Tuesday, August 6, 2019

'Love hormone' has stomach-turning effect in starfish


Sea stars are strange creatures!
If you could take love, bottle it, and sell it, you'd be a billionaire by tomorrow. That's what some scientists are trying to do. Scientists at the Queen Mary University of London are seeing how oxytocin, the 'love hormone' works in starfish. Oxytocin, more commonly known as the 'love hormone', is important for sexual reproduction in humans, other mammals, and even nematode worms, but this study shows that in the common European starfish (Asterias Rubens) it is important for feeding. The findings could be instrumental in saving the coral reefs, a major food supply for the crown of thorns starfish. Oxytocin in starfish causes starfish to have rapid and immediate hunger. However, in mice, oxytocin, has been known to cause nausea and lack of eating. The hope is to find a way to hide this expressive gene.




Scientists at Queen Mary University in London are trying to find an accessible and effective way of dosing a correct amount of chemically inactive oxytocin near the coral reefs to prevent the starfish from completely consuming the coral reefs.

Image result for oxytocin


Starfish feed naturally by climbing on top of prey such as mussels or oysters and adopting a rigid humped posture so that they can employ the pulling power of lots of tiny tube feet on the underside of each arm to pull apart the two valves of their prey.




Professor Elphick of Queen Mary University of London states, "What is fascinating is that injecting the hormone in starfish induces what is known as fictive feeding. The starfish are behaving as if they are feeding on a mussel or an oyster but no mussel or oyster is there to be eaten."




If scientists are able to come up with this noneffective oxytocin replacement for starfish, then the coral reefs may be saved from being eaten. Every year miles and miles of coral reef are destroyed by environmental factors, especially human interactions. If we can help limit their destruction, we may be able to preserve them for future generations. This oxytocin research seems like a good place to start!

Argentina Drug Offers Hope to Cystic Fibrosis Families

Cystic fibrosis (CF) is a genetic disease located on chromosome 7 that affects the exocrine glands in the body. It causes abnormally thick mucus, leading to the blockage of the pancreatic ducts, intestines, and bronchi which often results in respiratory infection and progressive worsening of lung function. Life expectancy for this disease is currently 47 years.


Three years ago, a new medicine called Orkambi was discovered in Argentina that was designed to reverse one of the genetic flaws that make CF as damaging as it is. The studies of this drug have had mixed results, but one of the more optimistic results said that it has nearly halved the disease progression of CF. While this drug has the potential to help many people affected by CF, it is not accessible to all. The official price of the drug is around $100,000 a year, and at this price England, along with other countries, has determined that the price is not worth the effectiveness of the drug. Families will not take no for an answer, “She’s our child, nothing else matters – I’d lose my house before I take her off the treatment,” says Nina White from Kent, mother of seven-year-old child with CF.

With the hope of a treatment families have turned to private companies and are spending $8,000 a month for the treatment. “We’re going month-to-month, everyone’s digging in. It’s completely unsustainable,” says White. Even though the price is unsustainable, White has noted remarkable improvement in her daughters condition and will do whatever she needs to to keep her daughter on the treatment. Since Orkambi is not patented, another company in Argentina has began producing a similar drug for only $23,000, a significant reduction in price that may make the drug accessible to more families.

I believe that this advancement has the potential to help thousands of people affected by the genetic disorder cystic fibrosis. I want to be glad that another company found a way to produce the drug for cheaper, but people can not forget about the 20 years and billions of dollars that the original company poured into research to discover the drug. I hope there is a future where this drug will become accessible for every patient diagnosed with CF to increase life span and quality of life.

Mission Impossible? Maker of Plant-Based Burger Struggles to Meet Chains’ Demand

The article, “Mission Impossible? Maker of Plant-Based Burger Struggles to Meet Chains’ Demand”, by Neil Vigdor is about the impossible burger made by Impossible Foods in California. These burgers are known as impossible because they are not actually made of meat; however, they seem to resemble meat very closely. They taste like, cook like, and look like meat. They have been sold to White Castle and Red Robin, two famous chains. The demand for the burger has increased dramatically since its introduction. Vegans and vegetarians are the main target group, because this is a food item they are not able to regularly enjoy. Even some carnivores are interested. 


Above is a picture of the impossible burger. It appears to look the same as a regular burger. 


