BioQuakes

AP Biology class blog for discussing current research in Biology

Our close cousins, Denisovans

Denisovans

Evolution is the change in the heritable characteristics of biological populations over successive generations. Evolutionary processes give increase biodiversity at every level of biological organization, including the levels of species, individual organisms, and molecules.

We once thought that the neanderthals were the only relatives but recent studies show that the Denisovans also interbred with humans.

This picture represents the spread of the Denisovans.

Modern humans are now the only human lineage left alive but others not only lived alongside modern humans, but also interbred with them, leaving behind DNA in the human genome. But with enough evidence, it has been proven that the mysterious Denisovans are relatives of modern humans. Denisovans also harbor a small amount of especially exotic DNA, probably from breeding with “super-archaic” humans that split from the others over 1 million years ago.

Previous research discovered that while Denisovans shared a common origin with Neanderthals, they were just as genetically distinct from Neanderthals as Neanderthals were from modern humans.

This diagram shows the spread of human.

According to researchers, ancestors of Oceanians interbred with a southern group of Denisovans, while the ancestors of East Asians mixed with a northern group.”The implication is that there were at least three instances of modern humans interbreeding with archaic humans — one with Neanderthals and two with Denisovans,” Browning said. “To me, this suggests that modern humans weren’t so very different from Neanderthals and Denisovans. There are signs that intermixing with archaic humans was occurring in Africa, but given the warmer climate, no one has yet found African archaic human fossils with sufficient DNA for sequencing,”

 

 

i-motif: A new form of DNA discovered

Australian researchers have discovered a new structure of DNA called i-motif. This form of DNA is in the shape of a twisted knot, vastly different from the conventional double helix model. i-motif basically looks like a four-stranded knot of DNA. In the i-motif form, the C bases on the same strand of DNA bind to each other instead of their complementary pairs.

File:G-quadruplex.gif

(Photo: Wikimedia Commons)

How did scientists discover i-motif?

i-motif previously haven’t been seen before, apart from in in-vitro (which means under laboratory conditions and not in the natural world) To detect i-motif, scientists used a tool made up of a fragment of an antibody molecule. This antibody could recognize and attach to i-motifs. Researchers showed that the i-motif structures mostly formed at the G1 phase -when mRNA is synthesized- in a cells life cycle. The i-motifs show up in promoter regions and in telomeres in the chromosome.

While scientists aren’t really sure the actual reason for their existence, some researchers suggest that they are there to help switch genes on and off and affect whether or not a gene is actively read.

Whatever the reason for their existence, they have potential to play an important role in how and when DNA is read. Prof Marcel Dinger at the Garvan Institute for Medical Research says, “It’s exciting to uncover a whole new form of DNA in cells — and these findings will set the stage for a whole new push to understand what this new DNA shape is really for, and whether it will impact on health and disease.”

The Behavioral Causes of Obesity

Obesity is a big issue that is affecting the world today. Obesity is mostly caused by abnormal eating habits, which include overeating, but little is known about what causes overeating. To further understand the behaviors that lead to overeating and obesity, scientists from the Centre for Genomic Regulation and the Pompeu Fabra University in Barcelona, Spain conducted research on mice. There findings were published in Addiction Biology.

The scientists put the mice in an environment where they are only fed high calorie foods. Their diet consisted of chocolate bars and their normal food. As the mice started to gain more weight, they started to become addicted to chocolate and started binge-eating it. They would eat the chocolate over their normal food, even though they were more full from eating their own food. Their new binge eating habits also changed their eating schedule. They started eating during the day, rather than at night.

In conclusion, this research made scientists aware that some people can be trapped in a binge eating state which can lead to obesity. Obesity is not just a metabolic disease, but is caused by behavioral issues. This research is helpful because people can now take preventative measures and go to therapy to change these eating habits. This research is very interesting because it can help solve obesity issues. To learn more about obesity behaviors and treatment, click here and here. 

