BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: Genes (Page 1 of 3)

How the “unknown” of the human gut microbiome gets in the way of metagenomic studies…

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On November 12, 2019

In Student Post

Did you know that the greatest concentration of bacteria lives in your gut? At two or three years old we have a balanced microbiome. While we know a lot about the human gut microbiome, there is a lot that is unknown about it. There has been a lot of improvement in finding an “unknown microbiome” for example, shotgun metagenomics enables researchers to take a sample of all genes in all organisms and allows them to find an abundance of microbes in many different environments.

What we know: 25 Phyla, ~2,000 Genera, ~5,000 Species, ~80% Metagenome mappability, and 316 million genes

What is unknown?: Undetected unknowns, hidden taxa and strain-level diversity (~20% sequences not matching microbial genomes), functional unknowns (~40% genes without a match in functional databases)

For example, one study where researchers studied a stool sample from 2 lean African men and a stool sample from 1 obese European. In the stool, they found 174 new species never seen in the human gut before and 31 new genome species (which can help in later studies). Found within these new species was, Microvirga Massiliensis which has the largest bacterial genome acquired from a human, along with Senegalvirus which is the largest virus in the human gut. We definitely know a lot more about the human gut microbiome than we did, even though there is a long way to go.

However, organizing large numbers of draft genomes from uncharacterized taxa is challenging, and while performing well for bacteria, assembly-based metagenomic tools are less effective when targeting new eukaryotic microbes and viruses.

The human gut microbiome intestines in an obese person vs. a lean person

To make improvements in uncovering “hidden strain-level diversity” it is vital to alter sample-specific associations from the metagenomes and to additionally incorporate as many genomes for each species in reference databases. Most species are “open”, meaning they don’t have an upper bound on the size of accessory genomes and it may seem impossible to reclaim all strain-level diversity; however, preserving “the effort of cataloguing strain variants remains crucial for an in-depth understanding of the functional potential of a microbiome.”

The difficulty is that the microbiome contains viruses. The “functional unknown” of the human gut microbiome is the broadest and most challenging to delve and study further into because there is little known about understanding its pathways and genes. There is one creation though, that helped try and find out what was “unknown” about the microbiome, called the Integrated Gene Catalogue. The Integrated Gene Catalogue of the human gut microbiome which consists of 10 million genes. It groups genes into thresholds, thus the genes then fall into sub-units of gene-families. Locating these genes is only a small part of finding out what they actually do. For example, out of 60.4% of the genes that were annotated, 15-20% of the genes have been discovered, but are stilled labelled “function unknown.” These results show how little is known about genes, their functions, and what is current in microbial communities. There is not enough investment in microbiome research. It is difficult because there could be viruses that can be discovered; however, not enough time is being put into finding it.

Lastly, there is a lot of research going into the human gut microbiome. For example, Fecal microbiome transplantation is where stool from a healthy donor gets placed into the other patients intestine, this transplant usually occurs when more bad bacteria take over the good bacteria in the intestine. However, it could cause more disease which is why further investigation in the human gut can solidify that transplantation could overall prevent a bad bacteria take over. The microbiome field is open to all technologies. Understanding the function of the microbiome still remains the largest challenge researchers face, along with the biggest challenge that “targeting specific genes are irreplaceable”, technology should be able to provide solutions (including microbial transcriptome, metabolome, and proteome, and the automation of cultivation-based assays to scale-up the screening of multiple taxa and genes for phenotypes of interest.)

 

Cracking the Code one Gene at a Time

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On October 26, 2019

In Student Post

Cells are one of the most important objects in the human body, yet scientists still have yet to truly understand the underlying mechanics. Recently researchers have observed how RNA transcription occurs in real, live cells. For the longest time scientists have observed RNA transcription extracellularly. Until now they have only been able to observe how RNA polymerase 2, a DNA copying enzyme, and other enzymes “by breaking cells apart and measuring the activity… outside the cellular environment.”

 

Image result for rna transcription

Process of RNA Transcription

The molecules involved in RNA transcription have been studied profusely, but only frozen in time. Now we can use “a highly specialized optical microscope” to watch how RNA polymerase copies DNA into mRNA. Researchers then labeled certain molecules with a tag so that they glowed when looked at. An issue with this method, though, is that there are so many of these molecules in the nucleus that if we were just to examine the reactions after adding the fluorescent tag, we would just have a glowing nucleus. The scientists have combated this by suppressing the signals from other reactions. This, along with the ultra-sensitive microscope allows us to focus on one gene and transcription occurs for it.

