BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: genetics (Page 1 of 4)

How Parental Metabolism Influences a Child’s Long-Term Health

A new study published in Diabetologia by researchers at Lund University and the King Edward Memorial Hospital and Research Centre in Pune, India, highlights how a child’s long-term risk of developing type 2 diabetes and cardiovascular disease can be influenced by the metabolic traits of their parents. Using data from over 2,400 participants in the Pune Maternal Nutrition Study, researchers analyzed parent and offspring relationships related to cardiometabolic traits such as body mass index (BMI), blood glucose levels, cholesterol, and insulin function at three different developmental stages: 6, 12, and 24 years of age.

The study found that maternal genes had the strongest influence on a child’s blood sugar and cholesterol levels throughout their early life and into adulthood. This influence was seen even at birth, where the mother’s genes had affected the baby’s birth weight. These findings suggest that maternal contributions, through both genetic inheritance and the prenatal environment, play a dominant role in shaping how a child regulates glucose and lipids. On the other hand, paternal genes had a larger impact on insulin-related functions over time, showing a stronger paternal influence on the child’s insulin sensitivity and secretion as they aged.

Participants in the study underwent tests measuring insulin sensitivity and the function of insulin-producing cells. The results showed that if the father had impaired insulin secretion or insulin resistance, these traits were more likely to appear in the child later in life. Researchers noted that this type of information could be valuable for early interventions, such as promoting physical activity, which is known to improve insulin sensitivity and lower the risk of developing type 2 diabetes.

This research provides insight into parent-of-origin effects, where the influence of a trait differs depending on whether the gene is inherited from the mother or the father. These findings have implications for developing preventive strategies targeted at parents, particularly mothers during pregnancy, to help reduce their children’s risk of cardiometabolic diseases.

This connects to what we learned in AP Biology because this study shows the concept of parent-of-origin effects and their connection to epigenetics and genomic imprinting. While classical Mendelian inheritance assumes equal contribution from both parents, this study shows that gene expression can be modified depending on the parent from whom the gene is inherited. Furthermore, the maternal effect observed in this research connects to the role of the prenatal environment in influencing phenotypic outcomes. This reinforces the idea that both genetic and environmental factors inherited from parents can significantly shape an individual’s physiological traits and disease risk over time.

On a more personal note, this topic stood out to me because I’ve seen how family health traits can run deep. What are some ways that schools and communities could help families better understand and manage their health risks across generations?

A family walking through a meadow at Gwynns Falls-Leakin Park

Simultaneous Tracking: CRISPR’s Major Upgrade

Software updates on your iPhone can often feel unnecessary. Waiting for your smartphone to complete an increasingly lengthy update, only to discover seemingly minimal changes in one area—like fixing bugs or improving compatibility—can be frustrating.

People using smartphones at a railway station

Smartphone users at a railway station.

For the past decade, scientists have been able to edit DNA with remarkable precision, revolutionizing genetic research with the use of CRISPR-Cas9 technology. Specifically, CRISPR-Cas9 technology is a type of gene editing technology that allows scientists to use enzymes to molecularly cut and/or modify specific portions of DNA or RNA to discover the roles these genes play in a variety of disorders and diseases. According to the National Library of Medicine, CRISPR-Cas9 “makes it possible to correct errors in the genome and turn on or off genes in cells and organisms quickly, cheaply, and with relative ease.”

This is what makes CRISPR technology so amazing! The technology’s ability to, according to the Broad Institute, “easily be matched with tailor-made “guide” RNA (gRNA) sequences designed to lead them to their DNA targets,” makes the technology distinctly efficient and customizable in a way other gene-editing tools are not.

Although this type of genetic technology has led to significant discoveries regarding the roles of genes in cancers and autoimmune disorders, CRISPR has had a key limitation: it could only target one gene at a time. However, in a recent study, researchers at Yale University discovered a new upgrade in CRISPR technology that allows for simultaneous genetic modifications and tracking across multiple genes at once, a notable change from past CRISPR abilities.

CRISPR-Cas9 Editing of the Genome

Illustration of CRISPR-Cas9 Editing of a Section of DNA.

The research team’s new tool, called CRISPR-Cas12a, has the ability for researchers to “simultaneously assess the impact of multiple genetic changes involved in a variety of immune system responses.” Led by Dr. Sidi Chen, the team of researchers developed four mouse models that used this new technology to fine-tune and track changes in the mice’s immune system cells. The team distinctly focused on inducing and editing sets of genes in “different directions simultaneously.”

These models essentially allowed the scientists to study the genetic interactions of the mice’s immune system cells that contributed to diseases like cancer and even autoimmune and neurological disorders. In this way, Chen’s team was able to create an entirely new way of studying immune responses at the genetic level not only for mice cells but for human cells as well, which could eventually develop into the creation of new remedies and therapies for certain types of medical conditions and diseases.

This research directly connects to what we’ve studied recently in AP Biology. CRISPR-Cas12a and other gene editing technologies relate directly to the ability to manipulate transcription and translation during protein synthesis through gene regulation. Moreover, we learned in class that genes control traits by coding for different types of proteins and that cells can turn their genes “on” or “off” through a series of regulatory processes. CRISPR-Cas12a connects to our classwork because this technology allows scientists to modify multiple genes at once and observe how those changes can affect how certain cells function and what phenotypes are shown as a result. By editing multiple genes, scientists can study how genes work together to create traits!

Cas12a (Cpf1) in complex with crRNA and target DNA

Structure of CRISPR-Cas12a with a guiding RNA (cRNA) and target segment of DNA.

Ultimately, CRISPR-Cas12a and other types of genetic technology have great implications for the future of medicine and genetic testing. The ability to edit multiple genes simultaneously has created promising hopes for the development of new, personalized medicinal treatments and the improvement of scientists’ understanding of genetic diseases and immune system disorders.

It is clear that the future of medicine is continuing to be crafted, one gene at a time—or in this case, many at once!

Beyond Genetic Scissors: How CRISPR-Cas12a Is Editing the Future of Medicine

Cas12a (AsSpf1) in complex with crRNA and target DNA

Imagine if your DNA came with a backspace key — thanks to CRISPR, it kind of does. This idea may seem crazy, and it is, but let me explain. CRISPR is a unique technology that allows scientists to edit parts of the genome by removing, adding or altering sections of the DNA sequence. How does it do this? Well it’s a little complicated. The CRISPR-Cas9 system has two fundamental molecules, the enzyme Cas9 and a piece of RNA called guide RNA (gRNA). gRNA is a small piece of pre designed RNA that contains bases complementary to a specific DNA sequence. This means that the gRNA will only bind to the targeted sequence and will “guide” the Cas9 to the right part of the genome. Cas 9 is playfully referred to as “genetic scissors” as it makes precise cuts in both strands of the DNA at the targeted spot in the genome. When the cell recognizes its DNA is damaged it activates repair mechanisms, allowing scientists to swoop in and insert, delete, or modify genetic material at that site.

