BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: DNA (Page 1 of 5)

Does Exposure to Toxins In the Environment Affect One’s Offspring’s Immune System?

A study has recently surfaced stating that maternal exposure to industrial pollution may harm the immune system of one’s offspring and that this impairment is then passed from generation to generation, resulting in weak body defenses against viruses.

Paige Lawrence, Ph.D., with the University of Rochester Medical Center’s Department of Environmental Medicine, led the study and conducted research in mice, which have similar immune system functions as humans. Previously, studies have shown that exposure to toxins in the environment can have effects on the respiratory, reproductive, and nervous system function among generations; however, Lawrence’s research is the first study to declare that the immune system is also impacted.

“The old adage ‘you are what you eat’ is a touchstone for many aspects of human health,” said Lawrence. “But in terms of the body’s ability to fights off infections, this study suggests that, to a certain extent, you may also be what your great-grandmother ate.”

“When you are infected or receive a flu vaccine, the immune system ramps up production of specific kinds of white blood cells in response,” said Lawrence. “The larger the response, the larger the army of white blood cells, enhancing the ability of the body to successfully fight off an infection. Having a smaller size army — which we see across multiple generations of mice in this study — means that you’re at risk for not fighting the infection as effectively.”

In the study, researchers exposed pregnant mice to environmentally relevant levels of a chemical called dioxin, which is a common by-product of industrial production and wast incineration, and is also found in some consumer products. These chemicals eventually are consumed by humans as a result of them getting into the food system, mainly found in animal-based food products.

The scientists found the production and function of the mice’s white blood cells was impaired after being infected with the influenza A virus. Researchers observed the immune response in the offspring of the mice whose mothers were exposed to dioxin. Additionally, the immune response was also found in the following generations, as fas as the great-grandchildren (or great- grandmice). It was also found that this immune response was greater in female mice.  This discovery now allows researchers to have more information and evidence to be able to more accurately create a claim about this theory.

As a result of the study, researchers were able to state that the exposure to dioxin alters the transcription of genetic instructions. According to the researchers, the environmental exposure to pollutants does not trigger a genetic mutation. Instead, ones cellular machinery is changed and the immune response is passed down generation to generation. This discovery explains information that was originally unexplainable. It is obviously difficult to just avoid how much toxins you are exposed to in the environment, but it is definitely interesting to see the extent of the immune responses in subsequent generations. We can only hope that this new information, and further discoveries, help people adjust what they release into this world that results in these harmful toxins humans are exposed to, and their offsprings.

 

 

 

Stem Cells and CRISPR

Many cells can reproduce but there are a few types of cells that are not able to reproduce. One of these types are nerve cells, the cells that cary messages from your brain to your body.  There are many ways nerve cells can be destroyed or damaged, by trauma or drug use.  Millions of people are effected by losing nerve cells and for so long no one could think of a way to recreate them; until the discovery of stem cells.

After fertilization, and when the newly formed zygote is growing, it is made up of a sack of cells.  Some of these cells are stem cells which develop according to their environment. Because of the behavior of stem cells, scientists theorized that if they placed stem cells in the brain or spinal chord, two areas that have an abundance of neurons, the stem cells would turn into a neuron because of the environment it was in.  But, when they tried introducing stem cells into the body, the immune system treated them as an foreign body, as it should. Our immune system has to treat anything that does not come from our body as an enemy or we could get extremely sick.  However, the downside is organ transplants, blood transfusions, etc. are dangerous because they could cause a serious immune rejection.

Someone experiencing a spleen transplant rejection

Cells have a surface protein that displays molecular signals to identify if it is self or foreign.  Removing the protein causes NK (natural killer) cells to target the cell as foreign. Scientist haven’t been able to figure out how to make a foreign cell not seem foreign until Lewis Lanier, chair of UCSF’s Department of Microbiology and Immunology, and his team found a surface protein that, when added to the cell, did not cause any immune response.  The idea would be to use CRISPR/cas9 to edit the DNA of the stem cells, and in doing so would remove the code for the current surface protein and add the code for the new surface protein.

After the scientists had edited the stem cells, to have the correct signal protein, they released them into a mouse and observed that there was no immune rejection. Truly amazing. Maybe brain damage could be helped by this science one day. Tell me your thoughts on Stem Cells in the comments!

For more information, please go check out the primary source of this article.

 

 

New anti-CRISPR Proteins Serving as Impediments to this Miraculous System.