Image result for fluorescent nucleus

Fluorescent Image of Living Cells

Through this new technique, we now have a much more detailed and intricate picture of how DNA, RNA, and enzymes function in transcription. This process can be replicated for many more reactions and will help us understand bounds more about ourselves and how we truly work.

I am personally very excited to see what new concepts and techniques will be discovered from this breakthrough. Genetics is the future of biology and using this to crack the code is one step closer to curing many genetic diseases. Combining this with other genetic breakthroughs like CRISPR is a cause for excitement in the future of biology. If you have any other ideas about why this could be useful please comment below.

 

The Rice That Can Clone Itself

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On March 12, 2019

In Student Post

A team of scientists has discovered that through the use of CRISPR, they were able to create a rice plant that can asexually reproduce. The problem with previous strands of genetically modified rice plants, those bread to have a higher yield, is that their progeny did not always carry this desired trait. So farmers have to buy new genetically modified seeds every year to ensure that they will get that same yield.

Image result for rice grains

That is where the magic of CRISPR comes into the equation. The first step in the process was editing the eggs of the plant by implanting a promoter that allows the egg to start the embryo growing process without a sperm. One issue still lingered, the process of meiosis that was occurring could not produce viable offspring because it only had half of the genetic material that the progeny would need. Another team of scientists from the French National Institute for Agricultural Technology discovered that by using CRISPR to turn off three specific genes they could stop the meiosis process and allow the plant to reproduce asexually.

Image result for rice plant

This process is still only 30% efficient at this stage. However, the offspring they do produce are able to asexually produce more clones of themselves. Now the process starts to try and make this process more efficient. I think these plants could have a major impact on the agricultural industry, especially with food shortages becoming more present as the human population rapidly increases.

What do you think? Have we overstepped our bounds by editing nature? Or have we pioneered a new solution for the world hunger question on everyone’s minds?

Could Messenger RNA Be the Future Chronic Disease Treatment?

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On January 12, 2019

In Student Post

What is mRNA and what makes it a good treatment option?

Messenger RNA (mRNA) sends signals to the cells to make certain proteins by changing the genetic coding. So mRNA has the potential to treat a variety of diseases because it can induce cells to make therapeutic proteins. This essentially makes the patient’s body cells into a treatment factory which would give patients a less invasive treatment option.

One of the obstacles with this treatment is how to deliver mRNA to the diseased area safely and efficiently. Researchers at MIT have found a new way to provide patients with mRNA. They made an inhalable form of mRNA. The goal would be to administer the mRNA similar to an asthma inhaler where powered mRNA medication would be sprayed into the lungs but as of now, the medication is only available in nebulizer form. However, there needed to be a way to stabilize the mRNA molecules using an aerosol method. So the researchers experimented with positively charged beta-amino esters which are biodegradable and are more easily broken down by the body. The upside to using a biodegradable material is that there would be a minimal accumulation of the substance in the area it was administered. Accumulation would cause unwanted side effects to the patients’ health.

To test out their new product MIT scientists put the mRNA molecule and polymers in spheres.  Then suspended those spheres in water droplets and distributed a mist through a nebulizer to mice. But the mRNA molecules that they put into the spheres coded for the production of the bioluminescent protein luciferase. Using the code for the bioluminescent luciferase, the researchers would be able to see if the mRNA had effectively made the protein that it coded for if it glowed. 

After 24 hours since administering the medication, the mice were producing bioluminescent proteins in their lungs which hints that eventually scientists could inject the code for therapeutic proteins in the mRNA and the cells would respond.  But as the mRNA levels dropped so did the protein production. That showed that only with repeated doses of the medication the mice would be able to continuously produce their own proteins. They also found that mRNA was evenly distributed throughout the five lobes of the lungs so the mRNA reached all the areas of the lungs which would be helpful in treating cystic fibrosis. This process could be the future treatments for chronic lung diseases as researchers work to make this product into inhaler form instead of the nebulizer for convenience purposes.

Microbiome Genes have Macro-significance

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On November 8, 2018

In Student Post

Ever been told that the little things matter in life? This same proclamation that you’ve been told by your elders rings true in your gut: one small modification to your human gut microbiome (a batch of bacteria that call your digestive tract home) can have drastic effects on your metabolism.