Because the burger has been such a success, the company now has a much higher demand. Some restaurants even want to use other impossible foods as meat substitutes in lasagna, tacos, and a slider version of the burger. The company will have to hire more to keep up. 
The most interesting part of the impossible burger is what it is actually made of. The “meat” is technically a GMO. The patties are made out of genetically engineered, soy based hemp protein. The article, “The ‘magic mix’ of ingredients responsible for the Impossible Burger’s taste and texture”, by Ricki Lewis offers more insight. The ingredient is known as soy leghemoglobin. When the burger is cooked, it reacts to produce heme which is what makes it turn red like meat. 
Unfortunately, the article by Lewis explains an unfortunate problem. As Vigdor mentioned, the demand for the impossible burger is very high. There is not enough land for soybeans in the United States to meet the demand that has been projected. Luckily, genetics is to the rescue. Through recombinant DNA technology, the soybean protein can be made in the cells of another species. It could be made in one that is easier than growing acres of soybeans to acquire it. Researchers have been able to put the gene that encodes for legHB into the genome of a single, complex celled fungus known as Picchia pastoris. This would allow the company to keep up with the demand. 
One of the problems with the burger not concerning the high demand is the controversy over GMOS. The second article offered more insight. Rather than yes or no, it appears to be both. The legHB protein is identical to the protein from soybean root nodules but the yeast used to make it would be genetically modified. 

I found this topic extremely interesting, because I am a vegetarian myself. I have not tried this burger, but I have had the beyond burger. I think that a plant based diet is a much more sustainable, and environmentally friendly way to live. However, I know it is not for everyone. The impossible burger offers a plant based version that still tastes like meat. While I have my own reservations about GMOS, I think genetics and using recombinant DNA to keep up with these demands is part of the answer to the environmental and food crises.

Monday, August 5, 2019

Accuracy of Genotyping Chips Called into Question

Genotyping chips are used to detect single-nucleotide polymorphisms, the type of DNA used by consumer genetic testing companies to detect variants in a persons genome. These genotyping chips have a false discovery rate of more than 85 percent when screening for rare variants, according to an article from BioRxiv. This finding highlights the danger of direct-to-consumer genetic testing, where customers could “interpret the results at these rare variants literally, without accounting for any possible laboratory errors,” Chiang, a human geneticist at the University of South California Keck School of Medicine, says. “That would be a legitimate concern.”

The chips in which this study came from were supplied by a manufacture named Affymetrix, owned by Thermo Fisher Scientific. They supply their chips to direct-to-consumer companies such as LivingDNA. The companies claim to warn customers not to take their results as a medical diagnosis, but most consumers are not aware of the level of uncertainty in this consumer genetic tests. Other direct-to-consumer companies like 23andMe claim to have a higher accuracy but are still susceptible to false positives in very rare variants.  

An example of a rare variant that may bring about false positives are the BRCA genetic variants. BRCA1 and BRCA2 variants are linked to breast and ovarian cancers, to which there are thousands of known rare variants. The direct-to-consumer companies MyHeritage and 23andMe both announced that they will soon begin providing genetic tests for three variants found on the BRCA1 and BRCA2 genes.


I believe that direct-to-consumer genetic companies are a great way to get the general public interested in genetics and their own genome. It has amazing potential to help people find family and see what part of the world their heritage originates from, but testing for rare genetic variants may still be out of the reach of consumer genetic testing companies. I think that being able to see that if someone has a variant of the BRCA gene would be very helpful in being able to start testing regularly and early to catch any sign of cancer, but with the present rate of false positives in rare variants I believe that we should wait to make this information available to the public until it becomes more accurate.

