Bowdoin Science Journal

Science

Seeing Without Light: Measuring Megahertz-Frequency Vibration on the Atomic Scale

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Scientists cannot take a picture of an atom. This is because visible light consists of waves so much larger than atoms that the two do not interact. Even supposed pictures of atoms, like this particularly famous one by British physicist David Nadlinger, show the radiation emitting from the atom – not the atom itself. So how else are we supposed to observe what happens at the atomic scale?

Vibration is an important key to link the quantum world with our own. Whereas visual observation is difficult on ultra-small scales, vibration still applies as a valid way to detect information. It’s like how you may be able to feel a splinter in your finger even though you can’t see it. For convenience, physicists often describe vibrations – periodic movement of atoms – as “phonons” (Chandler, 2010). Though phonons may sound like fundamental particles like protons or electrons, they aren’t. Phonons are just a way to describe complicated interactions between other fundamental particles into an easy-to-work-with particle form (Lewton, 2021). What we call heat is the same sort of approximation: it is an aggregate, easier way to describe the energy of the innumerable atoms in an object colliding like hundreds of billiard balls.

In Nature Physics, a team of researchers led by Caltech Professor Alkim Bozkurt recently created a device capable of reliably transforming phonons into detectable electromagnetic waves (2023). In their paper, published June of 2023, they describe an electrical circuit whose outputs vary with vibration.

Fundamental to the researchers’ design is a capacitor. Capacitors are circuit components that store electrical charges, i.e. electrons, on two parallel conducting plates separated by a small distance on their bodies. Capacitors are defined by their capacitance, which is the ability of a given component to hold charge. The key to Bozkurt et al.’s device is that capacitance depends on the distance between its parallel plates (2023). When the distance between the plates increases, capacitance decreases, and vice versa.

In the device described in the paper, Bozkurt et al. take advantage of capacitors’ properties to transmit photons (2023). The researchers connected the parallel plates of a calculator to a vibrating crystal lattice. When the lattice moves, the parallel plates – and thus capacitance –  change accordingly. Oscillating capacitance isn’t detectable on its own. However, voltage is a function of capacitance, and capacitance is the function of vibration. By hooking the capacitor up to a circuit whose output changes with voltage, we can observe the information carried by the phonons.

By hooking up the capacitor to a small transmitting circuit, the researchers can ascertain the phonons’ properties (Bozkurt et al., 2023). In operation, the wave transmitter must be tuned until the interaction between the moving capacitor and the transmitter creates a peak of detectable voltage in the transmitted wave. This peak occurs where the phonon frequency matches that of the transmitted microwave.

Say, for example, you have a crystal that vibrates at an unknown frequency 𝑓 that is greater than a millions of times per second. To find 𝑓, we attach the new device to the crystal. Then, once it begins vibrating, you must tune the transmitter’s electromagnetic wave output frequency to match the unknown 𝑓. When a peak of detectable voltage in the transmitted microwaves is observed, the output microwave frequency will equal to the unknown 𝑓. Thus, by measuring the microwaves, you will have indirectly measured the frequency of the vibrating crystal.

Such a device has practical applications well beyond measurement. The device can be used in parts of quantum memory units, interfacing with parts of quantum computers. It could effectively record the characteristic changes of a quantum system and then restore that state accordingly – something optical observing at such a small scale cannot achieve. Still, the invention is not quite able to match the phonon frequency as alternatives. Its outputs sometimes do not agree with the known vibration of the crystal. The paper cites possible next steps – including altering the transmitter – to increase its agreement with the known vibration of the phonons in testing (Bozkurt et al., 2023).

Still, this development is remarkable. The Caltech researchers produced a device that detects phonons at speeds of a billion times a second, orders of magnitude more sensitive than similar previous devices, with substantially improved reliability (Bozkurt et al., 2023). Other similar approaches rely on hard-to-create materials and suffer from short lifetimes at small scales.

Works Cited:

Bozkurt, A., Zhao, H., Joshi, C., LeDuc, H. G., Day, P. K., & Mirhosseini, M. (2022). A quantum electromechanical interface for long-lived phonons. Nature Physics, 19(September 2023), 1326–1332.

Brean, J. (2018, February 14). Stunning image of a single strontium atom wins British photography prize. https://nationalpost.com/news/world/stunning-image-of-a-single-strontium-atom

Chandler, D. L. (2010, July 8). Explained: Phonons. MIT News. https://news.mit.edu/2010/explained-phonons-0706

Lewton, T. (2021, March 24). The Near-Magical Mystery of Quasiparticles. Quantamagazine. https://www.quantamagazine.org/the-near-magical-mystery-of-quasiparticles-20210324/

 

 

Distributions, not Differentiation: New Studies Find Cell Proportions at the Heart of Neurological Specialization

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The human brain is organized into cortices, lobes, hemispheres, and more, with every designation serving as a location where a particular function necessary for survival is hosted. In understanding the cell types of the brain, scientists can further shape the understanding of the nature of human life. Current work strives toward comprehending the functions and capacities of the brain and developing stronger foundations for modeling brain physiology to support future research and medical applications. All of the advancements discussed originated from Alyssa Weninger and Paola Arlotta’s Science review article, A family portrait of human brain cells, which compiles recent findings in brain mapping research as aligned with the National Institute of Health’s BRAIN Initiative. In the article, Weninger and Arlotta summarize and discuss the work of multiple groups of neuroscientists that have developed new findings about the brain’s composition and variability across regions, individuals, and species (specifically five primates of interest and mice).

As suggested by the article, recent research from multiple teams of neuroscientists utilized a variety of study mechanisms to compare the composition of the brain. One of the most important tools used in the studies included single-cell profiling. This profiling technique analyzes cellular behavior through multiple methods that include their transcriptome (range of genetic information produced to control cell behavior), proteome (range of proteins produced by the cell), and epigenome (range of modifications and markings that control the genetic information expressed by a cell) to organize them into groups based on their functional similarities. Models that encompass these methods and human organoids (structures of organs derived from STEM cells that mimic organ tissue) are developed to model the brain and its cells. They are also used in mapping and developing comparative analyses to determine significant findings and understanding of the brain organization.

Comparisons of cell composition in regions across the brain resulted in findings from researchers under Siletti from the University of North Carolina at Chapel Hill and Jorstad from Harvard University. The two groups found that rather than mainly having different types of cells in different parts of the brain, some different parts of the brain shared the same cells but had different proportions of these cells. There were some exceptions, such as inhibitory neurons in the primary visual cortex, although the explanation of this finding is unclear. Such results change the understanding of evolutionary diversity in that diversification does not depend heavily on having many different cell types, but rather on having varying proportions of cells with small differences.

Jorstad’s group also developed a significant result in identifying differences in brain composition between human individuals. One cell type from 75 individuals was profiled and resulted in different classes of cells bearing contrasting levels of variability among individuals. Most of the explanatory factors were beyond demographic differences, such as gender, ancestry, or age. The reason for such differences is still unclear. Scientists are further encouraged to study bigger cohorts of people to further examine the origin of differences in variability across humans.

