Mutation Helps Even Carriers of 'Alzheimer's Gene' Avoid Alzheimer's

 

In this article written by Dennis Thompson of HealthDay, published by USNews, the author discusses new research on a cell function-boosting mutation that could help protect even carriers of Alzheimer’s disease from developing it. The mutation causes cells to produce a more powerful version of the protein humanin, which protects against cellular aging. 

Researchers examined over 500 participants, including people 100 years old or nearing 100, and their children. Of these people, they found that 12% of centenarians of Ashkenazi descent carried the P3S variant, which codes for higher levels of humanin. 

They then turned to genetically engineered mice altered to carry the APOE4 gene associated with a higher risk of Alzheimer’s. Researchers treated the mice with PS3 gene-produced humanin. The mice then displayed a marked reduction in amyloid beta, the protein associated with Alzheimer’s that builds up in the brain and impairs cognitive function. This research suggests that the P3S variant may be a reason why carriers of the APOE4 gene avoid Alzheimer’s.  

I found this research to be both fascinating and incredibly relevant to me. My grandmother died of Alzheimer’s, as have many of my other family members. Her caretakers were always giving her medications and I never understood how they helped. This research could lead to future treatments, and as there is a likelihood that I personally carry the APOE4 gene, I find it important to be well informed on the subject. Additionally, I believe it is important for all people to be educated on the disease. It is important to know the signs and symptoms, as dementia can be a common misdiagnosis before motor functions become impaired.   

Article: Mutation Helps Even Carriers of 'Alzheimer's Gene' Avoid Alzheimer's

Additional Info: A rare mutation protects against Alzheimer's disease, Stanford-led research finds

APOE4 Gene holder may be at a higher risk of contracting COVID-19

Researchers have recently discovered that a genetic variant that raises the risk of developing Alzheimer disease may also increase the dangers of COVID-19. They have discovered that a version of APOE gene called APOE4 in patients were more likely to test positive for COVID-19 than the APOE3 version. Studies have been also conducted with patients who have dementia that contracted the virus to show more serve symptoms or die, then further studies confirmed that the APOE4 showed a increase of serverity when contracted with COVID-19 than APOE3."Among nearly 400,000 participants in the large genetic database called the UK Biobank, only 3 percent have two copies of APOE4, while 69 percent have two copies of APOE3. The remainder have one of each version. But the APOE4 version was more common than expected among people diagnosed with COVID-19, the study found. Of 622 people who tested positive for the coronavirus, 37 had two copies of APOE4. On a population scale, that means about 410 of every 100,000 people with two copies of that version of the gene would test positive, the researchers calculate. That compares with 179 of every 100,000 people with two copies of APOE3 testing positive. "[1]
The APOE is a protein that is involved in the metabolism of fats in the body. When a person has the APO4 gene they risk of having a number of protein clumps in the brain tissue, which would cause Alzheimer and dementia. The APOE also helps the immune system suppress T cell proliferaiton and neutrophil act. This may be the reason of the rise of COVID-19 contraction in patients with APOE4 being at much more risk in contracting and severity of symptoms but more studies would need to be conducted in order to support the claim.

[1]https://www.sciencenews.org/article/coronavirus-covid-19-genetic-risk-factors-alzheimers-disease

[2]https://ghr.nlm.nih.gov/gene/APOE

[3]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2896842/#:~:text=In%20addition%2C%20apoE%20functions%20on,well%20as%20modulating%20inflammation%20and

SARS-CoV-2 May Trigger Genetic Alterations in Platelets

COVID-19, caused by the SARS-CoV-2 virus, is a major pandemic occurring at this very moment, affecting millions of people around the world. Its presence is terrifying enough, but recently, it was reported that blood-clotting cells in patients have been genetically altered due to the virus. Researchers at the University of Utah reported that these platelets are becoming “hyperactive,” ultimately leading to increased risk of life-threatening blood clots, such as a heart attack or stroke. Specific genetic processes seem to be affected, but it is still relatively unknown as to which processes cause these platelet changes. While researchers nationwide are currently studying whom this may affect most as well as how it could be prevented, clinical trials are either freshly underway or in the works.

As for what this means for us right now, we all must continue wearing masks, social distancing, and self-quarantining if we feel symptomatic. Until more research is conducted and a potential vaccine or cure is found for COVID-19, it is crucial to be aware of the serious health issues that remain even after the patient is cured.