Seems amazing right? The one catch is that CRISPR can only target, delete, replace, or modify one gene sequence at a time using a single guide RNA, making it difficult to study multiple genetic changes at once. However, a brand new study at Yale school of medicine has developed a new technologie that can help researchers simultaneously assess the impact of multiple genetic changes involved in a variety of immune system responses. This new tool is called CRISPR-Cas12a, and seems to have huge implications. Sidi Chen, an associate professor of genetics and neurosurgery at Yale School of Medicine and a pioneer in the field of CRISPR technology, led the lab in making four specially engineered mouse lines that allowed the scientists to study “complex genetic interactions and their effects involved in many disorders.”

Using Cas12a Chen’s lab was able to induce and monitor changes in the immune cell in response to gene editing, fine tuning sets of genes in different directions at the same time. The researchers were also able to generate rapid production of new disease and treatment models, including genetic disease in the liver, lung cancer, and skin cancer.

This all represents a huge step forward in the world of CRISPR gene editing, as according to Chen these developments will be a powerful tool for scientists developing new treatments for a wide range of diseases, from cancer and metabolic disorders to autoimmune and neurological conditions.

In fact CRISPR treatment has already been utilized with real patients. A clinical trial launched by the University of Pennsylvania in 2019 used CRISPR to engineer T cells that could better detect and attack cancer cells. The treatment entailed removing three genes that interfered with the immune system’s response to cancer and adding one gene that helped the T cells recognize cancer cells. While the trial focused on safety and the results were modest, the trial proved that CRISPR treatment can be done in a safe and meaningful way. This coupled with the work done in Chens Lab at Yale lays the groundwork for groundbreaking discoveries in the future. 

As a student of AP bio the work being done in the world of CRISPR gene editing is especially interesting as we recently just finished our unit on molecular genetics which centered around DNA, RNA, and Gene Regulation/Expression, topics that are very relevant to CRISPR technology. Having this background made me more curious as I researched the topic. For example we learned in class that before DNA can be transcribed, helicase needs to “unzip” the DNA, which made me wonder what unzips the DNA so the gRNA can bind to the complementary bases? Does Cas9 unwind the DNA due to its job as the “genetic scissors”? Or is helicase itself involved?

Another question I had connected to what I learned in AP bio was about frame shifts. If CRISPR cuts targeted spots in the genome, then how do researchers prevent frame shifts that could cause totally different proteins to be produced? 

If you know the answer to any of these questions please let me know in the comments!

CRISPR-Cas9: The Future of Genetic Medicine

One of the most important discoveries in modern biology is CRISPR-Cas9, which has transformed our ability to precisely edit genes. It was once discovered to be a bacterial immune system, but it has now evolved into a cutting-edge tool that can treat hereditary illnesses that were previously believed to be incurable.

Deoxyribonucleic acid (DNA) orbit

In an interview with biochemist Virginijus Šikšnys, he discusses how CRISPR-Cas9 has made its way from the lab to clinical settings. Šikšnys was one of the authors of the groundbreaking 2012 paper that demonstrated how the Cas9 protein could be used to precisely edit DNA. He and his colleagues showed how Cas9, an efficient genetic modification tool, could be reprogrammed to target and cut any desired DNA sequence, making it an effective genetic modification tool.

What’s incredible is how quickly these discoveries have moved from basic research to real-world treatments. Sickle-cell disease is one of the first illnesses to be treated with CRISPR. This gene-editing technology has already been used to correct mutations in blood cells, offering hope for those suffering from genetic disorders that were previously untreatable.

CAS 4qyz

Despite its success, CRISPR-Cas9 is still evolving everyday. Current treatments are often performed ex vivo, which means that the patient’s cells are removed, altered in a lab, and then returned.. The next step for CRISPR is to be used in vivo, or  directly within the human body. This will require overcoming challenges such as effectively delivering the CRISPR machinery to the right cells and tissues in the body.

CRISPR-Cas9 directly ties into several important topics that we’ve explored in AP Biology, especially those about DNA structure and gene expression. CRISPR relies on our understanding of DNA’s double-helix structure and how the genetic code is stored in nucleotide sequences. This system uses the precise targeting of specific DNA sequences, allowing for gene editing by cutting or modifying the genetic code, which connects to how mutations affect gene function, a concept we’ve studied in gene expression and regulation.  Additionally, CRISPR’s origins in bacteria as an immune system illustrate key ideas from our lessons on prokaryotes and their genetic systems, showing how bacteria store viral DNA to protect themselves from future infections, which is a mechanism that has been repurposed for gene editing in humans.

Cas12a (Cpf1) in complex with crRNA and target DNA

I chose to write about CRISPR because it fascinates me how a discovery meant to protect bacteria from viruses has now become a tool with the potential to cure diseases in humans. The topic of editing genes to treat illnesses like sickle-cell disease or cystic fibrosis makes me feel hopeful for the future of medicine and biology.

Sickle Cell Disease (SCD)

What are your thoughts on the potential of CRISPR to revolutionize medicine? What ethical concerns do you think need to be considered as CRISPR technology advances? What other diseases do you think CRISPR might be used to treat in the future? Leave a comment below!

New CRISPR Technology Can ‘Press Pause’ on Specific Genes

Scientists have discovered a new version of CRISPR that is reversible rather than permanent.

This new genetic tool is known as the IV-A CRISPR system. Traditional CRISPR technology works by producing short RNA strands that help the system locate matching DNA sequences. Then, when the target DNA is identified, the Cas9 enzyme binds to it and cuts, disabling the gene. IV-A CRISPR disables the gene without cutting the DNA by continuously influencing it. This system temporarily turns off genes, offering greater control. For example, researchers could turn off a gene and later turn it back on to see the effect it has.

The schematic diagram of CRISPR-Cas9

Diagram of Cas9 enzyme

Looking ahead, Pausch and his team plan to study how CRISPR molecules change while silencing genes, then explore medical applications. The system could enable precise genome editing, temporary gene expression control, or modify epigenetics, changes in gene function that do not involve changing the DNA sequence. Further research and discovery could lead to huge benefits for both medicine and agriculture. I think that it is amazing the range of possibilities that this technology could have for society but I also wonder about potential controversies that could arise. What do you think? If you have any thoughts that you would like to share please write them in the comments!

This relates to the AP biology topic of genetics. It relates to what we have learned about RNA and DNA. mRNA is made from DNA through transcription and then it is used to make proteins. For CRISPR, they use another kind of RNA in a completely different way. They use it to find a matching DNA sequence rather than code for a protein. It also relates to what we have learned about gene regulation. Both traditional CRISPR technology and IV-A CRISPR are essentially repressing for the gene by influencing the DNA, impacting transcription.