Striped Field Mouse

 

The Genetic Secrets in Monkey Poop!

 

We’ve learned that two distinct species cannot produce viable hybrid offspring, BUT…

A researcher from Florida Atlantic University has documented that two genetically distinct species of guenon monkeys in Gombe National Park in Tanzania, Africa, have been successfully mating and producing hybrid offspring for hundreds or thousands of years! How did she learn this? From their poop!

Earlier Knowledge: Previous studies showed that guenon monkeys’ widely varying physical traits keep them from interbreeding because of mate choice. In other words, a male monkey won’t be attracted  to/mate with a female unless her face matches his. Therefore, blue monkeys and red-tailed monkeys (two different species) wouldn’t be expected to mate. The two species currently live in close proximity to each other in narrow riverine forests along Lake Tanganyika in Gombe National Park, and Kate Detwiler has been studying them for years.

 

Red-Tailed Monkey https://www.flickr.com/photos/derekbruff/13353495075

Blue Monkey https://commons.wikimedia.org/wiki/File:Blue_monkey_(Cercopithecus_mitis_stuhlmanni)_pair.jpg

 

 

 

 

 

 

The Breakthrough: Kate Detwiler, author and an assistant professor in the Department of Anthropology in FAU’s Dorothy F. Schmidt College of Arts and Letters, challenges this claim that red-tailed and blue monkeys don’t mate. She studies the extent and pattern of gene flow from “red tailed” (Cercopithecus ascanius) monkeys to “blue” monkeys (Cercopithecus mitis) due to hybridization. Detwiler observes and studies the two monkey species in Gombe National Park, and recognizes hybrids by combined markings of the two parent species. She estimates 15% of the population are hybrids!

The Evidence: Detwiler uses mitochondrion DNA extracted from the monkey species to show movement of genetic material from one guenon species to another. More specifically, she examined fecal samples and found that all of the monkeys (hybrids, blues, and red-tails) have red-tailed mitochondrial DNA traced back to female red-tailed monkeys. Using mitochondrial DNA was the best option because it is more abundant than nuclear DNA and only comes from the mother. In her study, her control group was a group of blue monkeys outside the park; when she extracted DNA from these monkeys, she found that they only had blue monkey DNA. Upon studying the hybrid monkeys, Detwiler found no consequences of cross breeding.

Detwiler’s Theory: The key finding made from Kate Detwiler’s study is that blue monkeys in Gombe National Park emerged out of the hybrid population. She speculates that red-tailed monkeys got to Gombe Natoinal Park first and thrived. Male blue monkeys had to leave their original homes outside the park and then mated with red-tailed females. How was the hybrid population sustained? Detwiler believes that the monkeys have learned socially that if you grow up in a hybrid group it is okay to mate with any other monkey.

So What? “The Gombe hybrid population is extremely valuable because it can be used as a model system to better understand what hybridization looks like and how genetic material moves between species,” said Detwiler. This is especially important because hybridization often occurs in response to environmental changes, and climate change is happening now! Who knows what hybrids we will see in the future? Check out the full article here to read more about this fascinating study!

 

 

 

 

Single father birds taking care of their babies

 Researchers at University of Bath, studied six different populations of plovers located across Africa, Asia and Latin America. The three populations of plover birds had a balance in the sex ratio of males to females and shared parenting of their offspring. The scientists found that in populations when there were more males than females, or vice versa, the parenting roles shifted leaving the males to look after the chicks.

Professor Tamás Székely, Professor of Biodiversity at the Milner Centre for Evolution at the University of Bath said: “When there are more males in the population, the females have more opportunities to find partners and so they are more likely to leave the family and mate with multiple partners in the breeding season, leaving their male partner to look after the chicks.”

According to the researchers, it is harder for male plovers  to get another partner. Therefore, they are more likely to stay monogamous and be the primary parent and invest time in raising their offspring. Influencing mate availability, the adult sex ratio can change social behaviour with divorce, infidelity, and parental antagonism due to being more common in sex-biased populations.