Article: https://www.sciencedaily.com/releases/2020/06/200630125129.htm

Related Article: https://directorsblog.nih.gov/2020/06/11/searching-for-ways-to-prevent-life-threatening-blood-clots-in-covid-19/

Gene In Worms Promote Age and Reproduction, but Supress Immune Response

A study is being done by geneticists to see how a gene in worm DNA is affecting the worm's lives. First, they noticed that the worms were producing more offspring and were living longer unless exposed to a disease. They recognized the gene, TCER-1 as responsible for producing the protein that has this affect. At first, they though the gene would increase immune response along with reproductive capabilities. They observed the complete opposite. What was observed was that the worms with the gene produced more offspring but fought off diseases worse. When exposed to Alzheimer's disease protein, which paralyzes worms, worms with the gene survived nearly 1/3 of the time that worms with the genes did. Although, the gene made it possible for sick worms to produce healthy offspring.



Recently, a similar gene was discovered in humans. While not a worry at the moment, scientists say it is a "warning bell"(Saey). Particularly this could affect anti-aging therapies as some can cause unexpected frailty. Personally, the research is important and is something humans need to keep an eye on. It is especially important now that humans are living longer and longer and as more resistant diseases are beginning to emerge.





https://www.sciencenews.org/article/gene-may-help-worms-live-longer-not-healthier
https://www.nature.com/articles/s41467-019-10759-z

The Possible Heredity of COPD

COPD affects several Americans across the country each year. COPD is short for chronic obstructive pulmonary disease. It is a combinations of many of different conditions that negatively affect the lungs along with damage and inflammation tot he airways. Physicians do not look at the genetic factor that may take place in developing this disease when believing that someone may be at risk. There are many risk factors that have a severe affect on causing COPD and making it significantly worse. There may also be a genetic link to determine the risks of individuals that may be at a higher risk for developing COPD in the future.

The genetic link that some people may have to COPD is called AAT. Also known as alpha-1 antitrypsin. The only way to be at risk for COPD would be to have a deficient of AAT. It has been determined by the National Heart, Lung, and Blood Institute, that about 100,000 individuals living in the United States have an AAT deficiency that increases their risk of developing COPD. A person who lives in an environment with clean air and is a non-smoker can still be diagnosed with COPD if found with a deficient in AAT. There is not a specific test that physicians do to determine if someone has an AAT deficiency, therefore they may never even know if they have it. Instead, they look for the following signs, shortness of breathe, wheezing, a persistent cough, and regular respiratory infections.  Individuals that are AAT deficient have a chance of developing COPD at the early age of twenty years old.

In order to try and prevent the development of COPD is to stay away from many risks factors such as smoking and polluted air. The only way that an individual can be AAT deficient is if it is passed down through both parents carrying the deficient gene. If the gene is passed along through only one parent then the individual will not be AAT deficient, but it could be passed on to their children. The AAT deficiency may not be as common as the risk factors that contribute to COPD. People who is AAT deficient should talk to their doctor, reduce their vulnerability to the risk factors, and make lifestyle changes if necessary. Personally I believe that people should be aware of the risk factors and avoid them as much as possible whether they have the deficiency or not. By ensuring good health, taking the necessary steps to be educated on the risk factors can decrease the amount of people suffering from this disease.

Article: https://www.medicalnewstoday.com/articles/323348.php
Related Article: https://www.ncbi.nlm.nih.gov/books/NBK1519/

Key Gene to Accelerate Sugarcane Growth is Identified

Sugarcane lines have been known for having constraints on culm development. This means that the sugar’s storage capacity is physically limited, restricting the volume of sucrose and biomass produced. However, a study performed by the Bioenergy Research Program has discovered the gene ScGAI that place an important role in regulating culm development in sugarcane. ScGAI mediates the regulation of developmental hormones such as ethylene and gibberellins. Both hormones are used by sugarcane farmers to accelerate sugarcane ripening by degrading the plants’ DELLA proteins. In some lines, the ScGAI gene is silenced and has resulted in taller and richer plants. “The study shows that the ScGAI gene is a fundamental component of sugarcane development and can be a target for genetic manipulation to permit intervention in the speed of plant growth by regulating DELLA proteins”.

The researchers next step are to move this experiment and produce field tests to see if they can mimic the same results as they did inside the greenhouse. This article relates greatly to the video shown in class ‘Food Evolution’. With the production of ScGAI-rich sugarcane plants, farmers would be able to cut back on adding hormones such as ethylene and gibberellins and still produce the same results.

Article link
Related article

Breakthrough: Researchers fix Alzheimer's gene

         Researchers have been studying the gene in the development of Alzheimer's gene,  apolipoprotein (APOE), a great deal and they know that having one copy of the APOE4 gene makes the risk of developing Alzheimer's 2 to 3 times more likely. "The E4 version of the gene seems to be particularly damaging to the brain, with several studies showing that this genetic variant increases the risk of toxic amyloid beta and tau buildup.