CRISPR-Cas9 systems are bacterial immune systems that specifically target genomic sequences that in turn can enable the bacterium to fight off infecting phages. CRISPR stands for “clusters of regularly interspaced short palindromic repeats” and was  first demonstrated experimentally by Rodolphe Barrangou and a team of researchers at Danisco. Cas9 is a protein enzyme that is capable of cutting strands of DNA, associated with the specialized stretches of CRISPR DNA.

Diagram of the CRISPR prokaryotic antiviral defense mechanism.

Recently, a blockage to the systems was found by researchers which are essentially anti-CRISPR proteins. Before, research on these proteins had only showed that they can be used to reduce errors in certain genome editing. But now, according to Ruben Vazquez Uribe, Postdoc at the Novo Nordisk Foundation Center for Biosustainability (DTU), “We used a different approach that focused on anti-CRISPR functional activity rather than DNA sequence similarity. This approach enabled us to find anti-CRISPRs in bacteria that can’t necessarily be cultured or infected with phages. And the results are really exciting.” These genes were able to be discovered by DNA from four human faecal samples, two soil samples, one cow faecal sample and one pig faecal sample into a bacterial sample. In doing so, cells with anti-CRISPR genes would become resistant to an antibiotic while those without it would simply die. Further studies found 11 DNA fragments that stood against Cas9 and through this, researchers were ultimately able to identify 4 new anti-CRIPRS that “are present in bacteria found in multiple environments, for instance in bacteria living in insects’ gut, seawater and food,”  with each having different traits and properties.  “Today, most researchers using CRISPR-Cas9 have difficulties controlling the system and off-target activity. Therefore, anti-CRISPR systems are very important, because you want to be able to turn your system on and off to test the activity. Therefore, these new proteins could become very useful,” says Morten Sommer, Scientific Director and Professor at the Novo Nordisk Foundation Center for Biosustainability (DTU). Only time will tell what new, cool, and exciting discoveries will be made concerning this groundbreaking system! What else have you guys heard? Comment below!

CRISPR used to Control Genetic Inheritance in Mice!

Scientists around the world have been using CRISPR/Cas9 in a variety of plant and animal species to edit genetic information. Although this has been tested recently on insects, it is currently moving towards testing mammals. It happens to be more difficult with mammals due to the longevity between generations. However, It’s been done!!

UC San Diego researchers have developed a new active genetic technology in mice. Graduate student Hannah Grunwald, Assistant Researcher Valentino Gantz and colleagues led by Assistant Professor Kimberly Cooper, layed the groundwork for further advances based on this technology, including biomedical research on human disease.Image result for mice

“To demonstrate feasibility in mice, the researchers engineered an active genetic “CopyCat” DNA element into the Tyrosinase gene that controls fur color. When the CopyCat element disrupts both copies of the gene in a mouse, fur that would have been black is instead white, an obvious readout of the success of their approach. The CopyCat element also was designed so that it cannot spread through a population on its own, in contrast with CRISPR/Cas9 “gene drive” systems in insects that were built on a similar underlying molecular mechanism.”

The project duration was two years, and the researchers used many ways to “determine that the CopyCat element could be copied from one chromosome to the other to repair a break in the DNA targeted by CRISPR”. Some gene that was originally existent on only one of the two chromosomes was copied to the other chromosome. They were able to convert one genotype from heterozygous to homozygous, and they were able to tell in that there were  as many as 86 percent of offspring that inherited the CopyCat element from the female parent instead of the usual 50 percent.

The test was successful for the female mice’s production of eggs, but not for the males production of sperm. The researchers predict this is a possibility to a difference in the timing of male and female meiosis.

As this test was only the beginning, researchers such as those at UC San Diego hope to soon move on to research on human disease. They say that “Future animal models may be possible of complex human genetic diseases, like arthritis and cancer, which are not currently possible.”, and with their hard work, their research can lead to miracles.

Planet of the (CRISPR-Edited, Cloned) Apes

Several months ago, scientists in China cloned five gene-edited macaque monkeys. The clones were made through the somatic cell nuclear transfer method (SCNT)—a process in which a viable embryo is created from a body cell and an egg cell—that was used to produce the first primate clones around a year ago. In this instance, however, the monkeys’ genomes were first edited using CRISPR-Cas9—a unique genome editing tool that enables geneticists to edit parts of the genome by removing, adding, or altering sections of the DNA sequence—to show symptoms of sleep disorders by eliminating BMAL1, one of the positive elements in the mammalian auto-regulatory TTFL, which is responsible for generating molecular circadian rhythms. The result? The monkeys exhibited a wide range of circadian disorder phenotypes, including elevated night-time locomotive activities, reduced sleep time, reduced circadian cycling of blood hormones, increased anxiety and depression, and other schizophrenia-like behaviors. 