The finding of varying cell proportions held as Jorstad’s group conducted interspecies comparisons, comparing human compositions with other primates (specifically chimpanzees, gorillas, rhesus macaques, and marmosets). The exceptional cognitive ability found in humans was largely supported by differences in proportions of brain cell types rather than the variability of cell types. Additionally, faster evolutionary divergence may explain the differences in gene expression found between supportive tissue, known as glial cells, in the brain. This allowed for further species-specific development across primates. Only a limited number of gene patterns specific to humans were found, most of them concentrated in parts of the brain with human evolutionary change. As such, scientists have come to understand that attributes of the human brain are derived from very few cellular or molecular changes, leaving differences in cell proportions as the most prominent explanatory factory for human brain development. Furthermore, understanding the brains of related primates and their relation to human brains will help scientists develop new models for brain pathways and understand the kinds of questions that they will be able to answer with such knowledge in the future.

Neuroscientists today continue to work hard toward developing human brain models. Current studies are focusing on developing accurate organoids – three-dimensional tissue models of stem cells developed to mimic organs in structure and function. Velmeshev’s group of researchers worked towards profiling different cortical (outer layers of the upper brain) areas and related areas in fetuses to track developments across human births. Kim’s group of researchers investigated single-cell transcriptomes of the thalamus (the processor of sensory data) during its development but was missing an investigation of the thalamus cellular compositions. The work of these scientists contributes to the idea of molecular mechanisms as the driver of cellular diversity in the brain, but also calls for more innovation in external biological investigations to better model the brain and further study its composition. In doing so, neuroscientists will come even closer to understanding one of the most complex systems in the human body and develop more answers for current-day neurological problems.

Bibliography

Weninger, Alyssa, and Paola Arlotta. “A Family Portrait of Human Brain Cells.” Science, vol. 382, no. 6667, Oct. 2023, pp. 168–69, https://doi.org/10.1126/science.adk4857.

mRNA: Unpacking the Research that led to the COVID-19 Vaccines and the 2023 Nobel Prize in Medicine

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        By 2023, 81.4% of the United States population have received at least one dose of the COVID-19 mRNA vaccine, and just about everyone has heard of these lifesaving shots (CDC, 2023). But how many of us actually know how they work? In general, vaccinations expose the body to a weakened strain of a virus that initiates an immune response so that the virus can be recognized, and quickly neutralized, in the future (Jain, 2021). This works because of the structure of our immune system, which is split up into innate immunity and adaptive immunity. Innate immunity is the immediate response that our bodies put up when exposed to a pathogen; it sends out macrophages to gobble up infected cells, creates an inflammatory response to kill off the infection, and uses a host of molecules and pathways to destroy the virus. Adaptive immunity involves the presence of B and T cells, which arise in a viral infection and create immunological memory through antibodies and memory cells so that a future infection of the same virus is immediately recognized and shut down. Vaccines work to stimulate this adaptive immunity, while minimizing innate immunity.

        mRNA vaccines use this same basic principle, but instead of injecting a weakened strain of the actual virus into someone, they instead inject a piece of mRNA, or messenger RNA, which codes for a viral protein that stimulates this immune response (Jain, 2021).

Figure 1: The methodology of mRNA vaccines. Adapted from Jain, et. al., 2021

mRNA vaccines are much easier to make than traditional vaccines because they don’t require growing and inactivating a virus, and they don’t carry the risk that live vaccines have of infecting the subject, but up until recently, they weren’t even remotely possible because in vitro mRNA would create a huge inflammatory response when entering the body (Karikó, 2005). However, Hungarian biochemist Katalin Karikó and her colleague Drew Weissman were undeterred, and their research to create mRNA without an inflammatory response paved the way for mRNA vaccines and won them the Nobel Prize in Medicine in 2023 (Karikó, 2005).

        Karikó and Weissman’s research focused on in vitro mRNA’s stimulation of Toll-like receptors (TLRs), which recognize pathogens and activate signaling pathways leading to an inflammatory response (Karikó, 2005). They discovered that mammalian mRNA, which doesn’t stimulate an immune response, contains many base pair modifications, whereas bacterial RNA, which is known to stimulate a response, has no modifications (Karikó, 2005). In vitro mRNA, grown in a lab rather than from mammalian cell cultures, also has no, or very few, modifications. This led the researchers to question whether base pair modifications were how cells distinguished between foreign and non-foreign RNA, and thus which pieces of RNA stimulate an immune response (Karikó, 2005). They discovered that in vitro RNA activates three main TLRs known for activating an inflammatory response, but that nucleoside modifications limit that activation. Most importantly, they discovered that the suppressed immune response is proportional to the number of nucleotide modifications, and that these modifications also increase the stability of in vitro mRNA in the body, another original roadblock in the usage of mRNA for vaccines. (Karikó, 2005).

Figure 2: The use of base modifications to suppress inflammatory response of RNA. Adapted from Nobelprize.org

        Combined with later research also by Karikó and Weissman discovering that modified base-pairs also create increased protein production and other research designing more stable lipid carriers to deposit the mRNA into human cells, mRNA became a promising new vaccine technology, eventually allowing the COVID-19 vaccines to be produced in record times, shortening the pandemic and granting all of us our lives back. But the road to Karikó’s research being recognized, and especially the road to the Nobel Prize, was not predetermined. Karikó’s research was long overlooked, in part because of her identity as a Hungarian immigrant. She was “demoted four times” at UPenn, being told that her research didn’t measure up to their standards, but she continued to persevere, making her both a scientific success story, and a personal one (Shrikant, 2023). The COVID-19 vaccines created by Pfizer and Moderna were the first mRNA vaccines to be released, but future research is focusing on creating a universal flu vaccine and possibly even an HIV vaccine, all using mRNA technologies, which could drastically improve the landscape of viral infections, both in the US and across the globe.  

 

Literature Cited

Karikó, K., Buckstein, M., Ni, H., & Weissman, D. (2005). Suppression of RNA Recognition by Toll-Like Receptors: The Impact of Nucleoside Modification and the Evolutionary Origin of RNA. Immunity, 23(2), 165–175. https://doi.org/10.1016/j.immuni.2005.06.008

 Karikó, K., Muramatsu, H., Welsh, F. A., Ludwig, J., Kato, H., Akira, S., & Weissman, D. (2008). Incorporation of Pseudouridine into mRNA yields Superior Nonimmunogenic Vector with Increased Translational Capacity and Biological Stability. Molecular Therapy, 16(11), 1833–1840. https://doi.org/10.1038/mt.2008.200

 Jain, S., Venkataraman, A., Wechsler, M. E., & Peppas, N. A. (2021). Messenger RNA-Based Vaccines: Past, Present, and Future Directions in the Context of the COVID-19 Pandemic. Advanced Drug Delivery Reviews, 179, 114000. https://doi.org/10.1016/j.addr.2021.114000

 The Nobel Prize in Physiology or Medicine 2023. (n.d.). NobelPrize.Org. Retrieved October 22, 2023, from https://www.nobelprize.org/prizes/medicine/2023/press-release/