A. Sloan Devlin, assistant professor at Harvard medical school, carried out a study that proved the importance of the gut microbiome. She first located the gene in “an abundant gut bacterium” for an enzyme that processes bile acids. She then removed that gene from the bacterium. Next, she “colonized” “germ-free” mice with one of two types of the gut bacterium: either with the bile-processing enzyme or without the bile-processing enzyme. The results were surprising.

Credit: mcmurryjulie on pixabay

After both mice were fed the same high-fat, high-sugar diet, the mice without the bile-processing enzyme “had more fat in the liver and gained weight much more slowly than the other group. They also used proportionately less fat and more carbohydrate for energy.” Changing one single enzyme in a gut bacterium appears to change “whether the host is using [primarily] fats versus carbohydrates” for energy.

Even more staggering was the “correlation of lean body mass to energy expenditure.” Typically, in humans and mice, the more lean body mass an organism has, the more energy it expends. However, for the mice without the bile-processing enzyme, this relationship “broke down.” Devlin hypothesizes that this change could be due to a “signaling,” a process in which “physical states in the body trigger a cascade of genes to switch on or off.” Researchers can use this knowledge to treat diseases: figure out which microbiome bacteria activate which genetic switches, and better treatment for genetic problems such as, acid imbalances, metabolic disorders and obesity, may become a reality.

Devlin is sure to stress that this groundbreaking microbiome research is just her “first step.” Although this study was carried out on “germ-free” mice, Devlin dreams that one day she may use her research to improve the health of her own species: as Devlin states, her research brings her “one step closer to humans.”

 

A Gene In Your Ears For Sour Taste?

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On October 11, 2018

In Student Post

Unlike the other four human tastes, our process of detecting sourness has always been a mystery, and scientists were definitely not expecting to find the answer in a  protein normally found in the inner ear.

https://pxhere.com/en/photo/994259

This protein, coded by the gene scientists refer to as Otop1, usually functions as part of the vestibular system to maintain balance. Given this more commonly known function of the protein, scientists were shocked to find its use for both balance and detecting the acids often associated with sour taste. The association is actually not as far- fetched as one might think. Otop1 codes for the synthesis of calcium carbonate crystals which rest on the hairs of the inner ear and detect gravity to help humans stand upright. Researchers found that the tongue also uses these crystals to detect sour taste. Calcium carbonate, a relatively basic compound, dissolves when it comes into contact with acid, which reaction can be detected by the brain and interpreted as sour taste.

How could such a protein find its way to use in both our senses of balance and taste?

The answer lies in evolution. If a certain protein proves advantageous over generations, organisms with it in surplus may evolutionarily find other uses for the it. Recently scientists have actually found several proteins for sensory organs that double as homeostatic sensors in other tissues. Otop1 is only one of many; smell receptors are found in the kidney in surplus, as are sweet taste receptors in the bladder.

Although we have unearthed a lot about the human body over the years, there is always so much more to learn!

Fighting the mosquito disease problems with… mosquitos?

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On October 10, 2018

In Student Post

Since the discovery of CRISPR-Cas9 system (Clustered Regularly Interspaced Short Palindromic Repeats), gene editing has become a highly debated topic. One of the reasons backing the use of CRISPR-cas9 is to prevent diseases. These diseases include mosquito-borne diseases such as zika, dengue fever, and malaria.  Malaria in particular kills around 3,000 children every year. Various groups of scientists have worked on genetically modifying mosquitos to stop the spread of malaria by making female offspring sterile and unable to bite, making male offspring sterile, or making mosquitos resistant to carrying diseases. A point of concern was if the modified gene would stay relative and would carry from generations. In order to make offspring, genes from both parents must be used, resulting in the offspring carrying the modified gene only half the time.  In particular cases, mutations would occur in the altered DNA, which nullified the genetic changes.  This has been solved by developing a gene drive, which makes the desired gene dominant and occur in the offspring almost 100% of time.  This entails almost the entire mosquito population could have this modified gene in as little as 11 generations.

Image by Author

Recently, the government of Burkina Faso, a small land-locked nation in west Africa, has approved for scientists to release mosquitos that are genetically modified anytime this year or next year.  The particular group of mosquitos to be released first is a group of sterile males, which would die rather quickly.  Scientists want to test the impact of releasing a genetically modified eukaryotic organism in the Africa. It is the first step in “Target Malaria” project to rid the region of malaria once and for all.

 

One of the major challenges in gaining allowance to release the genetically modified species was the approval of the residences, who lack words in the local language to describe genetics or gene editing.  Lea Pare, who leads a team of scientists modifying mosquitos, is working with linguists to answer questions the locals may have and tp help develop vocabulary to describe this complex scientific process.