Sunday, August 4, 2019

Knockout mice are guide to new genes for eye and skin disorders

The article, “Knockout mice are guide to new genes for eye and skin disorders”, discusses the role mice play in discoveries about humans concerning certain disorders. There is a lot of information known about albinism. Albinism is a disorder that affects the pigment of hair, skin, and eyes. It can vary from extreme to mild. Scientists have been able to connect a lot of genes to 
Above is an image that depicts the difference between a transgenic mouse and a knock-out mouse (https://www.jidsponline.org/article/S0022-202X(15)52560-8/fulltext)


the disorder, however there is still a lot unknown. At UC Davis, researchers have used mice to target certain disorders genetically. They use “knock-out mice” in which an existing gene is inactivated to learn more about its function. 
Albinism in humans is just starting to be understood. However, it is very hard to look at the genetics of humans. We can easily sequence a genome, but it is harder to figure out the tie between a gene and a disorder. Luckily, through the mice, we are able to do this much more easily. Mice are not as variable, so it is easier to find the connections. While humans are not mice, through the discoveries in mice, it makes it considerably easier to find the target genes in humans. It allows us to focus on more specific genes which is a lot less daunting than the whole genome. 
There has been success in using these knock-out mice. The article, “300 blind mice uncover genetic causes of eye disease”, explains how genes linked to vision disorders have been identified. Three quarters of these had been previously unknown. Through finding the analogous genes in humans, we will be able to locate the cause for blindness genetically with much more ease. 
The reason mice are a prime candidate for the study as well as many other studies is because their genetic background has become so consistent in a laboratory setting. This creates a pretty reliable control and leaves less room for variables and discrepancy. 

Once these genes for disorders are pinpointed in mice, the knowledge can be applied to humans. I think it is amazing how all living organisms, that we know of, are based on the same genetic code. Through this, it allows us to make discoveries into our own species through research on the genetics of another. Having more insight into these hair, eye, and skin disorders will have all sorts of positive consequences. Scientists will be able to understand certain ailments and be better equipped to treat them. 

California Mountain Lions

        Puma concolor, or the mountain lion goes by many names. Puma, cougar, catamount and panther are just a few. While the mountain lion goes by many names, it's genetic code remains relatively the same. Although the mountain are not in direct danger of extinction, their population is decreasing at a high rate. The mountain lion itself is what is known as a indicator species. This means that the speices can be used as a great reference on how an environemnt is doing, and how well the environement has remained connected. The large cat also acts as an umbrella species. These "umbrella species" are extremely important biologically and ecologically. Umbrella species are usually greatly monitored and protected beceause in protecting them, many other species become protected indirectly. Due to this, conservation techniques have been put in place in many areas where the puma exist. However in a recent study to observe how geography changes genes, researchers stumbled upon something rather interesting.
      431 mountain lions from various location were used in a study to collect data about the levels of genetic diversity among the species. In order to accomplish this 12 microsatellites loci were analyzed in each cat. After looking closely at the data gathered, it was found that each cat had distinct genetic  subdivisions that were specific to the region they were from. It was found that cats from coastal regions displayed more heterozygosity than the cats sampled from inland areas. Heterozygosity is important in population genetics, as the heterozygote advantage plays a large role in species survival. Scientists came to the conclusion that geographic barriers like the Los Angeles Basin, the San Fransisco Bay and the Central Valley turned out to be enormous barriers to natural gene flow of the species. The disruption of gene flow can result in many things particularly different allele frequencies among the species. Metapopulations in Southern California have exhibited normal gene flow but recently human development has increased how hard it is for populations to travel, which in turn decreased gene flow. With this, human development has displaced many of these large cats leading them to environments their ancestors did not inhabit before, or into urban areas. These new environments present challenges for the species, one which they may not actually be able to survive.
    In essence this study provided conservationists with a ton of new data to analyze, think about and act upon in the coming years. Most importantly, it displayed an important concept. Conservation genetics, and genetic preservation. This study indicates that not every case can be treated the same way. Each population of these cougars has different genetic subdivisions, and faces different enviroenmtal cahllenges. From this work, scientists hope to come up with movement corridors in unpopulated regions, to help the pumas travel from area to area, and increase biological diversity.  Landscape-level conservation is not only crucial to the survival of this species, but crucial in helping the species become more heterozygotic.
      This study was awesome because it really shows the connectedness of species between each other. In protecting the mountain lion, you protect the big horn sheep, which in turns help stabilize plant growth, and the list goes on and on about the connectedness of the mountain lion to almost everything it interacts with. Population genetics are studied extensively with animal populations, and I hope to work with wildlife one day, so reading these articles get me excited for the future. Hopefully measures can be put in place so that these animals can travel more freely and give themselves a fighting chance against their ever-changing environment.