The study, published in Nature Communications, took data collected over 10 years from six wild shorebird populations that were closely related but displayed different parental strategies.

Dr Luke Eberhart-Phillips said: “We found that the chicks had a 50:50 sex ratio at hatching in all these species, and that the skewed adult sex ratios were caused by a difference in survival of male and female juveniles, although it’s still unclear why this happens.

“Our study highlights the knock-on effects that differences in survival rates between the sexes can have on population dynamics and social behaviour.”

The researchers continue to investigate how sex ratio and population affects social behavior.

Brain Scans Suggesting Schizophrenia?

Schizophrenia is a mental disorder that usually starts between ages of 16 and 30. The symptoms vary from individual to individual, but common symptoms include hallucinations, delusions, and distorted perception. It is suspected usually in teens that have anxiety, depression, or sleep problems. However those symptoms do not always mean this teen has or will develop schizophrenia, usually only about ⅓ of these teens actually develop schizophrenia.

Researches now may have found a special “fingerprint” for the brain to determine if schizophrenia is likely before symptoms emerge. This “fingerprint” is really folds found within the brain. The method looks at MRI scans of the brain and the correlation between the amounts of folds in certain areas, reflecting the strength of connections in these areas. Researches composed an experiment to see how effective this method was at determining one’s likelihood of developing schizophrenia.

Photo Credit: Jurgitta (https://commons.wikimedia.org/wiki/File:Schizophrenia_brain_large.gif)

The research team collected MRI scans from a group of people in Switzerland, averaging the age of 24. The participants in this study included 79 people with suggestive symptoms of developing schizophrenia and 44 healthy control individuals. The researchers followed all of the participants for four years and found that 16 people in the high-risk group developed schizophrenia. After looking back through the brain scans, the researchers found that 80% of the time, the relationship between the folding patterns of the brain and the individuals who developed schizophrenia correlated. The individuals that developed schizophrenia brain scans seemed to have a “disorganized brain network”, meaning the folds of their cortical regions didn’t go hand in hand as much as the folds in the controls and the high-risk people who didn’t develop the illness. (The cortical regions of the brain refer to the cerebral cortex).

Although not yet perfected, this technique could be very useful in determining out of the individuals who have schizophrenia symptoms, their likelihood of actually developing this disorder.

Climate Concerns and Rising Sea Levels: Antarctic Edition

    Photo Source

   Climate change has been a recent concern as it affects all aspects of human life. More evidence to climate change and the rise of sea levels was expressed in a very recent study conducted by IMAS PhD student: Alessandro Silvano. By doing so, he ultimately found that this process quickens the rate that ice melts and sea levels rise.

The study was conducted using ocean measurements off the coast of east Antartica. The study showed that glaciers are freshening the ocean, as the glaciers do not consist of salt. This dilutes the natural salt content of the ocean. He found that the melted water from the glaciers causes the ocean’s surface layer less salty and more buoyant, which prevented deep mixing during the winter months. Therefore it allowed warm water to retain its heat and melt glaciers from below. This process allowed the water to exist in layers, similar to when one attempts to mix oil and water. The study found a positive feedback mechanism, in which glacial melt water caused further melting of ice shelves, leading to an increase in sea level.

In some areas around Antartica, the study also found fresh meltwater decreased the formation and sinking of dense water. This results in decreasing the rate of ocean circulation, which stores heat and carbon dioxide. Because the cold glacial melt waters cause a slowing of the currents, which then decrease the ocean’s ability to decrease carbon dioxide and heat from the atmosphere. These two processes feed off of each other and induce and speed up climate change.

I enjoyed reading this article because I am personally passionate about decreasing the rate of climate change and educating myself on global warming. Backing global climate change due to its concerning effect – only one of which is sea level – with scientific evidence is important for gaining support of our communities.