 CDC. (2020, March 28). Covid Data Tracker. Centers for Disease Control and Prevention. https://covid.cdc.gov/covid-data-tracker

Shrikant, A. (2023, October 6). Nobel Prize Winner Katalin Karikó was “demoted 4 times” at her old job. How she persisted: “You have to focus on what’s next.” CNBC. https://www.cnbc.com/2023/10/06/nobel-prize-winner-katalin-karik-on-being-demoted-perseverance-.html 

 

Biomimicry Within Bowdoin: The Ongoing Development of Peptoids

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To solve complex human health issues, scientists have more recently turned to biomimicry. Biomimicry, also known as biomimetics, is a field that develops synthetic materials, systems or machines that are derived from the principles of natural biological processes (Nature). Concepts within biomimetics are currently being used to design regenerative medicine and newer drugs for diseases such as cancer. In fact, within Bowdoin, Professor Benjamin Gorske, is undertaking a comprehensive research on developing methods to create drugs that attempt to inhibit signaling pathways within cancer, or interrupt the signal transduction pathways involved in the development of plaques in Alzheimer disease. 

Professor Gorske explains that these aforementioned diseases can be addressed by “controlling the signaling proteins”. By interrupting the signaling process, the underlying issue of these diseases – which are often so diverse and hard to target – doesn’t need to be treated. However, a difficulty that comes with targeting signaling proteins is that they bind to other molecules over a vast space, and are implicated in many other signaling pathways. Therefore, these proteins cannot simply be targeted by small molecular drugs, as they would be impossible to effectively block the proteins and thus are called “undruggable molecules”. Instead, Professor Gorske turns to attempting to create a biological molecule that can mimic the other molecules that bind to the target signaling protein – which are normally much bigger than current drug molecules. 

One of the targets that Professor Gorske looks into in his lab are the signaling proteins within the Hippo pathway. The Hippo pathway normally controls the size of organs by regulating cell proliferation (division of cells) and apoptosis (programmed cell death) (Cell Signaling Technology). Ultimately, this pathway controls the expression of certain genes that are involved in the proliferation process. This pathway is involved in cancer when it is disregulated, as it continuously sends a signal to the nucleus to express these genes encoding for cell proliferation, thus leading to the uncontrollable growth of cancer. The Hippo pathway involves a lot of signaling proteins that are solely involved in this signaling pathway. Most of these signaling proteins contain a WW domain – a distinct functional unit of the protein that mediates the interactions these proteins have with other molecules (EMBL-EBI). All the signaling proteins with this specific domain in this pathway generally bind to proteins with polyproline type 2 helices (PPII). Professor Gorske’s lab aims to design a molecule to contain this PPII structural component to effectively target the signaling proteins (with the WW domain) in the Hippo pathway.

Fig 1: Diagram of the Hippo Pathway. The signaling protein YAP (yes-associated protein/transcription coactivator) is an example of a molecule with the WW domain.

However, we can’t utilize naturally formed proteins with these PPII helices as the proteases in our body would find the related drugs as foreign and destroy them. Thus these helices need to be made artificially, forming molecules called peptoids. Peptoids are a class of molecules that mimic the structure and function of helical peptides (Chongsiriwatana et al., 2008). They are very biostable, relatively easy to make, and most importantly proteases don’t destroy these molecules. Thus Professor Gorske has chosen to make specific peptoids that perhaps could target these signaling proteins in his lab.

Fig 2: Comparison of the general molecular structure of a naturally-derived peptide versus an artificially-produced peptoid.

However, an issue that arose with creating these peptoids is that the peptoids often folded to form polyproline type 1 helices (PPI) rather than PPII helices. This is due to the differences in orientation of the connected amides (subunits of the peptoids). This leads to peptoids with PP1 helices being much more compressed than peptoids with PPII helices. While they do work as good lung surfactants and other antimicrobials, they are not suitable to target signaling proteins. 

Fig 3: Comparison of the 3D structure of polyproline 1 helix (PPI) and polyproline 2 helix (PPII), and the orientation of the respective amide subunits.

Through experimenting, Professor Gorske has found out in his lab that the best way to encourage amides to connect in the desired PPII orientation is through adding side chains on the amide subunits, and the side chains are additionally thionated – the carbon is double bonded to sulfur instead of oxygen. Currently, he is investigating whether adding more than one thionated residue can lead to the whole peptoid to adopt the desired PPII helical structure. 

This method of creating peptoids that Professor Gorske is working to devise can be implicated in so many uses within medicine. As peptoid drugs can mimic biological molecules, they can more precisely target the required proteins, to help inhibit or promote signaling pathways back to normal. Professor Gorske’s research is therefore crucial to the ongoing development of medicine and healthcare. 

References

“Biomimetics Articles from across Nature Portfolio.” Nature News, Nature Publishing Group, https://www.nature.com/subjects/biomimetics. 

Chen, Yu-An, et al. “WW Domain-Containing Proteins Yap and Taz in the Hippo Pathway as Key Regulators in Stemness Maintenance, Tissue Homeostasis, and Tumorigenesis.” Frontiers in Oncology, vol. 9, 2019, https://doi.org/10.3389/fonc.2019.00060. 

Chongsiriwatana, Nathaniel P., et al. “Peptoids That Mimic the Structure, Function, and Mechanism of Helical Antimicrobial Peptides.” Proceedings of the National Academy of Sciences, vol. 105, no. 8, 2008, pp. 2794–2799., https://doi.org/10.1073/pnas.0708254105. 

Embl-Ebi. “What Are Protein Domains?” What Are Protein Domains? | Protein Classification, https://www.ebi.ac.uk/training/online/courses/protein-classification-intro-ebi-resources/protein-classification/what-are-protein-domains/. 

“Hippo Signaling.” Cell Signaling Technology, 2010, https://www.cellsignal.com/pathways/hippo-signaling-pathway.

 

The Possibilities of the CRISPR-Cas9 System

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          As humans continue to further explore the fields of science, they deepen their understanding of convoluted subjects through the use of advanced technologies. One of the notable technologies today is the CRISPR-Cas9 system, a highly precise DNA editing tool that allows for genome manipulation in humans, animals, and plants. CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats) works with a CRISPR-associated (Cas) nuclease, which was originally derived from a genome editing system used as immune defense by bacteria. To put it simply, if infected by a virus, the bacteria captures a small piece of the invading viruses’ DNA and inserts their own DNA to create a CRISPR segment (Tavakoli et al., 2021). With this segment, the bacteria can produce RNA segments that will attach to parts of the viruses’ DNA if it attacks again. The bacteria use the Cas9 enzyme to cut the viruses’ DNA apart and incapacitate it. 

          Scientists adapted the system so it could be inputted into the human genome and edit DNA. Researchers created small segments of RNA that have a “guide” sequence which binds to a target sequence in the DNA and attaches to the Cas9 enzyme (Tavakoli et al., 2021). The guide RNA (gRNA) identifies the intended DNA sequence and the Cas9 enzyme cuts the specific location, similar to how the process occurs in bacteria. The cell’s own DNA machinery is then used to add or delete pieces of the genetic material, known as gene knock-in and gene knockout, respectively. However, it can also alter the DNA by replacing segments with more customized sequences. CRISPR activation (CRISPRa) is used to up-regulate the expression of a gene while CRISPR interference (CRISPRi) down-regulates the expression of a cell (CRISPR Guide).