File:Macaque Monkey (16787053847).jpg

Macaque Monkey

Naturally, the results of the investigation triggered much backlash. According to Carolyn Neuhaus of The Hastings Center, the researchers viewed the suffering of the monkeys as a triumph, and failed to consider the moral implications of their investigation. “It’s very clear that these monkeys are seen as tools,” she told Gizmodo, the latter publication writing in a similar sentiment, “Their experiment is a minefield of ethical quandaries—and makes you wonder whether the potential benefits to science are enough to warrant all of the harm to these monkeys”. 

Nevertheless, the researchers involved in the experiment remain firm in their support of the experiment—the goal of which was to produce genetically identical monkey models of disease for biomedical research—on both moral and scientific grounds. “We believe that this approach of cloning gene-edited monkeys could be used to generate a variety of monkey models for gene-based diseases, including many brain diseases, as well as immune and metabolic disorders and cancer,” stated Qiang Sun, one of the research paper’s authors and director of the Nonhuman Primate Research Facility at the Chinese Academy of Science’s Institute of Neuroscience in Shanghai. Moreover, Reuters reported, “Xinhua [the state news agency] said the program, supervised by the institute’s ethics panel, was in line with international ethical standards for animal research”. Time will tell, ultimately, if the results of their experiment prove consequential on a larger scale. 

Scientist from China creates a baby resistant to HIV

The development of CRISPR technology has drastically progressed in the recent years, and He Jiankui, a scientist from China, took a step that most people judge to be crazy: he used CRISPR technology to create a human who is resistant to the HIV virus.

What is CRISPR? Good question.

CRISPR-Cas9 is a gene editing tool made from an ancient bacterial immune system. In bacteria, this system identifies DNA of invading viruses and send in different enzymes, such as Cas-9 to target and cut out a piece of DNA. Researchers quickly realized that almost any sequence of DNA can be cut out and modified the system to any sequence desired, even one that can prevent HIV. This is what Jianku’s work comprised of.

Jiankui and his team targeted the gene CCR5, a gene that provides the blueprint for the cell surface protein involved in the immune system, in the DNA of human embryos. The cell surface protein is usually involved in relaying information between cells, and HIV can use it to dock onto cells, infecting them with their own genetic material. Jianku eliminated the CCR5 gene to prevent HIV from docking onto any of the baby’s cells. However CRISPR-Cas9 induces mutations that scientist cannot fully control, and Jianku could not replicate the gene to the exact level. So, he instead created a “mixture of disrupted gene products”, which could potentially have a negative effect on human health.

At first glance, Jiankui’s experiment might be seen as beneficial, but Jiankui’s decision to create this human has been considered by other scientist as premature, drastic, and unethical, and has caused a lot of controversy. Although this was not the first time a scientist tampered with a human embryo, many scientists are outraged and believe that his experiment was a violation of human ethics. According to an article written by Allison Eck, the most notable ethical breach was conducting this experiment without the consent of other scientists, ethicists, regulators, or institutional review boards.

Debates over Jianku’s work have been circulating since the announcement of his experiment. Personally, I think that in the future, if we can prevent HIV and other harmful diseases that cause death, CRISPR can be an effective tool. However, as of now, we do not fully understand are aware of all of its effects. Therefore it is dangerous to test it on other humans. In the wrong hands, this powerful technology might be used in the wrong way and can cause huge repercussions. What do you think?

 

The Collateral Damage of CRISPR-Cas9

 

CRISPR’s ‘precise’ gene-editing has actually been damaging other parts of the DNA sequence, according to a recent study. Photo from this source.

Of the various gene-editing techniques, CRISPR-Cas9 is the fastest, simplest, and most accurate gene-altering method known to date. Comprised of simply two parts, CRISPR-Cas9 snips through targeted segments of DNA and causes a change in the genetic code. Scientists are hopeful that we can soon use this method to cut out mutations that code for HIV, cancer, and sickle cell disease. However, a study published in Nature Biotechnology has revealed an unwanted side-effect of CRISPR.

When using CRISPR-Cas9, there are two major molecules that create a mutation, or change, in a DNA segment. The first is an enzyme called Cas9. This enzyme works like a pair of scissors and that cuts the two helices at a specific location so DNA can be altered. The second tool used in this process is the guide RNA (gRNA) that binds to the DNA and ensures that the Cas9 molecule cuts the DNA in the correct place. Finally, after the incision, the DNA will seal itself back together, without a trace of the deleted segment.