         Researchers at the Gladstone Institutes wanted to find out why the effects of the E4 version of the gene is so threatening, specifically what the difference is between the E4 and E3 versions of the gene. To find this out the researchers examined the effects of the APOE4 on human brain cells by modeling the disease in human cells. They created brain cells using skin cells from people who did not have Alzheimer's and had two copiers of the APOE3 gene. 

        They found that in human brain cells the E4 protein has a pathogenic conformation. A pathogenic conformation means that if has an abnormal form that prevents it from functioning properly. This leads to a series of disease causing problems. They also found that is increased amyloid-beta production in human but not mouse, neurons. They expressed that this could explain the differences in some drug efficiency between human and mice.

        The scientists tried to correct the affects of the gene by applying a previously developed APOE4 "structure corrector". In previous studies this corrector changes the structure of APOE4 so that it behaves more like the inoffensive APOE3 gene. Applying it corrected the defects and eliminated the signs of the disease, restored normal cell function, and helped the cells live longer. 

      In my opinion, this discovery can change many things. It is important to have more insight about how efficient drugs are on mice compared to humans. This can tell researchers more information for future drug development. Also these findings if they can cure Alzheimer's with this method or even prevent it until a later age will make a great difference. People will live longer lives and the emotional tole that this disease has on people and their families can be avoided or lessened. 

Link to article: 
https://www.medicalnewstoday.com/articles/321455.php
Link to another site:
https://ghr.nlm.nih.gov/gene/APOE

Experimental drugs rewire brain connections in autism

       

       The University of Texas Southwestern in Dallas has recognized two possible new treatments for autism spectrum disorder, targeting the impact of a faulty gene on neural communication. Autism it a serious developmental disorder that weakens the ability to communicate and interact. It often works as a canopy for autism spectrum disorder (ASD). It is categorized by repetitive behaviors, and impaired social communication. According to the Centers for Disease Control and Prevention (CDC), around 1 in 68 children in the United States have been diagnosed with ASD. Treatments for ASD often focused on addressing the behavioral symptoms and helping people with the disorder to learn better communication strategies. Till now, very few efforts have targeted the biological causes of autism.

       The two potential treatments that could restore the neurotransmission processes affected by the absence of a gene known as KCTD13. JCTD13 gene encodes a protein with the same name, and its expression level have linked with abnormal brain size, arguing on the loss and the gain of the chromosomal segment that contains this gene consult a substantial risk of autism and evolving delay. KCTD13 is not tied to the size of the brain but it is tied to synaptic transmission, or neurotransmission; this is the neurons ability to transmit information. KCTD13 deletion did not result in increased brain size, increased embryonic cell proliferation, and changes in migration. The deletion of KCTD13 impairs brain function in a major way, and they found a way to repair the damage, but they have more work to do before they try these treatments on people. The findings give us a clue as to what pathways are altered and where to look. The absence of KCTD13, increases the level of RhoA (a protein) which impairs synaptic transmission. To counteract the effect of the gene deletion, the researchers of the University tested different types of RhoA-inhibition drugs: Rhosin and Exoenzyme C3.

       Rhosin and Exoenzyme C3 were successful in restoring normal synaptic transmission in under 4 hours, the incubation of brain slices in RhoA inhibitors could reverse synaptic abnormalities within the relatively short time frame of a few hours. Exoenzyme C3 is currently being tested in clinical trails for the treatment of spinal cord injury. If successful, they hope that these trials will smoothen the path for further tests of the drug’s potential in ASD treatments, as well. First, we would like to know if RhoA levels are altered in the mouse, who lacks the chromosomal segment that contains KCTD13. Secondly, determine if the abnormal locomotor behavior in the KCTD13 mice might be rescued by treatment of the whole animal with RhoA inhibitors. And in the end, genetic models of autism were predicted to alter the RhoA pathway.

References:

Cohut, M. (2017, November 02). Experimental drugs rewire brain connections in autism.