Figure 1. Gene Knockout
Figure 2. Activation of Target  Gene with CRISPRa

                                       Note. Adapted from CRISPR Guide, Addgene, 2022.

          There are many potential applications in cancer immunotherapy, treatment of genetic diseases, improving plant genetic variation, and more. For example, there have been advances towards mitigating the effects of blood disorders such as sickle cell disease (SCD). In those with SCD, the misshapen red blood cells can block blood vessels, thus slowing or stopping blood flow. Effects of this fatal disease are anemia, chronic pain, strokes, and organ damage. In this instance, CRISPR technology is not used to directly rectify the disease-inducing gene variant. Instead of restoring adult hemoglobin, it works to increase the levels of fetal hemoglobin, an oxygen carrier protein that only fetuses make in the womb (Henderson, 2022). Since it’s not affected by the sickle cell mutation, it can be a substitute for the defective adult hemoglobin in red blood cells (Henderson, 2022).

Figure 3. Hemoglobin Switching in Infants

Note. Adapted from CRISPR Clinical Trials: A 2022 Update, Henderson, 2022, Copyright 2022 by Innovative Genomics Institute.

         As seen in the diagram above, SCD symptoms begin during infancy when levels of fetal hemoglobin decrease. The blood stem cells are harvested from the blood and then the genomes are edited to activate the fetal hemoglobin gene. Next, chemotherapy eliminates the disease-inducing blood stem cells from the person’s body, and the genome-edited stem cells are put back into the bloodstream through an IV, creating a new blood stem cell population that produces fetal hemoglobin (Henderson, 2022). This technique is ex vivo genome editing, where the editing occurs outside the body to prevent the risk of lingering and unwanted CRISPR components in the body. Those treated for SCD in CRISPR clinical trials show normal to near-normal hemoglobin levels with at least 30% as fetal hemoglobin (Henderson, 2022).

          It raises the following questions: is it possible to select certain features in humans that are seen as favorable or desirable? Is it possible to have almost complete manipulation of physical features or to enhance the body’s biological processes to unlock superhuman abilities only seen in movies? These human experimentations would be best measured if implemented during the early stages of life so as to let the body integrate the changes and develop properly. Perhaps we could alter ourselves to increase muscle mass, heighten athletic ability, or augment intelligence. In regard to altering the human genome, there are certain limitations as to what can and can’t be done without violating certain ethical boundaries. 

          This can be seen in the case of He Jianku, a Chinese scientist who used CRISPR to edit two embryos, both of which are now living babies. Though there was little information that only came from He himself and the Chinese government, it has been said that sometime in late 2017, He injected the two embryos with a CRISPR construct that would delete a 32-base-pair in the CCR5 gene on chromosome 3, leading to a non-functional CCR5 protein (Greely, 2019). He sought to achieve humans who could not contract AIDS because they don’t have this functioning protein (Greely, 2019). Though this theory was later proved wrong and the CRISPR construct did not fulfill his intentions, he managed to induce never before seen changes that led to the production of non-functional proteins. His actions prompted the Chinese court to convict him on the basis of deliberately violating medical regulations (Greely, 2019). Could it be argued that pushing the boundaries are necessary for scientific growth and greater human evolution? How far is too far? As CRISPR and other gene editing tools continue to develop, we can keep imagining the unnerving yet exciting possibilities that are awaiting.

 

Literature Cited

CRISPR Guide. (n.d.). Addgene. 

Greely, H. T. (2019). CRISPR’d babies: human germline genome editing in the ‘He Jiankui affair’. Journal of Law and Biosciences, 6(1), 111-183.

Henderson, H. (2022). CRISPR Clinical Trials: A 2022 Update. Innovative Genomics Institute.

Tavakoli, K., Pour-Aboughadareh, A., Kianersi, F., Poczai, P., Etminan, A., & Shooshtari, L. (2021). Applications of CRISPR-Cas9 as an Advanced Genome Editing System in Life Sciences. BioTech, 10(3), 14. 

What are genome editing and CRISPR-Cas9? (2022). MedlinePlus.

The Chronic Lyme Debate

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Second possibly only to mosquitos, ticks are the most reviled insect found in New England nature. Like mosquitos, which are notorious vehicles for viruses such as Zika and West Nile, blacklegged ticks (deer ticks) spread Borrelia burgdorferi infection, resulting in Lyme disease. Affecting over 30,000 people a year in the United States, mostly in the northeastern states, Lyme disease is a bacterial infection which causes both local and global symptoms. Early symptoms include fever, muscle fatigue, swollen lymph nodes, and, mostly notably, an erythema migrans rash. Left untreated, patients may develop facial palsy (partial facial paralysis), arthritis, central nervous system inflammation, and heart palpitations. Diagnosis of Lyme disease is based primarily on symptoms and the possibility of exposure to Lyme-carrying ticks, although laboratory tests of patient serum for anti-B. Burgdorferi antibodies may also be considered. Treatments usually consist of a several week course of antibiotics. 

Although the majority of Lyme disease patients recover after initial treatment, 5-20% of patients continue feeling symptoms such as fatigue, muscle pain, and difficulty concentrating. This disorder, called post-treatment Lyme disease syndrome, falls under a broader category of disorders referred to as “chronic Lyme disease.” Also included in this category are patients without a history of Lyme disease but with Lyme-like symptoms; patients with other recognizable disorders seeking an alternative diagnosis; and patients with positive serological results for anti-B. Burgdorferi antibodies but no past exposure to ticks or other routes of infection. 

The majority of chronic Lyme patients fall into the middle two categories: those with symptoms but no history and the misdiagnosed. Moreover, in clinical trials, traditional treatment routes for Lyme disease such as antibiotics have not been effective in alleviating symptoms. Because many of those diagnosed with chronic Lyme do not match the diagnostic criteria for traditional Lyme disease, most scientists and physicians reject the diagnosis. However, a small but very vocal group of patients and physicians fervently believe in the existence of chronic Lyme disease. They are represented by powerful advocacy groups such as the International Lyme and Associated Diseases Society (ILADS) and the Lyme Disease Association (LDA). These groups have been effective at lobbying politicians and regulators to get protections for chronic Lyme sufferers, even as the physician community become increasingly convinced of its inaccuracy.

Although Lyme disease may seem a relatively simple disease with a clear cause (tick-borne bacterial infection) and treatment plan (antibiotics), the controversy over chronic Lyme disease reveals complexities. And this particular controversy doesn’t seem to be abating. It seems that the concept of chronic Lyme disease, like the disorder it purports to describe, is here to stay.