The Giant Y Chromosome: How White Campion Defies Genetic Expectations

Researchers at the University of Buffalo in New York were baffled upon discovering that the Y chromosome of the plant species Silene latifolia, commonly known as white campion, had grown to an enormous size. Typically, in most organisms, the Y chromosome is much smaller than the X chromosome due to genetic degradation over time. However, this particular plant species defied expectations, exhibiting a Y chromosome five times larger than its X chromosome.

Silene latifolia, a species of flowering plant in the carnation family, is known for its distinct sexual dimorphism. Unlike humans, who possess relatively small Y chromosomes, this plant’s Y chromosome has accumulated an astonishing number of genes and repetitive sequences over evolutionary time. Researchers had initially hypothesized that this accumulation was due to an inefficient method of removing non-essential DNA, leading to the bloated genetic material. However, upon further examination, they discovered that the Y chromosome had actively been acquiring genes, making it a key player in the plant’s development and function rather than a withering relic of evolution.

(MHNT) Silene latifolia - flower

Curious to understand this genetic anomaly, the researchers at the University of Buffalo used advanced sequencing technology to map out the entire Y chromosome of Silene latifolia. What they found was remarkable—rather than shedding genetic information like most Y chromosomes, this one was thriving with active, functional genes. Some of these genes were directly related to traits that differentiate male and female plants, including genes regulating flower development and reproductive structures. In essence, this Y chromosome was not a shrinking vestige but a powerhouse of genetic activity.

Such an unusual discovery prompted scientists to investigate whether this phenomenon extended beyond white campion. By comparing its genetic structure to closely related species, they found that some of its relatives also exhibited expanded Y chromosomes, though none to the same extreme. This suggested that the genetic inflation of the Y chromosome was a unique evolutionary path taken by Silene latifolia, possibly influenced by environmental pressures or the plant’s reproductive strategy.

While the discovery of a massive Y chromosome might seem like a niche topic, its implications stretch far beyond botany. Scientists are particularly interested in how this research could inform our understanding of sex chromosome evolution across species, including in humans. The study challenges the traditional view that Y chromosomes inevitably degrade over time and raises the possibility that, under certain conditions, they can expand and acquire new functions.

Furthermore, the research team speculates that the inflation of the Y chromosome may be linked to the plant’s ability to adapt and survive in different environments. By accumulating useful genes, the Y chromosome might be playing a significant role in the plant’s evolutionary fitness. This newfound understanding could lead to broader discussions about the role of sex chromosomes in adaptation and survival, not just in plants but across the biological spectrum.

This topic relates to AP Biology because it connects to the concept of sex-linked traits and chromosomal evolution. In Unit 5, Genetics, we learn about how sex chromosomes determine biological sex and how genes on these chromosomes influence inheritance patterns. The discovery of the expanded Y chromosome in Silene latifolia provides a real-world example of how sex chromosomes can evolve differently in various species. While in humans, the Y chromosome is known for its limited genetic material and degradation over time, in this plant, the Y chromosome has taken a drastically different evolutionary route. Understanding these mechanisms helps reinforce key concepts about gene linkage, chromosomal mutations, and natural selection in genetics.

I came across this fascinating discovery about Silene latifolia and its massive Y chromosome, and it completely challenges what I thought I knew about sex chromosome evolution! Instead of losing genes, it has actively gained them, influencing traits like flower development and reproduction. I love learning about weird exceptions like this because they challenge the “rules” of biology.

This makes me wonder: could similar expansions happen in other species, even outside of plants? And what does this mean for our understanding of sex chromosome evolution in general? Why might this plant have taken such a unique evolutionary path? Do you think environmental factors could play a role?

CRISPR: Ethical Dimensions and The Race for the New Agricultural Revolution

Peter Paul Rubens - Adam and Eve, after Titian, between 1628 and 1629

In the book of Genesis, Satan tells Eve that “God knows that when you eat from [the tree of knowledge] your eyes will be opened, and you will be like God.” As molecular biology and genetic science discover and elevate human knowledge, scientists find themselves considering compelling ethical questions. CRISPR, or clustered regularly interspaced short palindromic repeats, is one of these methods that demands ethical scrutiny. Throughout the course of human history, innovation and technological advancements provoke these philosophical investigations. And for inventions of great destructive and creative potential, a fundamental question arises which confront both CRISPR and the atom bomb. Is it just for humanity to wield divine power? 

On June 28, 2012, CRISPR pioneer Jennifer Doudna and her colleagues published a groundbreaking paper titled “A Programmable Dual RNA-Guided DNA Endonuclease in Adaptive Bacterial Immunity.” Just as Oppenheimer’s atomic bomb started the nuclear arms race, Dr. Doudna recalls how she “remember[s] thinking very clearly… [publishing this paper is] like firing the starting gun at a race.” Despite the extraordinarily dense title, the paper actually revealed revolutionary systems for editing DNA. CRISPR technology’s access to modifying DNA has led to advancements in crop resilience, medical breakthroughs, and anthropological knowledge. Using an enzyme called Cas9 that temporarily separates the 5’ and 3’ strands of DNA similar to the effects of helicase during transcription, scientists can access the nucleobases and match a guide RNA up to the relevant strand. If the guide RNA is complementary, then Cas9 will cut the DNA strand. At this point, the repair mechanisms inherent to cell regulation pounce on the DNA strand in an attempt to repair it. In the repair process, the cell must use an identical DNA strand as a template strand to repair the broken one. But scientists are clever, so at this point, a specially engineered and previously inserted DNA strand becomes the template strand. In Summary the CRISPR process takes advantage of the cell’s repair system by cutting DNA and presenting the cell with the blueprint for how to reconstruct it.

But how does this insertion end up changing our DNA? After all, how can such a tiny difference in DNA affect any biological processes when a single strand of human DNA is six feet long when uncoiled? The answer lies in DNA transcription and translation. After transcription in which a messenger RNA complementary to the template DNA strand is synthesized and processed, the mRNA leaves the nucleus and travels to the cytoplasm where translation occurs. The mRNA is effectively the blueprint for a corresponding amino acid. The mRNA enters a ribosome, where anticodons on tRNA read for the codons on the mRNA. As tRNA carries amino acids into the ribosome’s A site, the right codon-anticodon match will trigger a transfer of the amino acid from the tRNA in the P site to the one in the A site, which shifts over into the P site as its predecessor exits through the E site. The process chugs along until the polypeptide chain is complete, at which point a growth factor terminates the synthesis. Triplets of codons correspond to specific amino acids. As a result, having the right nucleobases and codons in place is crucial for attaining the desired amino acid. Thanks to CRISPR, scientists can now identify weaknesses in present DNA structures and engineer potential solutions by inserting the right DNA instructions. 