Such a precise process seems flawless. In theory, one should be able to cut out the unwanted genetic material and our DNA should perfectly repair itself. Unfortunately, senior group leader and director of the study at Wellcome Sanger Institute in England, Allan Bradley, stated that “CRISPR is not as safe as we thought.” Through a systematic and tedious approach, Bradley and his colleagues edited a series of mouse and human cells with CRISPR and then examined DNA base pairs father and farther away from the cut site. By examining millions of base pairs, the team landed upon unsettling news.

Bradley and his team found that huge chunks of DNA were inadvertently deleted, mutated, and rearranged millions of base pairs away from the cut site. The DNA was mutated so immensely that cells lost function in 15% of cases. Because these CRISPR-induced mutations were shown so far away from the cut site, this information could have easily been overlooked in other studies.  

This research poses questions on the accuracy of such gene-editing methods. What are the long-term effects of genetic engineering with CRISPR? How can we ensure that base pairs so far away from the cut site aren’t altered? Although this is somewhat discouraging news for the CRISPR community, this newfound information is motivating more researchers to improve CRISPR technology before making it widely accessible.

Read the full article here.

The Cure Before Being Born

lab mouse – Photo credit to Wikimedia Commons

A team of researchers from the University of Pennsylvania and Children’s hospital of Philadelphia has seen exciting results in their experiment on mice fetuses with an inherited liver disease.  The team removed the amniotic sac containing the fetus from the mother’s uterus, before injecting in a vein of thee fetus near the liver with CRISPR. This was to ensure that the genetic modification would be in the liver cells and would not affect any other vital organs. The fetus was then placed back into the uterus and the mother was thankfully unaffected by the modification, allowing for all the babies to be born without any issues.

The team used a more recently invented form of CRISPR called base editing instead of the well-known  CRISPR-CAS9.  Rather than cutting and inserting a sequence of DNA, a single nitrogenous base was replaced with another.  This newer method showed significantly less “genetic havoc”, unknown consequences for a cell that has been genetically modified with CRISPR.

The disease they targeted was a tyrosinemia type I, a mutation that effects 1 in 100,000 newborns globally, which causes causes the amino acid tyrosine to be metabolized into toxic products, which build up and cause damage to liver, and can eventually destroy it.   The scientist sought to disable the HPD gene, which creates enzymes that help to break down tyrosine.  By changing a cytosine base to thymine base, the toxic products are never produced.

Tyrosinemia type I – Photo credit to Wikimedia Commons

As the mice grew and developed, the researchers were astounded to find that despite only 15% of their liver cells having been the altered with the base edit, the genetically modified mice were surviving better and gaining more weight compared to those treated with traditional methods of drugs and monitored diet.

This is definitely a step in the right direction to eliminating genetic diseases, but base editing, especially for diseases due to multiple mutations might be more difficult, as many bases would need to be edited.  What do you think: more safe, yet possibly difficult base editing method or cut-insert method?

Message Intercepted – Commence attack on bacteria!

Tevenphage – Photo credit to Wikimedia Commons

While experimenting, a group of scientists noticed that a A virus, VP882, was able to intercept and read the chemical messages between the bacteria to determine when was the best time to strike. Cholera bacteria communicate through molecular signals, a phenomenon known as quorum sensing, to check their population number.  The signal in question is called DPO.  VP 882, a subcategory of bacteria’s natural predator, the bacteriophage, waits for the bacteria to multiply and is able to check for the DPO.  Once there is enough bacteria, in the experiment’s case they observed cholera, the virus multiples and consumes the bacteria like an all-you-can-eat buffet. The scientists tested this by introducing DPO to a mixture of the virus and bacteria not producing DPO and found that that the bacteria was in fact being killed.

The great part about VP 882 is it’s shared characteristic with a plasmid, a ring of DNA that floats around the cell. This makes it easier to possibly genetically engineer the virus so that it will consume other types of bacteria. This entails it can be genetically altered to defeat other harmful bacterial infections, such as salmonella.

Ti plasmid – Photo credit to Wikimedia Commons

Current phage therapy is flawed because phages can only target a single type of bacteria, but infections can contain several types of different bacteria.  Patients then need a “cocktail” with a variety of phages, which is a difficult due to the amount of needed testing in order to get approved for usage.  With the engineering capability of using a single type of bacteria killer and the ability to turn it to kill bacteria, phage therapy might be able to advance leaps and bounds.