What do you think about gene editing to possibly save millions?

Read the original article here.

View a video explaining how scientists can use genetic engineering to fight disease here.

GATTACA is Here!

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On March 17, 2018

In Student Post

            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

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On March 16, 2018

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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.

Potential cure to ALS, the disease that inspired the ice bucket challenge!

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On March 12, 2018

In Student Post

You all remember the ALS ice bucket challenge, that took social media by storm, in which people dumped ice water on their heads in order to raise money and awareness to ALS, a neurodegenerative disease that progressively destroys the motor neurons and eventually leads to death.

 

There is currently no cure to this horrible disease. However new genetic technology (CRISPR) may change all that.

In short, CRISPR is a new form of gene editing that allows scientists to change an organism’s DNA.

Scientists discovered that ALS is caused by a mutation in the C9orf72 gene. ALS is often caused by a significant repeat of a segment of DNA that becomes toxic. So, using CRISPR, scientists deducted which genes either protect against or cause these toxic DNA segments. This process was extremely effective and scientists found about 200 genes that affect ALS. For example, scientists found a gene that codes for a protein called Tmx2 that when removed from mice neurons caused the mice to survive whereas not removing them killed them. This means that scientists are beginning to figure out how to cure ALS.

Discoveries such as these are revolutionary as we can now find specific causes for previously fatal, cureless diseases  such as this. In addition, using this technology we can target these specific genes and save lives.

However, whenever we discuss gene editing we must ethically consider when does this become too far? Where is the line between helping to cure people and helping to destroy society by designing babies?

To answer my own question, I think it is crucial that we take any step possible to help find cures in situations such as this. That being said, there are clear limits that must be respected. The line is definitely hazy. Let me know in the comments your thoughts about gene editing!

But for now, let’s enjoy this scientific win and hope that ALS can be officially cured. Good job ice bucket challenge for bringing attention to a serious issue that may now actually be cured.

Original Article: https://www.sciencedaily.com/releases/2018/03/180305111517.htm

A New Addition to Gene Altering Technology

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On March 11, 2018

In Student Post

Today, there is new technology that allows genes to be edited. This is called CRISPR. CRISPR can fix genetic defects that lead to disease, improve food nutrition, and even resurrect extinct species. A research team in Japan created a new technology in addition to CRISPR that can change a single DNA base in the human genome. This is called Microhomology-Assisted eXcision or MhAX. The team called this new technique “absolute precision” in their article published in the Nature Communications journal.

MhAX originated when a group of researched wanted to have a better understanding on single nucleotide polymorphisms (SNP), which are single DNA mutations that can contribute to hereditary disease. In order to discover that these SNPS cause disease, researchers need to compare two genetically matched “twin cells.” However, twin cells are difficult to make because twin cells are not completely identical-they have a single different SNP. MhAX gives a new way to make twin cells.

The research teams used an extensive process to make the edits. First, the SNP modification and fluorescent reporter gene is inputed into the cell. This allows for researchers to see which cells are changed. The researchers then created another same DNA sequence, called microhomology, that was stationed on each side of the fluorescent gene. This allowed for sites where CRISPR can enter and trim the DNA. In order to leave only the SNP in, the research team used microhomology-mediated end system (MMEJ), a repair system that can remove the fluorescent gene. This technique, according to the team of researches, is precise and they are hopeful that it will be used to gain a better understanding of disease mechanisms which could potentially lead to gene therapies.

MhAX is very interesting because it is an additional technique to CRISPR that can help alter genes. It is very fascinating to read about the future of genetics and the new technology being created that can changes genes connected to diseases and improve the lives of people. For more information on MhAX, click here and here. Based on this research, how do you think this technology will be used in the future?

 

 

 

Transporting Organs from Pigs to People!

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On March 8, 2018

In Student Post

The shortage of human organs for transplants is one of the biggest problems facing the medical field, about 22 people die on waitlists for organs die every day in the United States. But there is a newfound hope! A recent discovery using CRISPR-cas9 gene editing may address this challenge.

Scientists have been dreaming about transplanting organs from pigs into people for years, a process called xenotransplantation, but they have been held back by threatening viruses in the pigs DNA called PERVs. PERVs are present throughout the pig genome and would infect a person who receives a pigs heart, lung, kidney, etc. This infection could be fatal and may cause a human epidemic. Scary right? However, scientists at well-known laboratories had a breakthrough this past summer using CRISPR-cas9 and created healthy pigs with no traces of PERV genes!