 

Works Cited:

CDC. (2022, January 19). Lyme disease home | CDC. Centers for Disease Control and Prevention. https://www.cdc.gov/lyme/index.html 

Chronic symptoms. (2018, April 11). Lyme Disease. https://www.columbia-lyme.org/chronic-symptoms 

Feder, H. M., Johnson, B. J. B., O’Connell, S., Shapiro, E. D., Steere, A. C., & Wormser, G. P. (2007). A critical appraisal of “chronic lyme disease.” New England Journal of Medicine, 357(14), 1422–1430. https://doi.org/10.1056/NEJMra072023 

Lantos, P. M. (2011). Chronic Lyme disease: The controversies and the science. Expert Review of Anti-Infective Therapy, 9(7), 787–797. https://doi.org/10.1586/eri.11.63 

Mosquito-borne diseases | niosh | cdc. (2020, February 21). https://www.cdc.gov/niosh/topics/outdoor/mosquito-borne/default.html 

Whelan, D. (n.d.). Lyme inc. Forbes. Retrieved April 2, 2023, from https://www.forbes.com/forbes/2007/0312/096.html 

The role of info chemicals in seabird plastic ingestion

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Short-tailed Shearwater (Puffinus tenuirostris), Ryan Shaw (2009)

Plastic debris is widespread in our waters with more than a quarter of a billion metric tons of plastic suspended in its global oceans. This abundant plastic pollution is being consumed by hundreds of organisms, ranging from tiny zooplankton to giant baleen whales. Seabirds are especially at risk, with a projection model concluding that over 99% of all seabird species will have ingested plastic debris by 2050. The consumption of plastic is incredibly harmful to seabirds as it reduces the storage volume of the stomach which ultimately leads to starvation and death. In the last few years, it has been discovered that the plastic problem is much more complicated than we thought before as many seabirds rely on their sense of smell to locate their prey instead of just visually. A 2016 study has brought to light this common misconception of marine organisms consuming plastic debris solely based on visual cues and has introduced a new factor: dimethyl sulfide (DMS). 

DMS is an infochemical used by foraging organisms as a way to find prey in marine environments. The production of DMS is from the enzymatic breakdown of its chemical precursor, dimethylsulfoniopropionate (DMSP), which increases when zooplanktons eat, letting other marine organisms know of the presence of a new meal. Plastic debris is an excellent substrate for biota that produce these infochemicals due to its convenience in biofouling, which is the accumulation of organisms on a surface. Since plastic debris can be easily fouled by DMS-producing organisms, then the debris can also produce a DMS signature that is significant enough to lead seabirds and similar organisms to consume it. 

To prove this, scientists examined the sulfur signature of plastic beads from the most common types of plastic found in the ocean. These plastic beads were tested for sulfur signatures after either being exposed to marine conditions or never being exposed to these conditions. The beads exposed to marine conditions were deployed off the coast of California at the Bodega Marine Laboratory and Hopkins Marine Station at oceanographic buoys and then retrieved after approximately three weeks. After examining each plastic bead, it was found that the samples not exposed to marine conditions did not produce any DMS signature. However, every sample that was tested after marine exposure was found to have produced a DMS signature. Even after less than a month of marine exposure, these plastic samples were found to produce DMS signatures that were significant enough to be detected by seabirds.

Additionally, the study was able to predict the importance of DMS and plastic ingestion patterns within seabirds through data analysis. Plastic ingestion data was analyzed from 55 studies among 25 procellariiforms––the order under which seabirds fall––to determine that DMS responsiveness has a significant positive effect on the frequency of plastic ingestion. Additionally, plastic ingestion patterns were predicted through calculations using data from previous studies to find that DMS-responsive species ingest plastic five times as frequently as non-DMS-responsive species.

The study has challenged the frequent assumption that marine organisms consume plastic because it is visibly mistaken for prey, suggesting rather that chemical cues like DMS play a role. This plastic ingestion has many implications, one such being that the semiannual movement patterns of seabirds between the Southern and Northern Hemispheres can create contact with plastic on a global scale rather than just a regional one. Although the primary focus of this study was on seabirds, they are not the only species that respond to DMS––sea turtles, penguins, and various other organisms have been shown to use DMS and DMSP as foraging compounds and could be impacted similarly. We must start mitigating the plastic waste we produce and work towards cleaning up our oceans. While this is a huge step to take, we can begin by looking for alternatives to plastic that are safer for the environment and reduce the amount of plastic that we use in our everyday lives.


References:

Savoca, M. S., Wohlfeil, M. E., Ebeler, S. E., & Nevitt, G. A. (2016). Marine plastic debris emits a keystone infochemical for olfactory foraging seabirds. Science Advances, 2(11). https://doi.org/10.1126/sciadv.1600395 

Eriksen, L. C. M. Lebreton, H. S. Carson, M. Thiel, C. J. Moore, J. C. Borerro, F. Galgani, P. G. Ryan, J. Reisser, Plastic pollution in the world’s oceans: More than 5 trillion plastic pieces weighing over 250,000 tons afloat at sea. PLOS ONE 9, e111913 (2014).

Wilcox, E. Van Sebille, B. D. Hardesty, Threat of plastic pollution to seabirds is global, pervasive, and increasing. Proc. Natl. Acad. Sci. U.S.A. 112, 11899–11904 (2015).

Ocean plastics pollution. Ocean Plastics Pollution. (n.d.). Retrieved April 2, 2023, from https://www.biologicaldiversity.org/campaigns/ocean_plastics/?adb_sid=71bc9f17-356c-492f-9204-f0e22e2752b6

The Contraceptive Brain Drain: How Birth Control Alters Women’s Brains

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There are millions of women taking steroids every day. But how is this possible? Are they just getting really buff? It feels like we always hear stories about how performance-enhancing drugs, namely steroids, are giving world-class athletes the boost they need to beat out their competition. But women across the globe are taking steroids every day as well, in the form of hormonal birth control. Despite their widespread use, side effects of hormonal contraceptives are largely unstudied, or have been until recently. In the last ten years, several studies have come out about the effect of taking a daily dose of steroids on women’s brains and mental health, which until now has been a severely neglected area where lack of knowledge affects millions of people worldwide. 

People take hormonal birth control, or hormonal contraceptives, for a myriad of reasons, from the obvious (preventing pregnancy) to the not-so-obvious (lessening iron deficiency) and everything in between. This type of medication simply refers to methods of pregnancy prevention that act on the endocrine system. The endocrine system controls growth, development, metabolism, and reproduction via signaling molecules called hormones. Two hormones in particular, estrogen and progesterone, control the menstrual cycle and are therefore the major components of hormonal birth control. Types of hormonal contraceptives come in many forms including the pill, the patch, the implant, injections, and hormonal intrauterine devices or IUDs, but despite the wide variety in the forms this medication takes, all of them contain one or both of these two hormones. As steroids, both estrogen and progesterone affect other body systems besides the reproductive system.