Secondary Source Article: The Washington Post: One of the most worrisome predictions about climate change may be coming true

Not All Giraffes Are Just Giraffes

Up until now Giraffes have been considered a singular species with nine subspecies.  Recently scientist from Senckenberg and the Giraffe Conservation Center have studied the genetic makeup of giraffes throughout the continent. The samples were taken through skin biopsies of the Giraffes. The analysis of these samples have proved that there is not “only one, but at least four genetically highly distinct groups of giraffes.” These giraffes also seem to not mate in the wild. This discovery of four genetically different groups of giraffes means that the traditional way of classifying giraffes is in need of an upgrade. The traditional  way of determining species of giraffes was based on coat patterns, horn structures, and geographical distribution. The new way of classifying species is based on their genetic structure. The four species based on genetics would be “southern giraffe (Giraffa giraffa), comprising two distinct subspecies, Angolan (G. g. angolensis) and South African giraffe (G. g. giraffa), (2) Masai giraffe (G. tippelskirchi), (3) reticulated giraffe (G. reticulata), and (4) northern giraffe (G. camelopardalis), which includes Nubian giraffe (G. c. camelopardalis), West African giraffe (G. c. peralta) and Kordofan giraffe (G. c. antiquorum) as distinct subspecies.” Not only did this study differentiate species but brought some older species of giraffes. This new discovery not only changes the way we refer to giraffes but how species conservation is carried out. Now not only is the giraffe under threat but their biodiversity is also under severe attack.

By LucaGaluzzi
https://commons.wikimedia.org/wiki/User:Lucag

If you want to read more on giraffe conservation you can click here.

A New Kind of DNA

Scientists at the Garvan Institute of Medical Research in Australia have discovered a new form of DNA in our cells. They’ve found that this DNA does not look the same as the traditional double-helix we are all familiar with, but instead is in the shape of a four stranded “knot”. This new DNA is called i-motif. Scientists not only know the shape of this new type of DNA, they also know how it differs from helical DNA and where it is located. Unlike helical DNA in which the Cs and Gs bind, the Cs on the same strand in the i-motif bind together.

Source: https://www.sciencedaily.com/releases/2018/04/180423135054.htm

In order to locate the i-motifs in the cells, researchers developed a new tool than can recognize this type of DNA. This tool is a fragment of an antibody that attaches to the i-motif DNA molecule. They used fluorescence techniques to find exactly where in the nucleus of human cells the i-motif DNA was.

Scientists also have concluded that the i-motifs most likely form at the late G1 phase. They appear in the telomere and promoter regions.

 

What You Eat Now Matters Later!

 

Researchers from the Novo Nordisk Foundation Center for Basic Metabolic Research at the University of Copenhagen have potentially uncovered the cause for developing obesity. This process involves precursor cells, the fatty acid palmitate and the hormone TNF-alpha.

^Above is a photo of fat tissue

What are precursor cells and how does it work? 

A precursor cell is an immature cell that has not undertaken a specific role in the body yet, for example a mature cell would be considered a muscle cell. When this cell comes in contact with the fatty acid palmitate and the hormone TNF-alpha it is disrupted. This interaction will cause future damage; it causes the cell to develop into a dysfunctional fat cell. Obese patients with type two diabetes will often contain these types of reprogramed cells.

How were these cells discovered?

The researchers collected physical data from multiple types of patients with 43 planned opporations. They retrieved fat tissue from 15 lean patients, 14 obese patients, and 14 obese patients with type two diabetes. When they compared the data from the three groups of patients they noticed that the fat cells from the obese patients with type two diabetes were not normal fat cells, they were reprogrammed cells that did not function like normal fat cells. Once they realized this, the researchers were able to recreate the reprogrammed cells by exposing precursor cells to the palmitate and hormone TNF-alpha. In just 24 hours they were able to complete the process successfully!

What can I do with this information?

These results illustrate how essential it is for you to maintain a healthy diet and lifestyle. It proves that your habits now will affect you in the future. This is why people should learn about how to live a healthy lifestyle at a young age. The younger the better, because it would decrease the chances of precursor cells to be transformed into abnormal fat cells for your future life.