I think that CRISPR will bear the greatest fruit in the agricultural sector (no pun intended). I think that there aren’t many ethical dilemmas when it comes to engineering more resilient and abundant crops, as few would oppose solving world hunger. However, regarding livestock and poultry, CRISPR could reveal some ethical problems, specifically when the well-being of the animal is sacrificed for more short-term agricultural gain. What do you think? Will CRISPR lead the world into a new era of food security, or will it open a Pandora’s box of moral issues just as the atomic bomb did.

 

Almost 200 new kinds of CRISPR systems were Revealed by Search Algorithms

Researchers at the McGovern Institute for Brain Research at MIT, the Broad Institute of MIT and Harvard, and the National Center for Biotechnology Information (NCBI) have developed a groundbreaking algorithm to efficiently explore large microbial sequence databases in search of rare CRISPR systems. These systems, found in diverse bact®eria from environments like coal mines, breweries, and Antarctic lakes, could offer new opportunities in biotechnology.

CRISPR, is a revolutionary technology that allows scientists to edit genes with. Originally discovered as a part of the bacterial immune system, CRISPR has been adapted for use in gene editing in a wide range of organisms. The technology works by using a small piece of RNA to guide an enzyme (often Cas9) to a specific location in the genome, where it can make precise cuts in the DNA. These cuts can then be used to disable a gene, repair a faulty gene, or introduce a new gene. CRISPR has many potential applications, including treating genetic disorders, creating genetically modified organisms, and studying gene function.

CRISPR illustration gif animation 1.gif

The algorithm, called Fast Locality-Sensitive Hashing-based clustering (FLSHclust), uses advanced big-data clustering techniques to rapidly sift through massive genomic datasets. It identified 188 new types of rare CRISPR systems, highlighting the remarkable diversity and potential of these systems.

CRISPR systems are part of bacterial defense mechanisms and have been adapted for genome editing and diagnostics. The new algorithm, created by Professor Feng Zhang’s lab, allowed researchers to analyze billions of protein and DNA sequences from public databases in weeks, a task that would have taken months with traditional methods.

The study revealed new variants of Type I CRISPR systems with longer guide RNAs, potentially offering more precise gene-editing tools with fewer off-target effects. Some of these systems could edit DNA in human cells and may be deliverable using existing gene-delivery technologies. Additionally, the researchers discovered Type IV and VII systems with new mechanisms of action that could be used for RNA editing or as molecular recording tools.

The researchers emphasize the importance of expanding sampling diversity to uncover more rare systems, as many of the newly discovered systems were found in unusual bacteria from specific environments.

This research shows the power of advanced algorithms in uncovering the vast functional diversity of CRISPR systems, paving the way for new biotechnological applications. The findings could lead to the development of novel CRISPR-based tools for genome editing, diagnostics, and molecular recording, with potential applications in medicine, agriculture, and environmental science.

In AP Biology, we learned molecular genetics. We learned the structure and function of DNA, gene expression, and genetic variation. CRISPR-Cas9 provides a real-world example of how these concepts are applied in biotechnology. It genetics we are taught that genes can only be passed down from generation to generation and can not be artificially altered. CRISPR technology goes against what we have learned. It teaches us that we can change the genes and DNA of organisms. We can learn about how CRISPR. is used to edit genes in model organisms like  fruit flies to study gene function. We can also use it to study its potential applications in agriculture to create crops with desired traits or in medicine to treat genetic disorders.

When I heard about CRISPR I immediately thought about the ethical concerns regarding the technology. What are the bad things about this technology? What if countries want to create super humans or weapons of mass destruction with CRISPR? This new technology raises many concerns. I definitely feel that this technology needs to be regulated and that only a select few are allowed to use it and experiment with it. What do you think?

The Humane Honey Bee

A recently published study in Molecular Ecology from Penn State introduced the fascinating world of worker honey bees and their altruistic characteristics. These characteristics are shown when worker bees assist the queen bee after being exposed to her pheromone. It involves deactivating their own ovaries, helping to share the pheromone with other workers, and caring for the queen and her eggs. What’s fascinating is that the genes responsible for driving this altruistic behavior can be inherited from either parent. However, the study revealed a twist: these genes only lead to altruism when passed down from the mother, not the father. This finding suggests that the origin of gene inheritance from the mother or father profoundly impacts honey bees’ behavior.

European honey bee extracts nectar

This study also lends strong support to the Kinship Theory of Intragenomic Conflict, which proposes that genes from both parents may be in conflict over which behaviors to support or discourage. As briefly talked about in class, genetic inheritance occurs due to genetic material, in the form of DNA, being passed from parents to their offspring. Genes, which consist of specific DNA sequences, contain the instructions for protein synthesis through the genetic code. Hereditary processes are utilized to read these DNA sequences and assemble proteins accordingly. In essence, genes are the segments of DNA that code for proteins. In the case of honey bees, genes inherited from the mother encourage altruistic behavior that ultimately benefits the queen’s reproductive success, while genes from the father tend to lean more towards self-serving behavior.

To get to these conclusions, the researchers conducted a series of experiments that involved cross-breeding different honey bee lineages. They assessed the responsiveness of worker bees to the queen’s pheromone and observed behavior. This investigation allowed them to identify the significance of maternal or paternal gene expression bias in shaping honey bee behavior. Overall, this study provides insights into the complex world of gene conflicts in honey bees and suggests that gene origin plays a vital role in shaping behaviors.

(Post includes edits suggested by Grammarly)

Unlocking Our Ancient Past: Exploring the Genetic Legacy of Extinct Cousins DNA

Have you ever wondered where we came from? Who we were? What genes truly lie within us, our mothers, fathers? According to a recent research article from ScienceDaily, Neanderthal genetics is one of them, and the genes still affect human life today. In this research article, the researchers from multi-institution teams, including Cornell University, have shown that Neanderthal genes comprise about 1 to 4% of the genome of present-day humans, mostly of those whose ancestors migrated out of Africa. These genomes are not surprising to the scientific community, but their effect on today’s society in human bodies is remarkable. Through a new plethora of computational genetic tools, researchers found the genetic effects of interbreeding between humans of non-African ancestry and Neanderthals that took place 50,000 years ago, as well as the effects on present-day human life. 

Close up of a Neanderthal in a museum

 In a study published in eLife, researchers reported that some Neanderthal genes are essential for specific traits in modern humans. Using an extensive dataset from the UK Biobank consisting of hereditary and trait information of nearly 300,000 Brits, the researchers examined more than 235,000 genetic variants likely to have originated from Neanderthals. They found that 4,303 of those differences in DNA play a vital role in modern humans and influence 47 distinct genetic traits. These genetic traits can include how fast someone can burn calories or a person’s natural immune resistance to certain diseases. Isn’t that unbelievable? How did something from so many years ago affect such a critical part of our lives? Even though they lived thousands of years ago, we all have a part of the Neanderthals in our genetics.