To study the impacts of taking a daily dose of steroids on other areas of the body, specifically the brain, Dr. Belinda Pletzer and her colleagues conducted a study in 2010. The brain is particularly susceptible to change due to an influx of synthetic hormones because it contains a very high quantity of hormone receptors. The brain needs to act as a “sponge” for these molecules since it plays an important role in creating the appropriate responses in the rest of the body. Pletzer’s study investigated how the sponginess of the brain would affect changes in its structure by comparing images of the brains of adult men, adult women during different stages of their menstrual cycle, and adult women taking hormonal contraceptives. To perform this comparison they used a technique called voxel-based morphology on MRIs of study participants (Pletzer et al., 2010). Voxel-based morphology measures differences in the concentration of tissue and the size and shape of different areas of the brain.

Overall, they found that women taking hormonal birth control had smaller areas of gray matter, or areas of the brain that have a high concentration of the cell bodies of nerve cells, when compared to “naturally cycling women” in both their follicular and luteal menstrual phases (Figure 1). Pletzer’s study also found interesting gendered differences in gray matter volume. While men had greater gray matter overall, the volume of gray matter in the prefrontal cortex, the pre-and postcentral gyri, and the supramarginal gyrus of both naturally cycling women and women taking hormonal contraceptives was higher than the volume of gray matter in these areas in men (Figure 2). These areas are involved in decision-making and problem-solving, controlling motor function, and emotional responses. However, the higher amount of gray matter in women in these areas was overshadowed by the larger volume of gray matter in men in the hippocampus, hypothalamus, parahippocampal and fusiform gyri, putamen, pallidum, amygdala, and temporal regions of the brain during the early follicular phase (A), mid-luteal phase (B), and in women taking hormonal birth control (C) (Figure 2). Many of these areas of reduced gray matter are ones of high importance for neurophysical ability and mental health.

Additionally, a study done by Rush University Medical Center showed an association between higher levels of gray matter and better cognitive function (“Everyday Activities Associated with More Gray Matter in Brains of Older Adults”). These findings suggest that taking birth control, and the associated decrease in gray matter, could be directly causing some of the symptoms women on hormonal contraceptives experience, such as brain fog, mood changes, and even anxiety and depression. For example, a smaller hypothalamus, one of the areas of decreased gray matter, is associated with heightened irritability and depression symptoms (“Study Finds Key Brain Region Smaller in Birth Control Pill Users”). Pletzer’s research and the work of others after her on the impact of birth control on structures of the brain represent important first steps in proving a causative relationship between birth control, symptoms associated with it, and structural changes in the brain.

Although this research has made some crucial preliminary steps into researching how taking a daily dose of steroids affects the brains of women taking hormonal contraceptives, the highly complex nature of the brain and its relationship with the regulation of the rest of the body means that further research is necessary. The sheer number of people that this issue affects means that it is essential to continue researching the impacts of this widely used drug. More importantly, knowing the potentially serious negative side effects enables millions of people to make more informed decisions concerning their health and their bodies.

 

Works Cited

Rush University Medical Center. (2018, February 14). Everyday activities associated with more gray matter in brains of older adults: Study measured amount of lifestyle physical activity such as house work, dog walking and gardening. ScienceDaily. Retrieved March 11, 2023 from www.sciencedaily.com/releases/2018/02/180214093828.htm.

Lewis, C. A., Kimmig, A. C. S., Zsido, R. G., Jank, A., Derntl, B., & Sacher, J. (2019). Effects of hormonal contraceptives on mood: a focus on emotion recognition and reactivity, reward processing, and stress response. Current psychiatry reports, vol. 21, no.11, 2019, p 115. PubMed Central, https://doi.org/10.1007/s11920-019-1095-z.

Meyer, Craig H., Kinsley, Elizabeth A. “Women’s Brains on Steroids.” Scientific American, https://www.scientificamerican.com/article/womens-brains-on-steroids/. Accessed 7 Mar. 2023.

Nemoto, Kiyotaka. “[Understanding Voxel-Based Morphometry].” Brain and Nerve = Shinkei Kenkyu No Shinpo, vol. 69, no. 5, May 2017, pp. 505–11. PubMed, https://doi.org/10.11477/mf.1416200776.

Pletzer, Belinda, et al. “Menstrual Cycle and Hormonal Contraceptive Use Modulate Human Brain Structure.” Brain Research, vol. 1348, Aug. 2010, pp. 55–62. ScienceDirect, https://doi.org/10.1016/j.brainres.2010.06.019.

Sharma, Rupali, et al. “Use of the Birth Control Pill Affects Stress Reactivity and Brain Structure and Function.” Hormones and Behavior, vol. 124, Aug. 2020, p. 104783. ScienceDirect, https://doi.org/10.1016/j.yhbeh.2020.104783.

“Study Finds Key Brain Region Smaller in Birth Control Pill Users.” ScienceDaily, https://www.sciencedaily.com/releases/2019/12/191204090819.htm. Accessed 7 Mar. 2023.

What Causes Aging? An Epigenetics Study From The Sinclair Lab May Have an Answer

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Dr. David Sinclair, A.O., Ph.D. Photo from the Sinclair Lab, Harvard Medical School (2023).

Aging, also known as “senescence,” is an inevitable process in all living things. Organisms small and large eventually break down, accumulating enough wear and tear in their cells that ultimately causes the body to stop functioning as a whole. While medicine and lifestyle improvements stave off aging, identifying its fundamental causes has been more challenging. In January 2023, scientists in Dr. David Sinclair’s lab at Harvard Medical School published a paper with experimental evidence supporting what Sinclair calls the “Information Theory of Aging,” where damage to the epigenome can cause aging.

After receiving his Ph.D. in molecular genetics from the University of New South Wales, Sinclair completed his postdoctorate at MIT where he co-discovered the role of sirtuin enzymes in limiting age-related cellular damage in yeast. In addition to teaching genetics and translational medicine at Harvard Medical School since 1999, Sinclair authored the popular book Lifespan: Why We Age – and Why We don’t Have To (2019). His breakthroughs in the science of aging have earned him a great deal of attention from the public eye, resulting in appearances on several popular media outlets, including CBS’s “60 Minutes” and TIME magazine (The Sinclair Lab, 2023).

Sinclair’s newest discovery, published as “Loss of epigenetic information as a cause of mammalian ageing” in January 2023, focused on the role of epigenetics in aging. The title specifies that epigenetic information loss, rather than genetic information loss, is a cause of aging. Genetics refers to the raw molecular information sequences stored in cells as deoxyribonucleic acid (DNA), which is physically condensed inside the nucleus into pairs of chromosomes. The material inside a chromosome is known as “chromatin.” The central dogma of molecular biology states that information in DNA sequences is read by the cell in the form of messenger RNA (mRNA) through transcription, and then ribosomes in the cell read this mRNA to make proteins through translation. DNA sequences that correspond to the production of a specific molecule are genes. The prefix epi- means “on top of,” so “epigenetics” refers to mechanisms that function “above” the molecules of DNA themselves, including reading DNA sequences, regulating gene transcription, and repairing mutated DNA. Like the DNA sequence, epigenetic changes are inheritable from parents to offspring.