The future:

Hopefully, this study sparks new ideas and discoveries regarding preventative obesity tactics. The researchers hope to discover a way to reverse the abnormal programing of the fat precursor cells. If researchers could figure out a way to reverse this programing how much safer could obese patients become? Could this research impact the education systems, forcing health classes earlier in students lives? This article interested me because I am always focused on how my decisions will affect me in my future, however I never thought of this with my eating habits.

The More You Sit, The More You Forget!

Researchers from the University of California, Los Angeles recently discovered a linkage between the memory of middle to older aged adults and their sedentary behaviors, actions that require little energy like sitting or lying down.

They concluded that long periods of sitting, like at a desk chair, affects the specific region of the brain that is involved in creating new memories, the medial temporal lobe. The UCLA researchers closely studied 35 people ages 45 to 75 years old, documenting their physical activity for two weeks prior to and during the study.  After the three months of research, they used a high resolution MRI scan and quickly noticed similarities between the thickness of each adult’s medial temporal lobe who spent on average the same amount of hours sitting everyday. The more hours spent sitting, regardless of any physical activity, the more thin the medial temporal lobe. “The participants reported that they spent from 3 to 7 hours, on average, sitting per day. With every hour of sitting each day, there was an observed decrease in brain thickness, according to the study. ”

Even though the findings of this study are preliminary, it suggests that “reducing sedentary behavior may be a possible target for interventions designed to improve brain health in people at risk for Alzheimer’s disease.” Becoming more active is always a great thing, but becoming conscious of how much time you spend being inactive and working to decrease that, could help you out more than you think. There is still more research to be done on this matter but this is a step in the right direction for improving life for those with memory related diseases and improving overall brain health.

To read more check out the full article here!

GATTACA is Here!

            In August of 2017 Scientists finally had figured out how to successfully edited genes in human embryos in order to treat serious disease-causing mutation using advanced CRISPER/Cas9. This is a  major milestone as it brings scientists closer to the reality of being able to genetically engineer babies in order to re

File:CRISPR-Cas9-biologist.jpg

Photo by J Levin W

pair faulty genes. This concept has always been feared due to the lack of success and safety of previous genetic tests, however, this study proves that scientists can now successfully edit genes.“We’ve always said in the past gene editing shouldn’t be done, mostly because it couldn’t be done safely,” said Richard Hynes, a cancer researcher at the MassachusettsInstitute of Technology who co-led the committee. “That’s still true, but now it looks like it’s going to be done safely soon,” he said, adding that the research is “a big breakthrough.” Genetic testing has also been regarded as unethical due to the possibility of eugenics, in which wealthy families would pay to have their embryos adjusted to get enhanced cosmetic traits such as height and muscle mass. “What our report said was, once the technical hurdles are cleared, then there will be societal issues that have to be considered and discussions that are going to have to happen. Now’s the time.” This successful study has come out only months after a national scientific committee recommended new guidelines for modifying embryos in which they strongly urge gene editing be used solely for severe hereditary medical conditions.

Crispr is coming soon to hospitals and medical facilities near you

In 2013, researchers demonstrated a type of gene editing ,called Crispr-Cas9, which could be used to edit living human cells. This means that DNA could be altered. It has been tested in labs, but now it is going to be tested on humans.
Crispr Therapeutics applied for permission from European regulators to test a code-named CTX001, in patients suffering from beta-thalassaemia, an inherited blood disease where the body does not produce enough healthy red blood cells. Patients with the most severe form of the illness would die without frequent transfusions.
If the trials are successful, Crispr, Editas and a third company, Intellia Therapeutics, plan to study the technique in humans with a bigger range of diseases including cancer, cystic fibrosis, hemophilia and Duchenne muscular dystrophy.