It was, in fact, the two early developers of that gene-editing technology, Harvard University’s George Church, and Luhan Yang, who first believed CRISPR’s guide RNA and a DNA-slicing enzyme could make precise, genome-wide changes to pig cells. Their results showed that CRISPR could “knock out” PERV genes at all 62 sites in the pig genome. However, there were some flaws in their experiments, they used a line of “immortal” pig kidney cells, which were chosen for their ability to survive in the dish. Earlier the team had tried to use genetically “normal” pig cells, but once the cells were edited they failed to grow normally. Yang says, “CRISPR’s hacking job of the DNA may have prompted them to stop dividing or self-destruct.” But when they exposed the cells to a “chemical cocktail” making them “immortal,” the growth of PERV free cells in the dish rose to 100%.  The next step was to actually produce piglets. The researchers inserted DNA containing the nuclei of the edited cells into the eggs taken from the ovaries of pigs in a slaughterhouse. They allowed each egg to develop into an embryo and implanted it in the uterus of a surrogate mother. Boom, healthy, PERV-free piglets!

https://commons.wikimedia.org/wiki/File:Cute_Piglet.jpg

After this huge finding, Church and Yang co-founded a company called eGenesis which focuses on the engineering of transplant organs and projects in laboratories around the world exploded. Currently, a transplant surgeon at the University of Maryland is gearing up to swap a pig heart into the chest of a baboon! However, obstacles still remain in regard to humans; the rejection of the organs once in humans, the physiological incompatibility, how to insert genes that will prevent toxic interactions with human blood, and (what I believe is most important) the ethical question.

 

 

 

 

What is that? Oh, it is the first ever hybrid bird species from the Amazon!!

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On January 18, 2018

In Student Post

According to the Science Daily article, A team of researchers from Scarborough revealed ,through a series of tests, a golden crowned manikin. This bird was first discovered in Brazil in 1957 ,but not seen until 2002.

“While hybrid plant species are very common, hybrid species among vertebrates are exceedingly rare,” says Associate Professor Jason Weir, senior author of the research.

A hybrid species forms when two parental species mate to produce a hybrid population, which then causes the birds to stop being able to freely interbreed with the parental species

The teams gathered genetic and feather samples over two trips to Brazil. They sequenced a large portion of the golden-crowned manakin’s genome including 16,000 different genetic markers. This led to the finding that 20 percent of its genome came from the snowy-crowned, and about 80 per cent came from the opal-crowned. In addition to that, the researchers used coalescent modelling to figure out at what point the golden-crowned split off from its parental species.

“The golden-crowned manakin ended up with an intermediate keratin structure that does a poor job of making either the brilliant white or the reflective iridescence of the parental species,” says Weir.

In its early existence, The golden-crowned manakin likely had duller white or grey feathers due to its keratin structure ,but eventually grew into yellow feathers to attract females. This led to unique color of the species.

“Without geographic isolation, it’s very likely this would never have happened because you don’t see the hybrids evolving as separate species in other areas where both parental species meet.”

 

 

 

Changing a baby’s DNA profile by physical contact?

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On December 12, 2017

In Student Post

Photograph by Vera Kratochvil, License: CC0 Public Domain

Recent research from the University of British Columbia and BC Children’s Hospital Research Institute proved that the amount of physical contact between infants and their caregivers can affect children at the molecular level. The study demonstrated that children who had been more distressed as infants and received less physical contact had an underdeveloped molecular profile for their age. This is the first study to show that the simple act of physical touching on human children can result in deeply-rooted changes in genetic expression.

The researchers measured a biochemical modification called DNA methylation in which parts of the chromosome are tagged with small molecules made of carbon and hydrogen. These molecules act as “dimmer switches” that help control how active each gene is and affect how cells function. The extent of methylation and where on the DNA it takes place can be impacted by external conditions, especially in childhood.

The team analyzed DNA methylation of 94 healthy children with records of received caregiving from the age of five weeks to four and a half years. The DNA methylation patterns the scientists gathered presented consistent differences between high-contact and low-contact children at five specific DNA sites. Two of the five sites are related to genes: one involves in the immune system, and the other in metabolism. The children who experienced higher distress and received little contact had a lower “epigenetic age” than what’s expected from their age. Such low epigenetic age is conceived as an underdevelopment of the child’s molecular profile. As medical genetics professor Michael Kobor said, “In children, we think slower epigenetic aging might indicate an inability to thrive.”