In another article by U.S.News, the idea of immune resistance through our body’s fight against COVID-19 is displayed. The results show that some people who have increased genes from their Neanderthal ancestors may have an increased likelihood of suffering severe forms of COVID-19. These genes, haplotype, increase the risks of hospitalization and not recovering from the virus, showing that having these traits while being able to burn calories fast may cause harm to us as well. As appealing as it might sound, I know it does to me that Neanderthal genes can help in various ways; it is also quite scary. The risk factors of diabetes, heart problems, and obesity can lead to death when mixed with the virus and the gene itself lingering within us. Since these genes are a part of our fundamental hereditary units and will continue to pass down from generation to generation, with all of these effects, this investigation commenced and evolved into an important and crucial step toward understanding where we came from and who we are. Therefore, these traits affect the lives of humans every day in COVID as well as provide multiple factors of traits that we live with every day, not even knowing where they came from.

Hospital HallwayNovel Coronavirus SARS-CoV-2

As an AP Bio student, in Unit 1, we talked about the parts of the cell along with the DNA that is within the cell. These cells are deeply related to what this topic is about, as the process in which genes work revolves around the cell that it is in. First, it starts with transcription, which is the process in which the genetic material is stored in DNA and replicated into a molecule of messenger RNA. The information goes from the DNA in the nucleus to the cytoplasm to carry out protein synthesis. In the cytoplasm, ribosomes make the proteins that create these specific effects mentioned above. Each gene carries instructions for the proteins that determine your features, such as eye color, hair color, height, and, in this case, immune resistance. These two must connect with each other to fully understand how these genes are still here thousands of years later. The answer is that the genetic material has been carried down for this time through each and every ancestor we have had. It’s pretty scary, if you ask me.

Diagram of a gene on a chromosome CRUK 020

I am not the only one who believes that these causes of our ancestral genes are threatening. If you are like me and want to continue learning about this, reach out! As well as anyone with first-hand knowledge of the research or possible medical intervention, please comment! Share your knowledge with me. The custom software discussed in the ScienceDaily link from UCLA is available for free download and use by anyone interested in further research. So, if you are an AP Bio student like I am or just interested in the genes defining us, even though they are from thousands of years ago, join the conversation. These traits and genes are just being figured out, as most of the work started in September 2023. No matter what fears you may have, to leave you with a sense of comfort after a long list of possible effects, modern human genes are prevailing over successive generations. Therefore, this research, although evolving with us, must continue.

Why Does our Hair Flow the Way it Does?

Do you ever wonder why your hair always naturally parts the same way? Our hair patterns can be described as our “hair whorl.” This denotes the direction in which the hair follicles orient themselves, as well as the number of times the hair rotates in a circular pattern. This can be either a single or double whorl. While this physical characteristic maybe be obvious to the naked eye, it is unclear why these patterns initially occur.

Boy with shiny short hair and whorls, rear view

In a recent study, the National Survey of Physical Traits cohort came together to understand whether or not our hair patterns could be determined by genetic characteristics. In China, Lead Investigator Sijia Wang determined that hair whorl can be a result of four genetic variances, also known as a polygenic inheritance. These variances occur at 7p21.3, 5q33.2, 7q33, and 14q32.13, which are specific locations on a DNA sequence. These variances affect hair patterns due to both cell polarity as well as cranial neural tube closure and extension.

This relates to AP Biology due to the effect of cell polarity on the hair whorl. In class we learned that non-polar (hydrophobic) molecules will move away from polar molecules. Hair cells are classified as epithelial cells, meaning they exist on the outer-most layer of our skin’s surface. They are polarized in sheet known as the planar cell polarity (PCP). The author’s logic makes sense in that a pattern will occur in the hairline if the polar molecules are moving away from those that are non-polar, or vice versa.

Blausen 0806 Skin RootHairPlexus

Additionally, because the whorls can be associated with neural tube closures and growths, it was believed that abnormally placed or shaped whorls can be related to a neurological deficit. However, Dr. Wang’s research did not confirm whether or not this was true.

Now it’s your turn — can you find your hair whorl?

 

Progress in Treating Huntington’s Disease Thanks to CRISPR Technology

Scientists have discovered a new way to treat Huntington’s disease, thanks to CRISPR technology. Their research has reduced symptoms of the disease in the mice that they tested on. 

Huntington’s Disease, which is a neurological disorder, is caused by a genetic mutation in the HTT gene. More specifically, repetitive and damaging sequences in the HTT gene cause Huntington’s disease. It causes progressive loss of movement, coordination, and cognitive functions. 

Researchers have discovered a possible solution to these symptoms: CRISPR technology. 

According to the article, “CRISPR is a genome-editing tool that allows scientists to add, remove or alter genetic material at specific locations in the genome.” One of the risks of CRISPR use is that it can affect off-target genes and molecules, causing unwanted alterations in chromosomes and genes. 

Gene

Study author Gene Yeo, PhD, explains how our cells struggle to copy repetitive DNA, which can lead to errors that cause repetitive sequences to increase with each generation. As we learned in class, the process to copy DNA is a complex one where there are many factors at play. DNA is replicated in a semi conservative manner, meaning that the old DNA strands are conserved and combined with the new, complementary strands. There is a replication fork, with a leading and lagging strand, on which DNA is replicated in the 5’-3’ direction. For replication on the leading strand, RNA primase adds RNA, DNA polymerase III adds nucleotides to the open end of the RNA, then a sliding clamp attaches to the DNA polymerase III and slides it along the strand, resulting in the leading strand being synthesized. 

The scientists directly targeted the RNA involved in the DNA replication process to remove toxic protein buildup that is responsible for the mutation in the HTT genes. They were able to complete this process using CRISPR, and without disrupting other important genes. 

After testing on mice, they reported that their research has resulted in improved motor coordination, less striatal degradation and reduced toxic protein levels. These improvements on the mice’s condition lasted for up to 8 months, and had no on other RNA molecules, making scientists optimistic that this treatment could be effective for humans. 

If You Give A Mouse…Sight!

In a recent study published in the Journal Of Experimental Medicine, researchers in China successfully used CRISPR Gene-Editing technology to restore sight to mice with retinitis pigmentosa.

That’s a lot of vocabulary all at once, so let’s establish some definitions first and foremost.  According to the National Eye Institute, retinitis pigmentosa is a “genetic disease that people [and animals] are born with…that [affects] the retina (the light-sensitive layer of tissue in the back of the eye)”. As for CRISPR Gene-Editing technology, YG Topics defines it as, “a unique technology that enables geneticists and medical researchers to edit parts of the genome by removing, adding or altering sections of the DNA sequence”.