The differences between genetics and epigenetics influence cellular reaction to damage. Damage to genes causes mutations, which are changes in the sequence of the DNA of that gene. Cells have mechanisms of repairing mutated DNA, but failure of these mechanisms can lead to cell death, or worse, cancer. Some DNA mutations, like those where a nucleotide is deleted, are irreversible.

By contrast, epigenetic mechanisms are more easily reversed. One epigenetic mechanism is DNA methylation, where a methyl group (-CH3) is added to a cytosine nucleotide by the DNA methyltransferase enzyme. This extra functional group blocks transcription factors from binding to promoter regions nearby the methylated cytosine, in effect “silencing” the gene as it cannot be transcribed into mRNA. DNA methylation is important for differentiating cells into specific cell types by enabling cells to only express the most pertinent genes while still containing the entire genome (Moore et al., 2012). DNA methylation is reversible with the help of TET dioxygenase enzymes (Wu and Zhang, 2014). Geneticists have found DNA methylation to be a way to assess molecular aging in cells as a sort of “epigenetic clock”. By analyzing methylation patterns of the genome (the “methylome”), scientists can find the biological age as well as the rate of aging in an organism’s cells (Hannum et al., 2012).

Figure 1: Methyl groups attached to cytosine bases in a gene block the enzyme RNA polymerase from binding to the promoter region of a gene, preventing transcription. Adapted from BOGOBiology (2017)

To investigate how changes to the epigenome affect aging in mice, Sinclair used a mouse system with induced changes to the epigenome (ICE). The genetically modified mice had a higher frequency of double-strand breaks (DSBs) in the DNA, which cause changes in the epigenome as cells are required to use their mechanisms of DNA repair more often . Sinclair’s method reduced the frequency of mutations by breaking the DNA strands in a way that left more whole unpaired nucleotides in the severed strand, making it more difficult for the cell to repair the DNA strand with a different sequence than before. While ICE mice had no significant difference in mutation frequencies versus control mice, DSBs in specific locations of the genome were observed as expected (Yang et al., 2023). Thus, any apparent changes in aging in the ICE mice of this study could be ascribed to the epigenetic DSB changes rather than mutations.

Figure 2: ICE treated mice after 10 months appear to have the physical hallmarks of aging, such as hair loss and reduced body mass, early compared to CRE control mice (Yang et. al. 2023).

The haggard appearance of the ICE 10 month old mice confirmed the early aging effects of the epigenetic changes (Figure 2). At the molecular level, analysis of DNA methylation at genome sites associated with age showed that ICE cells were approximately 1.5 times “older” than the control cells. With this artificially increased age came physiological consequences. ICE mice showed diminished short-term memory retention compared to Cre-control mice, as assessed by fear conditioning tests, and the ICE mice performed half as well in a Barnes Maze test as control, indicating decreased long-term memory. Additionally, ICE mice had decreased muscle mass and grip strength after 16 months. The authors attributed the cause of this accelerated aging to increased “faithful DNA repair” from the induced DSB breaks in the ICE mice, meaning that there were not significant mutations in the repair of DSBs.(Yang et al., 2023). During DSB repair, chromatin modifying factor proteins activate and move within a cell in a process known as “relocalization,” with repeated activation of this process known to cause epigenetic changes that silence genes normally expressed in young mice. Sinclair’s lab hypothesized that the relocalization of chromatin modifiers that occurs from repeated DSB repair associated with induced epigenetic changes lead to a gradual loss of cellular function associated with aging (Yang et al., 2023).

It may seem ironic that DNA strand break repair, a process meant to keep cells functioning when critical genes are damaged, is part of what ultimately causes the death of organisms. The fact that the mechanism implemented is epigenetic rather than genetic suggests that the effects of ageing may be reversible, like epigenetic mechanisms. In fact, Sinclair has shown that it is possible to partially undo the damaging effects of aging: after inducing OSK expression, which is a set of proteins known as “Yamanaka factors,” ICE mice exhibited some signs of rejuvenation in their eyes, kidneys, and muscles. Yamanaka factors like OSK are important in the fields of aging and regenerative medicine because they are keys to the synthesis of induced pluripotent stem cells, where somatic cells can become stem cells and potentially re-differentiate into other cell types (Takahashi and Yamanaka, 2006). The OSK treatment decreased the expression of age-associated markers in the kidney and muscle cells of the mice (Yang et al., 2023).

Sinclair’s experiments have shown the epigenome to be a key front in the investigation of aging, as the reversibility of changes to the epigenome can allow it to be a more accessible interface for scientists to interact with. The plasticity of the epigenome as demonstrated from the ability of Yamanaka factors to reverse the molecular indicators of aging mice show that there may be hope for science to bring this phenomenon to human epigenomes. Indeed, the news of reversing aging in mice made rounds in the media when Sinclair’s paper was published earlier this winter, and for good reason.

Works Cited

Al Aboud, N. M., Tupper, C., & Jialal, I. (2022). Genetics, Epigenetic Mechanism. In StatPearls. StatPearls Publishing. http://www.ncbi.nlm.nih.gov/books/NBK532999/

Bannister, A. J., & Kouzarides, T. (2011). Regulation of chromatin by histone modifications. Cell Research, 21(3), Article 3. https://doi.org/10.1038/cr.2011.22

BOGObiology (Director). (2017, October 11). Epigenetics: Nature vs. Nurture. https://www.youtube.com/watch?v=Q8BMP6HDIco

CDC. (2022, August 15). What is Epigenetics? | CDC. Centers for Disease Control and Prevention. https://www.cdc.gov/genomics/disease/epigenetics.htm

David Sinclair | The Sinclair Lab. (n.d.-a). Retrieved March 5, 2023, from https://sinclair.hms.harvard.edu/people/david-sinclair

Fernandez, A., O’Leary, C., O’Byrne, K. J., Burgess, J., Richard, D. J., & Suraweera, A. (2021). Epigenetic Mechanisms in DNA Double Strand Break Repair: A Clinical Review. Frontiers in Molecular Biosciences, 8, 685440. https://doi.org/10.3389/fmolb.2021.685440

Gilbert, S. F. (2000). Methylation Pattern and the Control of Transcription. Developmental Biology. 6th Edition. https://www.ncbi.nlm.nih.gov/books/NBK10038/

Hannum, G., Guinney, J., Zhao, L., Zhang, L., Hughes, G., Sadda, S., Klotzle, B., Bibikova, M., Fan, J.-B., Gao, Y., Deconde, R., Chen, M., Rajapakse, I., Friend, S., Ideker, T., & Zhang, K. (2013). Genome-wide Methylation Profiles Reveal Quantitative Views of Human Aging Rates. Molecular Cell, 49(2), 359–367. https://doi.org/10.1016/j.molcel.2012.10.016

Jin, B., Li, Y., & Robertson, K. D. (2011). DNA Methylation. Genes & Cancer, 2(6), 607–617. https://doi.org/10.1177/1947601910393957

Kulis, M., & Esteller, M. (2010). 2—DNA Methylation and Cancer. In Z. Herceg & T. Ushijima (Eds.), Advances in Genetics (Vol. 70, pp. 27–56). Academic Press. https://doi.org/10.1016/B978-0-12-380866-0.60002-2

Molecules discovered that extend life in yeast, human cells. (n.d.). EurekAlert! Retrieved March 5, 2023, from https://www.eurekalert.org/news-releases/664233.