The researchers intend to further examine whether the “biological immaturity” – epigenetic changes resulted from low physical contact – carries broader implications for children’s health, especially their psychological development. According to the lead author Sarah Moore, “If further research confirms this initial finding, it will underscore the importance of providing physical contact, especially for distressed infants.”

Build A Baby?!

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On December 10, 2017

In Student Post

Have you ever wanted a baby to be a super fast swimmer like Michael Phelps? How about a child who has more talent than Mozart? Well, that can’t happen.

According to the  New York Times Article, Scientists in Oregon have successfully modified the DNA of human embryos. This led to the new hope that designer babies are in our near future. But, designer babies are more likely to be seen in movies than in reality.

The main reason why designer babies are unlikely is because great vocals and amazing coordination does not come from a single gene mutation, or even from an easily identifiable number of genes.

Hank Greely, director of the Center for Law and the Biosciences at Stanford, said,“Right now, we know nothing about genetic enhancement,”. “We’re never going to be able to say, honestly, ‘This embryo looks like a 1550 on the two-part SAT.’”File:Baby Face.JPG

Physical traits, like height or arm length, will also be difficult to genetically manipulate. Some scientists estimate height is influenced by as many as 93,000 genetic variations. A recent study identified 697 of them.

Talents and traits aren’t the only thing that are genetically complex. So are most physical diseases and psychiatric disorders. The genetic message is not a picture book ,but it actually resembles a shelf full of books with chapters, subsections and footnotes.So talents, traits and most medical conditions are out of the equation.

But about 10,000 medical conditions are linked to specific mutations, including Huntington’s disease, cancers caused by BRCA genes, Tay-Sachs disease, cystic fibrosis, sickle cell anemia, and some cases of early-onset Alzheimer’s. Repairing the responsible mutations in theory could eradicate these diseases from the so-called germline, the genetic material passed from one generation to the next. No future family members would inherit them.

Although this is challenging, it is proven to be more possible for scientists to alter the genes that lead to genetic diseases.

Last but not least, it is illegal.
There are debates regarding ethics and “playing God”. “I’m totally against,” said Dr. Belmonte. “The possibility of moving forward not to create or prevent disease but rather to perform gene enhancement in humans.”

Other people are scared of a super children takeover.

“Allowing any form of human germline modification leaves the way open for all kinds — especially when fertility clinics start offering ‘genetic upgrades’ to those able to afford them,” Marcy Darnovsky, executive director of the Center for Genetics and Society, said in a statement. “ We could all too easily find ourselves in a world where some people’s children are considered biologically superior to the rest of us.”

In summary, genetic modification for babies will only be used in dire cases. Therefore, the only way I can have a red head child who can play the piano and the flute simultaneously with their feet is through Sims 4.

Not to worry… you’re someones (blood) type!

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On November 6, 2017

In Student Post

 

BLOOD

Blood types were first discovered in 1901 by Austrian immunologist, Karl Landsteiner. The classification of human blood is based on the inherited properties of red blood cells as determined by the presence or absence of the antigens A and B, which are carried on the surface of the red cells. So what is the difference between types A,B,AB and O blood?

This picture demonstrates the possibilities of different blood types and their characteristics.

 

Blood Type is Hereditary 

Hereditary is defined as genetic factors that are able to be passed on from parents to their offspring or descendants. If someone has blood type A, they must have at least one copy of the A allele, but they could have two copies. Someone who is type B must have at least one copy of the B allele.  Alleles are one or two or more alternative forms of a gene that arise by mutation and are found at the same place on a chromosome.

Blood types are either positive or negative.  It is important to note that blood cells do not have a charge, the + or – is used to determind specific traits of the cell. For example, the + or – is determined on wether or not the blood cell has the antigen “Rh factor”. If there is a + attached to your blood type, the antigen is present; if there is a – next to your blood type, the antigen is not present.

So What?

Dealing with blood types is very interesting because, according to “Scientific American”, blood type may affect brain function as we age, concluded from a new large, long-term study. However those with AB show a 10% increase of having cognitive problems. From that same study, it was determined that…

In addition to blood types affecting health, blood types also contribute to a persons personality.  According to James and Peter D’Adamo’s work, type A tends to be cooperative, sensitive, clever, passionate and smart where type B people tend to be balanced, thoughtful and ambitious.

Blood type’s current impact on society is very crucial because it gives insight to future diseases, the ability to donate blood to those who need it, and for new born babies be a backbone for their personality.

Comment your blood type below!