Since China is more lenient when it comes to human trials, several studies are already happened, but there was no conclusive data.
Katrine Bosley, chief executive of Editas, says the field of gene editing is moving at “lightning speed”, but that the technique will at first be limited to illnesses “where there are not other good options”.

The reason for this is because, as with any new technology, scientists and regulators are not fully aware of the safety risks involved. “We want it to be as safe as it can, but of course there is this newness,” says Ms Bosley.

Although Crispr-Cas9 has not yet been trialled in humans in Europe or the US, it has already benefited medical research greatly by speeding up laboratory work. It used to take scientists several years to create a genetically modified mouse for their experiments, but with Crispr-Cas9 “transgenic” mice can be produced in a few weeks.
Despite the sucesses, the field of gene editing has been hampered by several setbacks. Editas had hoped to start human trials earlier, but was forced to move the date back after it encountered manufacturing delays. Crispr has lost several key executives in recent months, while Cellectis had to suspend its first trial briefly last year after a patient died.

Crispr is in its beginning stages ,and although it is not yet mainstream, it is expected to be completely groundbreaking in the field of medicine.

Closer to Reality: Gene Editing Technology

In August of 2017, scientists in the United States were successful in genetically modifying human embryos, becoming the first to use CRISPR-cas9 to fix a disease causing DNA replication error in early stage human embryos. This latest test was the largest scale to take place and proved that scientists were able to correct a mutation that caused a genetic heart condition called hypertrophic cardiomyopathy.

CRISPR-cas9 is a genome editing tool that is faster and more economical than othe r DNA editing techniques. CRISPR-cas9 consists of two molecules, an enzyme called cas9 cuts strands of DNA so pieces of DNA can be inserted in specific areas. RNA called gRNA or guide RNA guide the cas9 enzyme to the locations where impacted regions will be edited.

(Source: Wikipedia Commons)

 

Further tests following the first large-scale embryo trial will attempt to solidify CRISPR’s track record and bring it closer to clinical trials. During the clinical trials, scientists would use humans- implanting the modified embryos in volunteers and tracking births and progress of the children.

Gene editing has not emerged without controversy. While many argue that this technology can be used to engineer the human race to create genetically enhanced future generations, it cannot be overlooked that CRISPR technology is fundamentally for helping to repair genetic defects before birth. While genetic discrimination and homogeneity are possible risks, the rewards from the eradication of many genetic disorders are too important to dismiss gene editing technology from existing.

 

The Weirder Side of CRISPR

If you’ve been following science news at all, you’ve heard of CRISPR, the gene-editing tool which is rapidly becoming a very hot topic. Since its discovery, CRISPR has been used for some truly extraordinary things. It’s also done some other things, which stray from medical miracles into the realm of the strange.

Alphr.com reports some of the weirder projects using CRISPR. This includes manufacturing super-dogs, as well as the possibility of bringing back the woolly mammoth! This is all being done as you read this through CRISPR CAS-9

Another project mentioned in the article is an effort to create organs in pigs suitable for human transplants. This has become a larger topic of conversation, as there is always an ample need for organs, and if this project comes to fruition, waiting lists for organ transplants could possibly be abolished completely.

To read the other weird projects using CRISPR right now, check out the article.

Comment below your thoughts on this article, and the uses of CRISPR in general. I, for one, would love to see a mammoth before my own eyes!

Crispr-Cas9 is the gateway to a new frontier in genetic engineering. Here’s The good and the bad.

For a number of years now, molecular biologists have been diving increasingly further into the field of genome editing. The latest development into the field is the emergence of CRISPR-Cas9. CRISPR-Cas9 has risen to prominence over other potential methods of genome editing due to its relatively simple construction and low cost. CRISPR-Cas9’s original primary and intended purpose was to help fix mutations within DNA, and with this it could theoretically help eradicate entire diseases. This application of CRISPR is wholly positive, however with the increasing prevalence of the technique other potential uses have been discovered, and some of these potential uses raise profound ethical questions.

