mitochondria, the energy-producing structures found inside cells. Mitochondria contain their own small genomes, known as mitochondrial DNA, and in many animals these genomes are inherited primarily from the mother. Because mitochondria regulate energy production, metabolism and several processes linked to aging, changes in mitochondrial DNA or mitochondrial condition could provide a way for maternal age information to affect offspring. Older mothers may pass on mitochondria with altered performance, or they may transmit molecular signals that influence how mitochondria function in the next generation. Gribble’s laboratory is considering this possibility alongside histone regulation, although the relative contribution of mitochondrial DNA remains unresolved.
Genetic variation also appears to shape whether maternal age effects are harmful, neutral or even beneficial. The researchers found that different rotifer genotypes did not respond identically to maternal age. In one strain, offspring produced by older mothers lived longer, a result that contrasts with the more common pattern of reduced longevity. This observation suggests that some genetic variants may protect offspring from the negative consequences of advanced maternal age or may convert an age-related signal into a physiological advantage. The result also emphasizes why maternal age cannot be understood as a universal biological switch. The same maternal condition may produce different outcomes depending on the inherited genome and the interaction between genes, epigenetic regulation and the environment.
The persistence of maternal age effects presents an evolutionary puzzle. If offspring of older mothers are often less likely to survive and reproduce, natural selection might be expected to remove the genetic or physiological processes that generate these outcomes. Yet maternal age effects have been documented across a remarkable range of species. One explanation is that natural selection becomes weaker late in life. In rotifers, most reproduction takes place early, and females may have already produced the majority of their offspring by the time they reach advanced age. Variants that harm late-born offspring may therefore experience limited evolutionary pressure if they have little effect on the number of descendants produced earlier. The same principle, in different forms, could help explain why age-related reproductive effects remain common across animal populations.
The most far-reaching implication of the work is that biological information may travel across more than one generation through mechanisms that do not fit a simple DNA-centered model of inheritance. If a grandmother’s environment or age alters molecular states in her offspring’s reproductive cells, those changes could potentially influence grandchildren or even later descendants. Such transgenerational effects are difficult to distinguish from direct maternal effects, because researchers must determine whether the observed trait is caused by the mother’s condition, by exposure during development, or by a change that persists through the germ line. Rotifers offer a practical system for separating these possibilities because their generations are short and their ancestry can be monitored under controlled conditions.
The researchers stress that results from rotifers cannot be transferred directly to humans, whose development, reproduction and aging are far more complex. Nevertheless, the basic biological principles under investigation—chromatin regulation, mitochondrial inheritance, genetic variation and the weakening of selection at later ages—are shared across many forms of life. Understanding how maternal age information is encoded and transmitted could eventually improve scientific models of health risk and disease susceptibility. It may also clarify why an individual’s biology is influenced not only by their own genome, but by the reproductive history and environments of previous generations. For now, the rotifer experiments are revealing that maternal age effects are neither necessarily permanent nor genetically uniform, and that their hidden mechanism may lie in the cell’s control systems rather than in the DNA sequence itself.
Subject of Research: Maternal age effects, epigenetic inheritance, histone modifications, mitochondrial inheritance and genotype-specific transgenerational effects in rotifers.
Article Title: Transgenerational and Intergenerational Maternal Age Effects Exhibit Complex, Genotype-Specific Patterns of Inheritance
News Publication Date: 13-Aug-2026
Web References: https://doi.org/10.1086/742104
References: Liguori et al., “Transgenerational and Intergenerational Maternal Age Effects Exhibit Complex, Genotype-Specific Patterns of Inheritance,” DOI: 10.1086/742104.
Image Credits: Michael Shribak; female Brachionus manjavacas rotifer and offspring.
Keywords: Maternal age effects, rotifers, Brachionus manjavacas, epigenetics, histone modifications, transgenerational inheritance, intergenerational effects, mitochondrial DNA, genetics, aging, longevity, natural selection.