Most inherent forms of blindness and loss-of-vision stem from genetic mutations, and thus retinitis pigmentosa is one of many forms of genetically caused blindness.  However, through CRISPR technology, the researchers in the study successfully edited the DNA of mice who had the mutation to eliminate retinitis pigmentosa and give them the ability to see.  The results of the study are very promising, as not only does retinitis pigmentosa affect mice, but human beings.  Thus, there is evidence that CRISPR could be used to cure blindness among everyday people.  Kai Yao, a professor from the Wuhan University of Science and Technology who contributed to the study said, “The ability to edit the genome of neural retinal cells, particularly unhealthy or dying photoreceptors, would provide much more convincing evidence for the potential applications of these genome-editing tools in treating diseases such as retinitis pigmentosa”.

In AP Biology, we discussed how DNA factors into the traits of a living being.  DNA is made up of 3 base codons that form up to 20 different amino acids.  These amino acids code for specific proteins.  Through a process of DNA transcription and translation, the DNA uses various forms of RNA to code for proteins, which help tell the cell what to do.  Thus, the way the cell acts is largely determined by its DNA.  Essentially, DNA codes certain traits through various amino acid sequences.  Mutations and alternations to amino acid sequences cause different traits, such as red hair, blue eyes, or blindness.

Thus, successfully altering the DNA of mice has huge implications for the human race.  CRISPR could potentially be used to edit the DNA of humans, and thus help limit and prevent certain genetic conditions.  Many diseases are based on genetic mutations, and if CRISPR Gene Editing technology is proven successful, we could potentially eliminate genetic diseases in a few decades.  While “much work still needs to be done to establish both the safety and efficacy” of CRISPR technology, some groundbreaking scientific treatments could be coming sooner than you think (Neuroscience News).

Мышь 2

Are You Predisposed to Being Overweight? New Genetic Variations Say Yes.

Recent studies composed by researchers from the Spanish National Cancer Research Centre and the IMDEA Food Institute show that people with a specific variation or version of a gene crucial to cell nutrition tend to accumulate less fat. This means that those with a particular change or alteration in this gene may be inclined to store less fat in their bodies. Prior research has shown that genetics only play a role in 20% of our body weight for the general population. This means that other external factors such as diet, exercise, and overall lifestyle have much more of an impact on body weight.

Past research has identified nearly 100 genetic variants which slightly increase one’s likelihood of having a high BMI. This new research identifies one additional variant. Typically genetic variations are only slightly different versions of a gene and often do not result in visible changes. But, this new variation challenges this idea. It affects the amount of fat the body stores, something which can strongly alter one’s physical appearance. What’s more, the researchers of this gene have found that it is more prevalent in Europe with just under 60% of the population having it.

Ácido desoxirribonucleico (DNA)

 

According to Alejo Efeyan, the head of CNIO’s Metabolism and Cell Signalling Group, the new research can help us to further understand the role which genes play in obesity, body weight, and fat accumulation. Efeyan says, “the finding is a step forward in the understanding of the genetic components of obesity.” Additionally, Ana Ramirez de Molina, the director of the IMDEA Food Institute, claims that a key understanding of cell pathways regarding cell nutrition may affect and spur the creation of not only obesity prevention but also personalized treatments. Essentially, understanding the new gene can help us to target obesity and body weight on an individual level rather than the population as a whole. She believes, “a deep knowledge of the involvement of the cellular nutrient-sensing pathway in obesity may have implications for the development and application of personalized strategies in the prevention and treatment of obesity.”

To find and research the genetic variant which influences fat storage and obesity a team from the IMDEA Food institute collected a variety of data from 790 healthy volunteers. This included body weight, muscle mass, genetic material, and more. The researchers found a “significant correlation between one of these variants in the FNIP2 gene and many of these obesity-related parameters.” Essentially their research proved that there is a connection between the specific gene and factors of obesity. The study has also been published in the scientific journal of Genome Biology. Although this gene may play a role in keeping body fat storage lower than others, it is important to note that it is not entirely a preventative measure against obesity or fat gain. Efeyan clarifies, “It is not at all the case that people with this genetic variant can overeat without getting fat.”

The genetic variation is present in a gene that specifically partakes in a signaling pathway that tells the cell what nutrients are available and needed. The gene signals to the cell what nutrition is necessary at a given moment. In our AP Bio class, we learned the intricacies of cell communication; how and why it can occur, the stages of it, and even the differences in the distances of communication. Connecting back to our AP Bio class, I wonder whether the gene interacts in an adjacent, paracrine, or long-distance manner. Also, how the distance can affect the communication of the gene to the cell regarding cell nutrition. We also learned about how genes in the nucleus of our cells can code for specific factors in our bodies and how they are a sort of ‘instructions’ for us to carry out. This connects to the research as we can see that a change in a gene can alter our body’s fat storage and connection to obesity. The genetic variation changed the ‘instructions’ for weight, fat storage, and obesity disposition. Additionally, the research stated that 60% percent of Europeans have genetic variation, I wonder what may have caused this. Was it a result of their diets, lineage, geography, or just a scientific anomaly? I invite any and all comments with a perspective and an idea as to what may have caused this, along with any comments regarding this research as a whole.

Obesity-waist circumference

 

 

COVID-19 on the Genetic Level

Similar to any other virus, the symptoms of COVID-19 are amplified in patients who are of old age, have additional complications, or are unvaccinated. For instance, researchers found that unvaccinated individuals ages 50 and older are 12 times more likely to die from COVID-19 than individuals who are vaccinated with boosters (Hesman Saey). Additionally, cancer patients, especially those who are immunosuppressed, are at a higher risk of facing the serious impacts of COVID-19. Research suggests that baseline immunosuppression increases the risk of a cytokine storm. Cytokine storms result in extreme immune responses towards a pathogen which can result in harmful conditions for the body or inSARS-CoV-2 without background​​​ some cases death. 

These factors play an important role in the severity of COVID-19, however, there are still some severe cases that are unaccounted for. Throughout the COVID-19 pandemic, one question that has perplexed many scientists is: why do certain healthy patients contract severe cases of COVID-19 while others merely experience the symptoms of the common cold? Recent research has found that genetics may be the answer. Studies have revealed that genes passed down from our ancient ancestors can both help and hurt individuals infected with COVID-19. A global study that took DNA samples from 28,000 patients infected with Covid-19 and about 600,000 healthy patients confirms this theory.

The two main genes taken i3D Structure of Legumin Proteinnto account are toll-like receptor 7 (TLR7) and TYK2. Variants in these genes are what can control the severity of a COVID-19 case. TLR7 is a gene whose protein is responsible for initiating an immune response by sending signals to other cells that a pathogen has invaded the body. If this process is not operating correctly, it is more difficult for the body to defend against a virus. So, if SARS-CoV-2 enters the body, a variation in TLR7 can cause a more severe case of COVID-19. TYK2 is responsible for producing interferons. A variation in TYK2 can cause an overproduction of interferons. When there is a virus present, such as SARS-CoV-2, the production of interferons can be helpful in the body’s defense. 

