Bowdoin Science Journal

epigenetics

Invasive Species: Ecological Shapeshifters?

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Watershed reeds of midcoast Maine provide a deeper look into the field of epigenetics

Forests, grasslands, and marshes are ecological battlegrounds. In the fight to hold territory, maintain access to resources, and reproduce, many organisms compete directly to occupy the same niche– the role played by a specific organism in an ecosystem. An organism’s ability to carry out these roles is dictated by its “fitness” or capacity to survive and contribute its genes to the next generation. Naturally, relative reproductive success is incredibly environmentally dependent. Most organisms are tailor-made to thrive within their native habitats via natural selection. However, this biological narrative is challenged by the proliferation of invasive species in competition with their native counterparts. In their 2016 study, Spens and Douhovnikoff argue that epigenetics may be key to understanding ecological invasiveness and that the common reed (Phragmites australis) is “an ideal model species” (Spens & Douhovnikoff, 2016) for studying this rapidly expanding subfield of genetics.

Among other things, greater phenotypic plasticity, or “the ability of individual genotypes to produce different phenotypes when exposed to different environmental conditions” (Fusco & Minelli, 2010), increases an organism’s potential to adjust to its surroundings and occupy a vast variety of niches. This becomes possible through epigenetics.  Epigenetic modifications alter gene expression without changing the underlying DNA sequence (Weinhold, 2006). Methylation, the process by which methyl groups are added to DNA, is the key turning genes “on” and “off” (Menezo et al., 2020). The addition of methyl groups prevents DNA-transcribing proteins from accessing the DNA strand, stopping the gene’s expression as a protein. This has the potential to create significant differences in structural and even cellular function among individuals that are otherwise genetically identical.

Clonal plants provide a unique opportunity to study environmental pressures on epigenetics, as these individuals can act as their own genetic control. Reeds are an excellent example of this: as facultatively clonal plants, they can utilize both sexual and asexual reproduction. Exploiting this integral feature, and the existence of multiple subspecies of reed in midcoast Maine, researchers studied the genomes of both native and invasive reeds in two separate locations, Libby and Webhannet. They addressed two questions: Do introduced subspecies exhibit greater epigenetic variation (indicating that epigenetics plays a role in the success of an invasive species)? And will the variation between subspecies genotypes be lesser than the variation within a single genotype’s epigenetic markers (suggesting that epigenetic variation can be used to adapt to an incredibly variable environment)?

Researchers sought answers by studying clusters of reeds called ramets. Since all the reeds within a ramet were genetically identical, they could selectively measure epigenetic variation. These clones were grown within heterogeneous microhabitats that contain varying combinations of nutrients and conditions. Extracted DNA fragments were compared based on the level of methylation among subspecies, genotype, and ramet.

In both sites, the invasive reed demonstrated greater epigenetic diversity than the native reed (Figure 1). Up to 71% of epigenetic variation at the Webhannet site is attributed to differences among genotypes. These results suggest that clones adjust to the demands of their environments via epigenetics, rather than genotypic adaptation. Flexibility of this kind allows for rapid specialization in response to the hyper-individualized environmental conditions of each ramet. Additionally, each site developed an epigenetic “signature” with both subspecies exhibiting distinct, location specific, morphological characteristics. The significant differences in epigenetic markers between sites hint at the potential for large scale shifts due to epigenetics, should genotype not be a factor in these differences. The distinct characteristics displayed by each species demonstrate the vast alterations necessary to survive in an environment with subtle differences.

Figure 1. Epigenetic markers clustered by species (native, introduced) and location (Libby, Webhannet). Differences within a single genotype were greater than variation between genotypes, particularly for the introduced species. Figure adapted from Spens and Douhovnikoff

While this study was small scale, it supports the position that epigenotype variation provides a strong competitive advantage in the natural world. It also suggests that further study would provide more valuable information about the relevance of epigenetics in ecology. In our rapidly changing environment, due to climate change and other human influences, these native genotypes are in danger of being displaced from their niches. Despite a species’ history with its habitat, subtle alterations can have vast impact on individuals that demonstrate low plasticity or tolerance for change. Introduced organisms who demonstrate more flexible epigenotypes have the potential to outcompete their neighbors, eroding local ecosystems beyond repair. This reality drives ecological research in the direction of epigenetics, not only for the sake of discovery, but also in hopes of protecting species who cannot adapt as quickly as we disrupt.

 

Works Cited

Fusco, G., & Minelli, A. (2010). Phenotypic plasticity in development and evolution: Facts and concepts. Philosophical Transactions of the Royal Society B: Biological Sciences, 365(1540), 547–556. https://doi.org/10.1098/rstb.2009.0267

Menezo, Y., Clement, P., Clement, A., & Elder, K. (2020). Methylation: An Ineluctable Biochemical and Physiological Process Essential to the Transmission of Life. International Journal of Molecular Sciences, 21(23), 9311. https://doi.org/10.3390/ijms21239311

Spens, A., & Douhovnikoff, V. (2016). Epigenetic variation within Phragmites australis among lineages, genotypes, and ramets. Springer International Publishing. https://link.springer.com/article/10.1007/s10530-016-1223

Weinhold, B. (2006). Epigenetics: The Science of Change. Environmental Health Perspectives, 114(3), A160–A167.