One of the main concerns of people skeptical about CRISPR is their assertion that once the door to the wholesale genetic editing of offspring is open, there is no going back. This, on its own, is a reasonable concern. The ability to choose a child’s sex, eye color, hair color and skin complexion is very likely to be made available to by CRISPR in the coming years. CRISPR does not yet have the capability to influence more abstract elements of the genome, such as intelligence and athletic ability, but this may not be far off. There are legitimate concerns that this is a slippery slope towards a dystopian society similar to the one seen in the movie Gattaca, where society is stratified into two distinct classes: those who are genetically engineered and those who are not.

Another concern raised by some scientists is the overall safety of genetic editing. A potentially very hazardous negative result of CRISPR is the possibility of an “off target mutation.” An off target mutation is the result of CRISPR mutating something other than the intended part of the genome and it could have disastrous consequences. Now, many scientists believe that with further advancements in the field the likelihood of something like an off target mutation occurring could be reduced to almost zero. However, it is important to examine the risks of any new process, and the prospect of something like an off target mutation occurring is certainly noteworthy.

For more information click here.

CRISPR: The Next Step for Cancer Treatment

CRISPR is a gene editing technique that is currently still being researched and expanded upon, however, upon recent discoveries, one can note the great advantages this technology brings to the table to enhance cancer immunotherapy .  More specifically, according to the Washington University School of Medicine, “these T cell immunotherapies can’t be used if the T cells themselves are cancerous.” However, there is more to this discovery. Let’s backtrack.

What exactly is CRISPR? “CRISPR technology is a simple yet powerful tool for editing genomes. It allows researchers to easily alter DNA sequences and modify gene function. Its many potential applications include correcting genetic defects, treating and preventing the spread of diseases and improving crops. However, its promise also raises ethical concerns.” For the sake of this article, we are just focusing on the benefits it has on cancer treatment solely. Also, what exactly are T cells? They are “a type of white blood cell that is of key importance to the immune system and is at the core of adaptive immunity, the system that tailors the body’s immune response to specific pathogens. The T cells are like soldiers who search out and destroy the targeted invaders.” On the other hand, T cells can become cancerous therefore not being able to accomplish their task of destroying invaders.

How does CRISPR enhance cancer immunotherapy? Scientists at the Washington University School of Medicine engineered human T cells that can attack cancerous human T cells. Additionally, they engineered the T cells to eliminate a harmful side effect known as graft-versus-host disease. This was all thanks to CRISPR. But, how exactly did they figure this out? Were there any flaws or bumps in the road?

Well, this type of treatment cannot work if the T cells they use are cancerous. Supercharged T cells can alternatively be used to kill cancerous T cells, but the cells can also kill each other because they resemble each other closely. This is where CRISPR came in, preventing the human T cells and cancerous human T cells from killing each other. Another benefit of this is that the scientists engineered the T cells so any donors T cells can be used without the fear of not matching the person in need of the T cells.

Overall, anything to better the prevention of cancer is a scientific win in most’s book. But, CRISPR is a controversial tool. Some think it should be put to use and some do not. However, will this technology alter other aspects of the human genome besides diseases and deadly occurrences? How will this affect our ethics as a community? Will our genetics continue to increasingly become more altered? Time will only tell.

What does the future hold for CRISPR-Cas9?

Genome editing, or the technologies in which scientists can change the DNA of an organism, is on the rise, especially with its latest development, CRISPR-Cas9, the most efficient method of all of the methods to edit DNA.

Like many other discoveries in science, CRISPR-Cas9 was discovered through nature. Scientists learned that certain bacteria capture snippets of DNA from invading viruses, making DNA segments called CRISPR arrays, helping them remember the virus to prepare for future invasions of that virus. When they are confronted with that virus again, RNA segments from the CRISPR arrays are created which target the DNA of the virus, causing the enzyme Cas9 to cut the virus’ DNA apart, which would destroy the virus.