The processes impacted by TRL7 and TYK2 directly relate to the body’s innate immune process. Innate immunity is the body’s first line of defense once a virus has passed through our innate immune system. The innate immune process involves mast cells which release histamines and macrophages which release cytokines. Interferons work in a similar way. All parts of innate immunity are focused on keeping the pathogen from advancing. Cell signaling is central to innate adaptive immunity, so any alterations in it would result in a less effective defense and therefore a more severe case of COVID-19. 

I found this COVID-19 study to be intriguing because this past January a few members of my household were infected with COVID-19. However, only one experienced extreme symptoms. Since all were vaccinated, it may be possible that the alterations in TLR7 and TYK2 are the reason for the differences in reactions among my family.

Would You Have Survived the Black Death?!?!

New research from McMaster University, the University of Chicago, the Pasteur Institute, and other organizations suggests that during the Black Death, 700 years ago, there were select individuals whose genes actually PROTECTED them from the devastating population-crushing Bubonic Plague.

Model of bubonic plague bacteria - Smithsonian Museum of Natural History - 2012-05-17

The Bubonic Plague, later nicknamed the Black Death after many realised people would develop blackened tissue on their body postmortem, due gangrene(the death of tissue due to lack of blood flow). “It remains the single greatest human mortality event in recorded history, killing upwards of 50 per cent of the people in what were then some of the most densely populated parts of the world.” (ScienceDaily.com)

The team researching this genetic phenomena collected DNA from the deceased 100 years before, during and after the Black Death. They collected samples from the greater London area, as well as some parts of Denmark to accurately represent Upon searching for evidence of genetic adaptation, they found 4 different genes prevalent in the pandemic survivors, all of which are protein-making genes that are used in our immune systems, and found that versions of those genes, called alleles, either protected or rendered one susceptible to plague. We in AP Biology will soon learn more about alleles in higher depth, for they are imperative in the genetics of almost every DNA-carrying organism’s survival.

People with two identical copies of a gene named ERAP2 were able to survive the Black Plague at significantly higher rates than those who lacked that specific gene. “When a pandemic of this nature …  occurs, there is bound to be selection for protective alleles in humans … Even a slight advantage means the difference between surviving or passing. Of course, those survivors who are of breeding age will pass on their genes”.- evolutionary geneticist Hendrik Poinar. Mr. Poinar’s analysis of this research poses a unique and interesting question. Does the natural selection that occurred during the Bubonic Plague mean that you and I have a higher chance of having this gene in our DNA? If another plague with a similar biological makeup to the Black Death, would our bodies be better suited to find it?

Scientists Discover Super-Protein Involved in Gene Replication

For over 50 years, it has been believed all factors that control gene activation in humans were identified and known to scientists. However, researchers from the University of California San Diego and Rutger’s have proved this theory wrong. 

Collegiate professors, and now pivotal contributors to modern science Dr. Jia Fei and James Kadonaga, have discovered a new protein that is involved in the regulation of RNA polymerase. Called NDF (nucleosome destabilizing factor), this gene-building molecule not only unravels nucleosomes, but also “turbocharges” RNA polymerase as it works its way along the DNA strand, improving the synthesis of replicating RNA.

But that’s not all this protein has to offer: NDF has also been found to be in an array of species and organisms, ranging from yeast particles to mammals. This widespread presence suggests that NDF is an ancient factor in the process of gene activation, and has been here since the very beginning. 

NDF works by first interacting with nucleosomes in cells, and then goes on to facilitate transcription– in other words, to replicate strands of RNA. Enzymes called RNA polymerases then come into play, and copy the RNA via dehydration synthesis. This process includes removing oxygen molecules and hydroxides from each nucleotide to covalently bind them together, producing a waste product of water molecules and, finally, a copy of the RNA strand. 

While this newly discovered protein is crucial for the elongation of RNA strands in many organisms, it is especially abundant in humans. Kadanoga reports that it is “present in all [our] tissues,” particularly in stem and breast cells. This makes sense, as NDF has actually been linked to breast cancer; Abnormally high levels of this protein lead to hyperactivity in gene synthesization, which increases the chance of a mutation occurring, and thus cancer. 

With all the remarkable characteristics of NDF, it is crucial that scientists today continue to explore the capabilities and effects of this gene-activating protein, and use it as a basis for studying diseases and phenomenons that occur in the process of gene replication.

RNA recognition motif in TDP-43 (4BS2)

Depiction of RNA strand.

CRISPR Mini | New Territory Unlocked

For over a million years, DNA has centered itself as the building block of life. On one hand, DNA (and the genes DNA makes up) shapes organisms with regard to physical appearance or ways one perceives the world through such senses as vision. However, DNA may also prove problematic, causing sickness/disease either through inherited traits or mutations. For many years, scientists have focused on remedies that indirectly target these harmful mutations. For example, a mutation that causes cancer may be treated through chemotherapy or radiation, where both good and bad cells are killed to stop unchecked cell replication. However, a new area of research, CRISPR, approaches such problems with a new perspective.

The treatment CRISPR arose to answer the question: what if scientists could edit DNA? This technology involves two key components – a guide RNA and a CAS9 protein. Scientists design a guide RNA that locates a specific target area on a strand of DNA. This guide RNA is attached to a CAS9 protein, a molecular scissor that removes the desired DNA nucleotides upon locating them. Thus, this method unlocks the door to edit and replace sequences in DNA and, subsequently, the ways such coding physically manifests itself. Moreover, researchers at Stanford University believe they have further broadened CRISPR’s horizon with their discovery of a way to engineer a smaller and more accessible CRISPR technology.

This study aimed to fix one of CRISPR’s major flaws – it is too large to function in smaller cells, tissues, and organisms. Specifically, the focus of the study was finding a smaller Cas protein that was still effective in mammalian cells. The CRISPR system generally uses a Cas9 protein, which is made of 1000-1500 amino acids. However, researchers experimented with a Cas12f protein which contained only 400-700 amino acids. Here, the new CasMINI only had 529 amino acids. Still, the researchers needed to figure out if this simple protein, which had only existed in Archaea, could be effective in mammals that had more complicated DNA.

To determine whether Cas12f could function in mammals, researchers located mutations in the protein that seemed promising for CRISPR. The goal was for a variant to activate a protein in a cell, turning it green, as this signaled a working variant. After heavy bioengineering, almost all the cells turned green under a microscope. Thus, put together with a guide RNA, CasMINI has been found to work in lab experiments with editing human cells. Indeed, the system was effective throughout the vast majority of tests. While there are still pushes to shrink the mini CRISPR further through a focus on creating a smaller guide RNA, this new technology has already opened the door to a variety of opportunities. I am hopeful that this new system will better the general well-being as a widespread cure to sickness and disease. Though CRISPR, and especially its mini version, are new tools in need of much experimentation, their early findings hint at a future where humans can pave a new path forward in science.