Your DNA Remembers: Correlating Epigenetics and Early Childhood Trauma through DNA Methylation

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What’s your earliest memory? Can you remember everything that happened between the ages of three to five? No? Me neither. Despite the gaps in your memory, your body—specifically your DNA—knows what happened to you. It shouldn’t be surprising that DNA has such a good memory. After all, it stores genetic information tracing back thousands of years. This of course prompts several questions, namely the following; how does DNA store my memories and how does that affect me?

Let’s start from the beginning. Epigenetics encompasses all heritable changes in gene activity that do not stem from a change in DNA sequences (Moore et al, 2013). DNA methylation introduces a particularly salient new epigenetic mechanism for gene regulation and cell differentiation. The key to DNA methylation lies within the special enzymes that modify the cytosine DNA base by adding a methyl group (Moore et al, 2013; Suelves, 2016). Interestingly, cell differentiation is partly driven by differing levels of DNA methylation. An overall increase in DNA methylation occurs during the differentiation process, while a decrease in it at cell-specific loci helps define cellular identity (Suelves et al, 2016). Additionally, the progressive decrease in overall DNA methylation can contribute to physiological aging and the development of cancer (Suelves et al, 2016). Overall, these altered cytosines play key roles in human development and health issues (Moore et al, 2013).  

This brings us to the second question: how does my DNA’s photographic memory affect me? Well, it turns out that choices such as diet, drinking, exercise, illness, and environmental conditions can all have an impact on genomic stability and gene-specific DNA methylation (Lim et al, 2012). So while you might not remember what happened as a kid, your DNA may already be internalizing those experiences. The Avon Longitudinal Study of Parents and Children patiently waited for years so they could specifically study how childhood experiences affect epigenetic markers in adolescence. A cohort of 13,988 children with due dates between April 1991 and 1992 were monitored for exposure to childhood adversity from birth to the age of eleven. Using changes in DNA methylation at the age of fifteen, researchers investigated whether the timing of adversity has epigenetic consequences across childhood and adolescence (Lussier et al, 2023). 

Each mother reported whether their child faced any of the following seven types of childhood adversity; caregiver physical or emotional abuse, sexual or physical abuse, maternal psychopathology, one-adult households, family instability, and neighborhood disadvantage as well as the timing that the adversity was present. Out of the 13,988 children, 609-665 showed signs of both adversity and a decrease in DNA methylation at 15 years old (Lussier et al, 2023). 

Within this sample from the original cohort, further DNA analysis identified twenty-two loci that showed significant associations between exposure to adversity and altered DNA methylation at the age of 15 (Lussier et al, 2023). Of the loci identified to be associated with decreased DNA methylation, the highest percent of loci were correlated with growing up in one-adult households (Lussier et al, 2023). None of the identified loci indicated that adversity may alter DNA methylation at birth or the age of seven, but instead only emerged in adolescence (Lussier et al, 2023).  

Researchers concluded that the ages between three and five years old are when children are vulnerable to adversity and the consequences of this adversity may biologically embed itself and later manifest itself in adolescence (Lussier et al, 2023). Additionally, the adversity-associated decrease in DNA methylation is correlated to have effects on the central nervous system (Lussier et al, 2023). Of course, it’s great timing that the altered DNA methylation becomes an issue during puberty. Especially since it’s associated with poor self-esteem and increased depressive symptoms. 

What’s the upside? There has to be a silver lining or else this article is just a doomsday proclamation. The ability to finally trace health complications back to epigenetic mechanisms due to latent childhood trauma provides an important piece of the puzzle of understanding complex diseases. However, the puzzle is far from solved. The cohort in this study was predominantly of European descent and further research into how the complexities of race factor into DNA methylation and childhood adversity is the next step in this journey.

Literature Cited:

Lim , U., & Song, M. (2012). Dietary and Lifestyle Factors of DNA Methylation. In Cancer Epigenetics (Vol. 863, pp. 359–376). Humana Press.

 Lussier, A. A., Zhu, Y., Smith B. J., Cerutti J., Fisher J., Melton P. E., Wood N. M., Cohen-Woods S., Huang R., Mitchell C., et al. (2023). Association between the timing of childhood adversity and epigenetic patterns across childhood and adolescence: findings from the Avon Longitudinal Study of Parents and Children (ALSPAC) prospective cohort. Lancet Child Adolesc Health. 7(8), 532-43. https://doi.org/10.1016/S2352-4642(23)00127-X

Moore, L. D., Le, T., & Fan, G. (2013). DNA methylation and its basic function. Neuropsychopharmacology, 38(1), 23–38. https://doi.org/10.1038/npp.2012.112

Suelves, M., Carrió, E., Núñez-Álvarez, Y., & Peinado, M. A. (2016). DNA methylation dynamics in cellular commitment and differentiation. Briefings in Functional Genomics, elw017. https://doi.org/10.1093/bfgp/elw017