 

How A Chemical From the Cypress Tree Could Advance Epigenetics Against Cancer

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On April 5, 2017

In Student Post

by Czechmate on Wikimedia Commons

Found in the essential oil extracted from the bark of a cypress tree, a chemical named hinokitiol shows potential to impact epigenetic tags on DNA and stop the activity of genes that assist the growth of tumors.

In order to develop an of understanding cancer, researches have had to comprehend the DNA methylation, an epigenetic function which controls gene expression. In regular DNA methylation, genes that work to fight against tumors are turned on, reducing the risk of cancer. However, if DNA methylation is negatively altered, then those cancer-fighting genes will be silenced, helping to progress cancer development. Scientists have tried to combat irregular DNA methylation and over-silencing of genes by creating epigenetic anti-cancer medications that reverse non-beneficial methylation effects. Like in most cases of medication usage, the users face unappealing side effects. Hinokitiol is attractive to scientists because it is a natural compound with many health benefits and way less side effects than modified drugs that can possibly cause mutagenesis and cytotoxicity.

 

Researchers from the Korea University College of Medicine tested the productivity of the hinokitiol chemical in a study by giving doses of it to colon cancer cells. It was found that this chemical helped to inhibit the colon cancer cells efficiency without affecting the colon cells without cancer. The scientists also found through careful inspection that the presence of hinokitiol decreases the expression of proteins DNMT1 and UHRF1; both of which are proteins that encourage carcinogenesis. In summary, the doses of hinokitiol appear to have allowed normal cells to remain healthy, while reducing the ability for the colon cancer cells to thrive and ceasing the production of proteins that promote cancer maturation.

Researchers are continuing their search for natural compounds, as opposed to artificial medications, that can prevent the flourishing of cancer in our bodies through playing a positive role in gene expression and DNA methylation.

http://www.whatisepigenetics.com/cypress-trees-epigenetically-protect-cancer/

 

 

https://commons.wikimedia.org/wiki/File:Raindrops_on_leyland_cypress.jpg

The Miracle of CRISPR/Cas9 in Gene Editing

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On April 5, 2017

In Student Post

Some scientists say, “you can do anything with CRISPR” and others are absolutely astonished and amazed.

CRISPR can rapidly change any gene in any animal or plant with ease. It can fix genetic diseases, fight viruses, sterilize mosquitos and prepare organs for transplant. The possibilities are endless – and the prospect of designer babies isn’t far off.

https://en.wikipedia.org/wiki/CRISPR#/media/File:Crispr.png

Dead Cas9 can fix a single base pair typo in DNA’s genetic instructions. It can convert a C-G into a T-A pair. Also, we can attach fluorescent tags to dead Cas9 so researchers can locate and observe DNA or RNA in a living cell. Dead Cas9 can also block RNA Polymerase from turning on a gene, in CRISPRi. In CRISPRa, a protein that turns on genes is fused to dead Cas9.

CRISPR can be used for anything involving cutting DNA. It guides molecular scissors (Cas9 enzyme) to a target section of DNA & works to disable or repair a gene, or insert something new.

Many scientists have been thinking of improvements for this miracle gene editor. RNA Biologist Gene Yeo compares the original Cas9 to a Swiss army knife with only one application – a knife. He says that by bolting other proteins and chemicals to the blade, they transformed the knife into a multifunctional tools.

CRISPR/Cas9 is special because of its precision. It is much easier to manipulate and use compared to other enzymes that cut DNA. By using “guide RNA” it can home in on any place selected by the researcher by chemically pairing with DNA bases.

While Cas9 does have some problems, scientists definitely see the potential for greatness with a few tweaks. They wanted to ensure permanent single base pair changes, and they increased that from 15 to 75 percent. Liu used a hitchhiking enzyme called cytidine deaminase.

Scientists researched chemical tags on DNA called epigenetic marks. When scientists placed the epigenetic marks on some genes, activity shot up. This provided evidence that the mark boosts gene activity.

Case can also revolutionize RNA biology. The homing ability of CRISPR/Cas9 is what makes this seem possible. It was found that Cas9 could latch on to mRNA.

CRISPR/Cas9 was first found in bacteria as a basic immune system for fighting viruses. It zeroes in on and shreds the viral DNA. Half of bacteria have CRISPR immune systems, using enzymes beyond Cas9.

Overall scientists predict that in the next few years, results will be amazing. The many ways of using CRISPR will continue to multiply and we will see where science takes us.