What do you think? Does this small CRISPR technology unlock a new realm of possibility or does it merely shed light on scientists’ lack of control over the world around us?

Unnatural Selection: The Future of The Future?

Imagine it’s Saturday night, you are snowed in until the morning and you need a way to pass the time. Like many people, you resort to Netflix. Upon browsing through the vast selection of horror, comedy, and romantic films, you decide you are in the mood for a documentary. Scrolling through the options, you stop at a title that grabs your attention: Unnatural Selection.

Since you are an AP Biology student, you immediately connect the words “Natural Selection” to the work of Charles Darwin, the study of genetics, and most importantly: evolution. In brief, natural selection is the survival and reproduction of the fittest, the idea that organisms with traits better suited to living in a specific environment will survive to reproduce offspring with similar traits. Those with unfavorable traits may not be able to reproduce, and therefore those traits are no longer passed down through that species. Natural selection is a mechanism for genetic diversity in evolution, and it is how species adapt to certain environments over many generations.

If genetic diversity enables natural selection, then what enables unnatural selection? Well, If natural selection eradicates unfavorable traits naturally, then unnatural selection essentially eradicates unfavorable traits or promotes favorable traits artificially.

The Netflix docuseries “Unnatural Selection” focuses on the emergence of a new gene-editing technology named CRISPR (an acronym for “Clustered regularly interspaced short palindromic repeats”). CRISPR is a revolutionary new method of DNA editing, which could help cure both patients with genetic diseases and patients who are at risk of inheriting unwanted genetic diseases. The two pioneers of this technology, Emmanuelle Charpentier and Jennifer Doudna, recently won Nobel Prizes in Chemistry for their work on CRISPR.

CRISPR illustration gif animation 1

Animation of CRISPR using guide RNA to identify where to cut the DNA, and cutting the DNA using the Cas9 enzyme

CRISPR works with the Cas9 enzyme to locate and cut a specific segment of DNA. Scientists first identify the sequence of the human genome, and locates a specific region that needs to be altered. Using that sequence, they design a guide RNA strand that will help the Cas9 enzyme, otherwise known as the “molecular scissors” to locate the specific gene, and then make precision cuts. With the affected region removed, scientists can now insert a correct sequence in its place.

Using the bacterial quirk that is CRISPR, scientists have essentially given anyone with a micropipette and an internet connection the power to manipulate the genetic code of any living thing.

Megan Molteni / WIRED

CRISPR is just the beginning of gene editing, introducing a new field of potential gene editing research and applications. But with great power comes great responsibility — and great controversy. Aside from the obvious concerns, people speculating the safety, research, and trials of this new treatment, CRISPR headlines are dominated by a hefty ethical dilemma. On one hand, treating a patient for sickle cell anemia will rid them of pain and suffering, and allows their offspring to enjoy a normal life as well. However, by eliminating the passing down of this trait, sickle cell anemia is slowly eliminated from the human gene pool. Rather than natural selection choosing the path of human evolution — we are. We are selecting which traits we deem “abnormal” and are removing them scientifically. Although CRISPR treatment is intended to help people enjoy normal lives and have equally as happy children, putting evolution into the hands of those evolving can result in more drastic effects in the future.

For our generation, CRISPR seems like a magical cure for genetic diseases. But for future generations, CRISPR could very well be seen as the source of many problems such as overpopulation, low genetic diversity, and future alterations such as “designer babies.” Humans have reached the point where we are capable of our future. Is CRISPR going to solve all of our problems, or put an end to the diverse human race as we know it? Comment how you feel down in the comments.

 

Paving The Way For Discovery: Gene Editing In Ticks

What is something that reminds you of summer and your childhood? For me, it is ticks. I know it sounds strange, but the constant reminders from my parents to “check for ticks” after long summer walks are ingrained in my memory. Although the practice of checking for ticks is common, we don’t often stop to question why, or take a moment to expand our knowledge as to just how dangerous a summer walk in long grass could be. Ticks, although tiny, are powerful, disease ridden organisms and have the potential to spread diseases to humans such as Lyme’s disease, Babesiosis, Anaplasmosis, Tularemia, etc. 

tick

Despite their ability to pass on such a vast variety of pathogens, research on ticks is extremely limited, especially in comparison to similar organisms like mosquitoes. The challenge when it comes to gene editing in ticks is that tick embryos are very difficult to inject due to high pressure in the eggs, a hard outer shell on the egg, and a wax layer outside the embryo created by Gene’s organ. In a recent study published in iScience, researchers developed a tick-embryo injection protocol that aimed to target gene disruption with CRISPR-Cas9 (using both embryo injection and Receptor-Mediated Ovary Transduction of Cargo. In this technique, researchers removed Gene’s organ to prevent the wax coating along with treating the eggs with chemicals such as benzalkonium chloride and sodium chloride to remove the outer shell and relieve the inner pressure. Gulia-Nuss, the co-author of the study and a molecular biologist at the University of Nevada, states: “Another major challenge was understanding the timing of tick embryo development. So little is known about tick embryology that we needed to determine the precise time when to introduce CRISPR-Cas9 to ensure the greatest chance of inducing genetic changes.”

Essentially, the CRISPR-Cas9 system consists of two main molecules that introduce a mutation to the DNA. The first is an enzyme known as Cas9. The function of this enzyme is to cut the strands of DNA at a specific location in order for pieces to be added or removed. As we learned in AP Bio, enzymes are key when it comes to DNA and DNA replication, for they play a variety of roles that allow DNA to replicate the way it does. For example, helicase untwists the double helix at the replication fork, topoisomerase relieves the strain of twisted DNA strands by breaking and rejoining them, and primase synthesizes short RNA strands that act as a primer. Without these enzymes and their very specific purposes, DNA would not be able to replicate. In the case of Cas9, it performs the essential job of cutting DNA in order for gene editing to occur. The second piece of the system is a piece of RNA called guide RNA. The guide RNA binds to a specific sequence in the DNA due to its RNA bases that are complementary to those of the DNA sequence. 

Prior to this study, no lab had displayed the possibility for gene editing in ticks, due to the daunting technical difficulties of such a task. This study is proof to embrace the difficulty and the challenges, in life and in science, for often the most difficult of tasks lead to the greatest outcome. In the case of this study, the discovery of ways in which to target the disruption of genes in ticks will pave the way to the uncovering of the molecular biology of tick-pathogen-host interactions, hopefully in the long run creating ways to prevent and control tick-borne diseases, a process that has the potential to save lives.

Page 1 of 4

Powered by WordPress & Theme by Anders Norén

Skip to toolbar