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

Offord, Catherine. Two research teams reverse signs of aging in mice. (n.d.). Retrieved March 14, 2023, from https://www.science.org/content/article/two-research-teams-reverse-signs-aging-mice.

Takahashi, K., & Yamanaka, S. (2006). Induction of Pluripotent Stem Cells from Mouse Embryonic and Adult Fibroblast Cultures by Defined Factors. Cell, 126(4), 663–676. https://doi.org/10.1016/j.cell.2006.07.024

What is Epigenetics? The Answer to the Nature vs. Nurture Debate. (n.d.). Center on the Developing Child at Harvard University. Retrieved March 5, 2023, from https://developingchild.harvard.edu/resources/what-is-epigenetics-and-how-does-it-relate-to-child-development/

Wu, H., & Sun, Y. E. (2009). Reversing DNA Methylation: New Insights from Neuronal Activity–Induced Gadd45b in Adult Neurogenesis. Science Signaling, 2(64), pe17–pe17. https://doi.org/10.1126/scisignal.264pe17

Wu, H., & Zhang, Y. (2014a). Reversing DNA Methylation: Mechanisms, Genomics, and Biological Functions. Cell, 156(0), 45–68. https://doi.org/10.1016/j.cell.2013.12.019

Yang, J.-H., Hayano, M., Griffin, P. T., Amorim, J. A., Bonkowski, M. S., Apostolides, J. K., Salfati, E. L., Blanchette, M., Munding, E. M., Bhakta, M., Chew, Y. C., Guo, W., Yang, X., Maybury-Lewis, S., Tian, X., Ross, J. M., Coppotelli, G., Meer, M. V., Rogers-Hammond, R., … Sinclair, D. A. (2023). Loss of epigenetic information as a cause of mammalian aging. Cell, 186(2), 305-326.e27. https://doi.org/10.1016/j.cell.2022.12.027

 

Ecology, Policy, and Science Communication: The Story of Biologist and Activist Erika Zavaleta

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Erika Zavaleta is an interdisciplinary scientist that has worked her career to make her research accessible, has broken down barriers for biologists of color, and is seen by many to be a trailblazer in her field. Zavaleta is a community and ecosystem biologist at the University of California Santa Cruz (UCSC) that focuses on global and regional environmental change, ecosystem functioning, and effective stewardship. She uses environmental policy, economics, anthropology, and outreach as tools to communicate her research to a larger audience as a scientist that aims to make the field accessible. She received her bachelor’s and master’s in anthropology and Ph.D. in biological sciences at Stanford University. Dr. Zavaleta is a Howard Hughes Medical Institute Professor in the Ecology and Evolutionary Biology department at UCSC. She is an appointed California Fish and Game Commission science advisor, an Ecological Society of America (ESA) “Excellence in Ecology Scholar,” ESA fellow, and a fellow of the California Academy of Sciences. Dr. Zavaleta has also co-authored over 75 papers and book chapters in the fields of conservation, ecology, and social sciences. In 2021, she received the Commitment to Human Diversity in Ecology Award from ESA due to her devotion to highlighting the voices of low-income, Indigenous, Black, and Latino backgrounds in the ecology and conservation field.

Dr. Zavaleta’s Conservation Science and Solutions Lab is interested in questions related to ecological responses to climate change, changes in biodiversity due to environmental variability, and conservation-based approaches to mediate these impacts. Some research projects currently taking place by her lab members are the impacts of land and water use changes on bat ecological communities, the impacts of community-led forestry conservation efforts in Brazil and Nepal, and the effectiveness of current conservation efforts in response to climate change. Through this research, Zavaleta’s group works to act as a link between ecology theory and research to develop and recommend effective conservation and management practices. The lab places an emphasis on collaborating with community partners, approaching research through a multidisciplinary lens, and furthering initiatives that promote inclusivity in the field of conservation and biology.

Zavaleta’s lab has supported initiatives that she founded at UCSC that provide mentorship and support for historically excluded scientists including the Doris Duke Conservation Scholars Program and the Center to Advance Mentored, Inquiry-Based Opportunities (CAMINO) in 2013 and 2017 respectively. The Doris Duke Conservation Scholars Program (DDCSP) is a national fellowship that aims to increase accessibility to the conservation field, mainly focusing on providing training and research experience for underrepresented students in science. DDCSP is carried out by five partners including the DDCSP Collaborative, the University of California at Santa Cruz, the University of Michigan, the University of Washington, and the Yale School of the Environment. CAMINO works directly with students at UCSC and provides academic and professional assistance from graduate and faculty mentors. The center pairs CAMINO scholars with funded internships where they can gain research experience regardless of their previous internships in the ecology and conservation field. Dr. Zavaleta currently serves as a faculty director for both of these programs.

Most recently, Zavaleta established a training called FieldFutures with biologist Dr. Melissa Cronin that emphasizes the importance of field-based education and research that prevent sexual harassment for scientists in the ecology and conservation field. As said on their website, “studies have shown that 64% of surveyed field researchers experienced harassment—and one in five experienced assault— while conducting fieldwork. Women, people of color, LGBTQIA+ people, and people with other marginalized identities are more likely to experience these problems.” Since fieldwork directly places scientists of all genders at greater risk of sexual violence, FieldFutures works to provide workshops that identify ways to increase prevention, provides a space for scientists to get hands-on experience in dealing with these situations, and offers protocols that can be used in the field. The “Futures” component of their name symbolizes their vision of a future for fieldwork free of sexual assault and harassment—and they are working towards getting closer to this prospect with each training.

I write about Dr. Zavaleta as a fellow Latina and future conservation biologist who not only admires her research and intellectual contributions to the field but also her dedication to making the field one that welcomes people like me. During my first and second summers as an undergraduate, I spent them as a Doris Duke Conservation Scholar at the University of California Santa Cruz (UCSC). I have heard first-hand Dr. Zavaleta’s passion for finding climate solutions, diversifying the field, and using public policy to enact impactful environmental legislation. She has not only shown her commitment to increasing diversity in the field, but she has also asserted her support for social movements around the country and pledged to incorporate their missions in her own work. In 2020 in a letter as director of DDCSP, she contended that

Science and conservation have long marginalized Black and brown voices, faces, and talents. The demographics of our country tell us that there should be five times as many scientists and professionals of color in ecology, evolution, and conservation as there are. The absence of diverse leadership in our field sustains this gap unless all of us work for change. We all have to speak up and act when we see racial inequities affect our peers, colleagues, students, and communities.

As a beneficiary of the initiatives she has passionately poured time and energy into, I can attest that programs like DDSCP have helped me and my peers realize that scientists like us—first-generation college students and people of color— can thrive in this field and use our experiences to connect to a greater audience in the scientific field. I wish to be as intentional and inclusive as Dr. Zavaleta moving forward as a scientist, educator, and science communicator and I hope that more people in this career follow her lead.