 

We use the same method in genome editing with CRISPR-Cas9 by creating RNA that binds to a specific sequence in a DNA strand and the Cas9, causing the Cas9 to cut the DNA at that specific sequence. Once this is done, the scientists create a sequence to replace the one that was cut to get the desired genome.

This technology is most prominently used to attempt to treat diseases, where the somatic cells’ genomes are altered which affect tissues, as well as prevent genetic diseases where the sperm or egg’s genome is changed. However, the latter causes some serious ethical concerns of whether we should use this technology to enhance human traits. But this begs the question that if we start using it more and more to prevent genetic diseases, will this open the door for it to be used in new ways?

CRISPR Defends Bacteria, and Helps Scientists Discover New Bacterial Defenses

Although CRISPR is known for being a gene-editing tool, it can be used in other areas, such as a defense mechanisms in bacteria. This discovery “Probably doubles the number of immune systems known in bacteria,” according to a microbiologist at the University of California. Bacteria have to defend themselves against Phages, which take control over bacteria’s genetic machinery and force them to produce viral DNA. Bacteria use CRISPR to defend themselves against Phages because it stores a piece of past invaders DNA so bacteria can recognize and fight of those future viruses.

 

Photo By J LEVIN W (Own work) [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)], via Wikimedia Commons

the researchers found that nine groups of bacterial genes were defense systems, and one system protected against plasmids. The data revealed a possible shared origin between bacterial defense systems and defense systems in more complex organisms. Some of the genes contained DNA fragments that are also  important parts of the immune system in plants, mammals, and invertebrates. The discovery of more bacterial defense systems poses the question of wether they will also be useful biotechnology tools like CRISPR is.Only 40% of bacteria have CRISPR, so scientists searched for other bacterial defense mechanisms. To do this, they looked at genetic information from 45,000 microbes, flagging genes with unknown functions located near defense genes, because defense-related genes cluster together in the genome. The researchers then used genomic data to synthesize the DNA and  inserted them into Escherichia coli and Bacillus subtilis, which can both be grown and studied in the lab. They then studied how well bacteria defended themselves during phage attacks with various genes detected. If eliminating certain genes deterred the bacteria’s defense, that determined that those specific genes were a defense system.

 

For more information, click here. For more information on CRISPR’s role in bacteria, click here.

The Child that Saved Millions

Thousands of years ago a child was born in west Africa with genetic mutation that altered the shape of his/her hemoglobin. This mutation wasn’t harmful because each person has two copies of every gene and the other gene was normal and so they lived and passed on their mutated gene that would save millions of lives.

The gene spread across all of Africa and into parts of southern Europe and India. Every so often two people with the gene would make a child that had two copies of the gene. The child would no longer be able to produce normal hemoglobin. As a result, their red cells became defective and clogged their blood vessels. The condition, now known as sickle cell anemia, leads to extreme pain, difficulty with breathing, kidney failure and even strokes. Most people with this disease die before 40.

In the early 1900s doctors in the U.S first noticed this disease and called its sickle cell anemia because of the way the cells look. Most cases were found in African Americans and studies showed that 8 percent of African Americans had some sickle-shaped blood cells, yet the vast majority had no symptoms at all.

By 1950 doctors had discovered that sickle cell anemia was an incomplete dominance trait and the people who had one copy of the mutated and one of the normal gene showed no symptoms. They soon found out the sickle cell anemia was not unique to the U.S in fact the gene turned up in high rates across Africa, southern Europe and into India. Genetically speaking this made no sense because having two copies of the trait was so deadly it would be most likely that the mutation would have become rarer with each generation.

In 1954 a geneticists Anthony C. Allison observed that people in Uganda who carried a copy of the sickle cell mutation had lower rates of getting malaria. Later research confirmed Dr. Allison’s findings. It seems that the sickle cells defend against malaria by starving the single-celled parasite that causes the disease. The parasite feeds on hemoglobin, and so it’s likely that it can’t grow on the sickle cell version of the molecule.

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