https://link.springer.com/article/10.1023/A:1024069014911

https://www.sciencedaily.com/releases/2018/12/181221142514.htm

https://www.scientificamerican.com/article/highways-fragment-southern-california-mountain-lion-gene-pool/
       

Fly antimicrobial defense system doubles as tumor-killer


In their experiment, tumor prone fruitflies produced more Defensin than normal fruit flies. Defensin is a protein that interacts with dying tumor cells in animal cells. By shutting down Defensin in the tumor prone animals, tumor cells begin to grow. This suggests that Defensin is actively killing cancer cells while sparing healthy cells. By using the fly version of Tumor Necrosis Factor, Parvy shows that this factor helps flag tumor cells for destruction and makes the cells more sensitive to Defensin's attack. It does this by bringing a protein called phosphatidylserine to the surface of the tumor cells. Defensin binds to these sites and terminates the cell.




An antimicrobial agent called Defensin kills tumor cells and shrinks tumor size in fruit flies, with help from a pathway that flags the cells for destruction.

Recent studies published in, eLife, show that there is the first evidence in live animals that antimicrobial peptides, AMps, which help protect against infection, can also defend against cancer!



Lead author, Jean-Philippe Parvy, a postdoctoral fellow at Cancer Reseach UK's Beatson Institute in Glasgow states that, "We used the fruit fly Drosophila melanogaster to investigate whether the machinery that is best known for its role in the recognition and elimination of harmful microbes is also capable of recognizing malignant cells in a living organism and eliminating them in a similar manner".



Image result for fruit flies
        Parvy's work could be instrumental to future treatments for cancer within humans if given more time. I believe that if scientists can use Defensin to target human Tumor Necrosis Factor, then a cure for cancer may be in the near future. Converting Defensin to a treatment suitable for humans is the next hurdle that scientists need to jump over. I believe that they can do this, and create more effective cancer treatments, hopefully without the awful side effects of traditional treatments.

https://www.sciencedaily.com/releases/2019/07/190730125311.htm

Saturday, August 3, 2019

One Gene Change 2 Million Years Ago Left Humans Vulnerable to Heart Attack

     Scientists currently believe that humans are the only species to get heart attacks caused by clogged arteries. New research suggests that a single DNA change 2 million years ago is at the heart of this. Dr. James Jeffrey, a cardiologist, believes this finding creates the link between genetic and environmental factors which cause atherosclerosis and inflammation of arterial walls. However, even chimpanzees do not suffer from this affliction, meaning these types of heart attacks are specific to humans.

     To find out why researchers led by Dr. Nissi Varky and Dr. Amit Varky looked at a gene known as CMAH.  This gene functions by creating a sialic acid sugar molecule known as Neu5Gc. In other mammals a functioning version of this gene appears to greatly reduce the likelihood of atherosclerotic damage in blood vessels. The problem is this gene seems to have been switched off in humans roughly 2 to 3 million years ago. The researchers hypothesize that a dangerous malarial parasite thrived in the presence of Neu5Gc which forced the human genome to evolve and shut down production of this gene. While this change benefited humans by causing resistance to these parasites, it may have caused humans to become more vulnerable to develop fatty deposits in arteries.

      To test this theory, the team compared rates of atherosclerosis is mice with a working CMAH gene and a genetically modified version of the gene not producing Neu5Gc. This test showed that mice with the non-working gene showed nearly double the fatty buildup in their blood vessels. The mice without the gene were then fed red meat, which naturally contains New5Gc which caused even more significant buildup of fatty deposits in blood vessels.

        The researchers believe that this could be a reason that diets high in red meat are linked to heart disease. The hypothesize that contact with Neu5Gc sets off an immune response which leads to a chronic state of inflammation within the blood vessels. This gene may be the reason why people who don't eat meat altogether still are at a high risk for heart attacks while our other mammalian ancestors are not, Currently heart disease is one of the leading killers in the United States. If a form of gene therapy was developed to target this gene, and also other genes involved in how the body reacts to Neu5Gc, a very large dent could be made in the number of people who are claimed by heart disease, which is rapidly rising.

Image result for Neu5Gc

Image result for atherosclerosis

https://www.usnews.com/news/health-news/articles/2019-07-29/one-gene-change-2-million-years-ago-left-humans-vulnerable-to-heart-attack