As humans’ storage of effective antibiotics depletes, time is ticking to find new ways to fight bacterial infections.  Are bacteriophages and bacteria-killing viruses like VP 882, the answers?

Your DNA Will Determine Your Coffee or Tea Addiction

The perception of taste varies according to the genetic makeup of different individuals. In fact, these taste genetics can determine whether a person will prefer coffee or tea.

What does this mean?

There is a version of a gene that increases sensitivity to the bitter taste of caffeine. Those with this gene tend to be coffee drinkers, as they are able to detect caffeine’s bitterness. Research was conducted to connect DNA gene variants to the recognition of bitter taste of chemicals, caffeine, quinine, and propylthiouracil, testing different people’s DNA from around the world. Analysts then calculated each person’s variants in the taste genes, creating a genetic score for how intensely the person tastes each of the bitter chemicals. Researchers connected these statistical analytics to said people’s lifestyle in relation to the beverages of their choice: coffee or tea.

It was determined that people who had the highest genetic score for detecting caffeine’s bitterness were 20 percent more likely to drink a lot of coffee, while those without or less of the increased sensitivity gene were stated to be tea drinkers.

Why is this important?

Prior to this research discovery, it was thought that people with “increased sensitivity” to bitter tastes would tend to avoid bitter foods or drinks. However the choice of drinking coffee or tea may not only result from this gene sensitivity. The study coauthor, Marilyn Cornelis, a nutritional and genetic epidemiologist at Northwestern University Feinberg School of Medicine, says “coffee drinkers may have learned to enjoy caffeine’s bitterness because it’s a sign of the buzz the chemical provides. But tea drinkers may not actually like the bitterness of propylthiouracil and quinine.” This means that tea drinkers may exist only as a result of the rejection of coffee, as caffeinated tea still gives the consumer a slight “buzz.” Although the role of bitter taste genes on whether a person is a coffee or tea drinker is still not completely certain, researchers have made strides with this last test report, as it is now known that taste genes are somewhat linked to coffee and tea consumption.

As an avid coffee drinker myself, I believe it is possible that I possess these taste genes. My dad, and his mom (my grandma) both are heavy coffee drinkers, so I think I can now say, “it is in my DNA to be addicted to coffee.”

Why Don´t We Grow Ears on Our Arms?

The Miracle of DNA Regulation

Now, the question posed is why we don’t grow ears on our arms. May I introduce to you: gene regulation. That’s right. Even though every single cell in your body has the same DNA, the body is able to ‘turn off’ different genes so that only ones that are necessary are read. This is why you do not grow ears on your arms, because those ear-making genes are ‘turned off’.

But… How?

This question has been plaguing scientists for quite a while, as we have discovered genes in the human genome that are ‘turned off’ but could potentially be quite useful such as the regeneration of limbs (same as a starfish or a crab). Now there has been a new breakthrough in how we understand gene regulation thanks to some researchers in Cambridge, Massachusetts. The binding domain’s function in gene regulation has been known for quite some time already. The mystery lied within the activation domain. It has now been discovered that the activation domain sort of acts as a net, capturing the molecules for gene regulation and anchoring the transcription ‘machinery’ by the gene that is to be transcribed.

But… How? What Does This Mean?

Well, the activation domain creates little droplets by mingling with transcription proteins that attract the transcription machinery stuff. It’s kind of like creating oil droplets in vinegar. This process is now called phase separation. This has grand implications for even more research on gene regulation and can even give more insight into diseases such as cancer. When do you think the next breakthrough will come? Do you think this is the key to unlocking how to turn genes on and off for good or is there much more work to be done?

 

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 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!

 

 

 

 

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.

 

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.

 

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.

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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 Cas9, too good to be true?

After its peak in popularity following its reveal as a possible “genetic modifier” in 2013, the CRISPR Cas-9 enzyme system has been the center of debate within the biology community. Thought to be the solution to all genetic and hereditary diseases by simply “cutting out” the fault gene, new research and studies have shown that a majority of people (65 to 79 percent) have antibodies that would fight cas-9 proteins.

“The study analyzed blood for antibodies to two bacteria from which Cas9 is derived: Streptococcus pyogenes and Staphylococcus aureus. The researchers’ concern stemmed from the fact that these bacteria frequently cause infections in humans, and so antibodies to them may be in our blood” states bigthink.com

While the overall effects are unclear, the study concludes that the result would be “significant toxicity” and an unsafe use of the gene editing tool.

What do you think? Is the current risk of using Cas-9 worth the reward?

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Cas9, photo by J LEVIN W

 

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