Source: https://www.sciencenews.org/article/crispr-inspires-new-tricks-edit-genes

Other Sources: https://www.neb.com/tools-and-resources/feature-articles/crispr-cas9-and-targeted-genome-editing-a-new-era-in-molecular-biology

8 Genes That May Be Affecting Your Sleep Patterns

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On March 2, 2017

In Student Post

Have you ever wondered why you struggle to fall asleep at night, while your sibling has no issues sleeping soundly for eight hours? What causes your sleep patterns? While your sleep may occasionally be affected by a particularly stressful event, leading to irregular sleep patterns, for

While your sleep may occasionally be affected by a particularly stressful event, leading to irregular sleep patterns, for many, it is simply caused by the way their brains and bodies work. New research has identified for the first time eight specific genes that are linked to insomnia or excessive daytime sleepiness. The data also revealed that some of the genes associated with disturbed sleep identified in this study seemed to be linked to certain metabolic and neuropsychiatric diseases too, like restless leg syndrome, schizophrenia, and obesity.

Richa Saxena, one of the co-authors and assistant professor of  anaesthesia at the Massachusetts General Hospital and Harvard medical school, explained why this research was so important: while “it was previously known that sleep disturbances may co-occur with many diseases in humans, but it was not known that there are shared genetic components that contribute both to sleep problems and these conditions.” Furthermore, while studies have previously identified genes linked to some sleep disorders, this is the first study that has specifically linked genes to insomnia.

Link to Original Image

The study looked at the prevalence of insomnia, sleep problems and excessive daytime sleepiness in 112,586 European adults who had participated in a UK Biobank study. All participants had their genes mapped, as well as additional information like weight and diseases/chronic conditions. The results revealed fascinating linkages between certain genes. For example, the genes linked to insomnia were most strongly related to those associated with restless legs syndrome, insulin resistance, and depression, while the genes associated with excessive daytime sleepiness were also linked to obesity. Saxena remarked again that “it was not known until this study that there are shared genetic components- shared underlying biological pathways- that contribute to both sleep problems and these shared conditions.”

Of course, this study is not 100% conclusive- people who have trouble sleeping are not necessarily at higher risk for restless legs syndrome, schizophrenia, and obesity. In reality, it is likely that many different genes contribute to both sleep problems and these medical problems, Saxena said. But this new study does suggest that these problems share genes and underlying pathways.

So what does this research do for the average person? Well, not much. Right now, it’s just fascinating news that there may be a genetic reason people with these disorders are more likely to have troubled sleep. However, there is hope that in the future researchers will be able to design and test various drugs to target these genes. This would bring immense benefits to people who struggle to keep normal sleep patterns, as well as helping individuals proactively avoid diseases they may be more at risk for (for example, obesity).

 

Transgender- Science Behind Sexual Identity

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On October 13, 2016

In Student Post

Stop Homophobia - NUS Sports Gay Protests, London

Darren Johnson Image Link

Transgender concepts have been a prevalent issue. It has been seen on a celebrity level with Caitlyn Jenner but on smaller levels as well. Schools are struggling to make decisions of whether to make bathrooms same-sex or unisex. While administrative figures are struggling to make accommodations for the increasing number and popularity of LBGT rights, society is also struggling to determine whether trans-gender identity is a social or biological doing.

One recent finding has shown that anatomical sex- gender identity and orientation- is determined in the womb. However, once the anatomy is settled, there is about a six month lag before the brain masculinizes or feminizes. Research has concluded that through some combination of genetics, hormones and the uterine environment, sometime between six months and delivery the sexual orientation is set in the brain. The only question that rises is what happens when the brain does not match the genitals.

Genetics has been proved to play a role in transgender identity. Researches studied a group of twins where either one or both were transgender.  In identical twins, 39% were both transgender. Of the fraternal twins, there were zero pairs where both were transgender. In fact a study in the Journal Biological Psychiatry, researchers found a gene variant that was associated with being a trans woman.

For the 61% of identical twins where only one is transgender, the prenatal environment, or womb, had a key role. While identical twins share genetic codes, the genes that get expressed or remain unexpressed differ. Identical twins have separate umbilical cords , separate amniotic sacs, and develop in separate locations of the womb. All these things can have an affect in the mixing of chemicals and the sexual identity process.

Lastly, the structure of the brain also plays a role. A 2014 study from the Journal of Neuroscience found that “differences in the brain’s white matter tracts [fall] along a perfect spectrum of gender identity with cisgender men and women at the ends and trans men and women in the middle.”

 

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