Retrieved November 08, 2017, from https://www.medicalnewstoday.com/articles/319945.php

Washington University School of Medicine. (2017, November 2). In autism, too many brain connections may be at root of condition: Learning, social issues may reflect neuronal miscommunication. ScienceDaily. Retrieved November 10, 2017 from www.sciencedaily.com/releases/2017/11/171102131330.htm

Cross-Cultural Evidence for the Genetics of Homosexuality

Scientists at the University Lethbridge in Canada have shown in their research there is evidence that common genetic factors underlie in homosexual preference in men in multiple cultures. In south Mexico there are individuals called muxes which describes them as being biologically male and being attracted to other males. In the Mexican culture, they are recognized as a third gender and have shown correlations with homosexual males in other cultures. There has been something recognized as the fraternal birth order effect, which means the likelihood of a male being attracted to the same sex increases if there are a multitude of older brothers born before him. In Western culture, the homosexual man recall higher levels of separation anxiety compared to the heterosexual man. This means at some point during their lifetime, they were left by an important figure. Molecular genetic studies have shown that Xq28, a region on the top of the X chromosome is responsible for both anxiety levels and and male homosexuality. This means there is a possible genetic predisposition for both in humans. As research continues on this topic, the outcome could have political affects, as some parties believe this life style is a choice while others do not. I believe it would be interesting to see if there is a real genetic reason for homosexuality and think it could help the argument of whether or not it is a personal choice, or there is a scientific reason behind it.

Scientific American

Sweet Tooth or Salt Tooth?

According to an article written for Live Science, some people may carry a gene that instead of a sweet tooth gives them a Salt tooth. During tests performed it was found that a gene called TAS2R48 had a higher taste for salt and was more likely to make someone consume more salt daily. Those who did not have this gene were less likely to over consume sodium daily leading to a lower risk of heart disease. A theory along with the research is that TAS2R48 enhances bitterness; explaining why people expressing this gene seem to avoid green leafy foods. This leads people to lean towards salty less bitter foods increasing sodium intake and increasing risk of heart attack.  The hope of researchers at the University of Kentucky college of Nursing is to identify which gene variant people have and hopefully be able to help them make better food choices seriously for them.

    

I think this research gives an amazing stride to the fight of obesity in America. With this research, people can find out why they crave some foods over other foods. Hopefully, with this knowledge people can become more aware if they are prone to a higher consumption of salty food and be more aware of diet that would be healthier for them.  

Next Generation of Children?

       There are multiple ways traits are inherited from parents to offspring, the one that will be the focus of this article will be traits that are inherited from the mitochondrial DNA.  A majority of the mitochondria is inherited from the mother to the offspring, this leads to a disadvantage in the case where the mother may have a mitochondrial disorder such as mitochondrial myopathy which the offspring will inherit. 

          Scientist's from Britain's Newcastle University to create children using DNA from the mother, father, and a donor female to prevent the inheritance of mitochondrial disorders. This technique is done by extracting the nucleus DNA from the egg of the mother and is inserted into the female donor egg. The DNA from the female donor egg is extracted before inserting the mothers DNA. By performing this  technique the end result is the embryo ending up with DNA from the mother and mitochondrial DNA from the donor female. 

         Although this is a new form of preventative medicine, I believe this can have some trouble being accepted worldwide for at least another decade since this technique can lead to not only preventing disorders but also to designing what your own child can look like by removing certain sections of DNA and adding a section of a donors DNA for certain traits that are desired to be expressed. 

https://medicalxpress.com/news/2017-03-uk-grants-babies-dna-people.html

https://www.mda.org/disease/mitochondrial-myopathies

Gene Mutations in brain-linked to OCD Behavior

Recent research have provided further evidence of how gene mutations can cause certain brain region to fuel behaviors associated with obsessive-compulsive disorder (OCD). The causes of OCD are still unclear, however, previous studies have suggested that the disorder could be due specific gene mutations. Northwestern University have pinpointed in their recent studies that gene mutations in the corticostriatal region of the brain is what's leading OCD-like behaviors on their test mice. The corticostriatal brain region is responsible for regulating repetitive behavior. The tests done in mice's brain have shown that there's synaptic receptors known as kainate receptors (KARs) that play a key role in the development of the region. By manipulating the KAR gene in mice's brain, it shows that it compels the mice to perform repetitive behavior. This could be a gateway to finding out why OCD occurs.

This is an interesting article since it was trying to figure out what a mental disorder like OCD is linked with genetics. The KAR gene mutation could effect the corticostriatal region of the brain in order to create the behavior.

http://www.medicalnewstoday.com/articles/316039.php

Possible Gene Manipulation for Diabetes Cure

First lets distinguish the types of diabetes without going into much detail. Type 1 results when the body's immune response destroys the cells responsible for producing insulin these cells are called beta cells. Type 2 occurs when your body can't effectively keep up with the insulin demands of your body.  

With diabetes type 1 and 2 on the rise within the United States and throughout the world, scientists are looking around every corner to find a way to either prevent or cure diabetes. Dr. Francesca and her team from Max Delbruck Center for Molecular Medicine have found a way to reprogram liver cells into pancreatic beta cells in mice. This reprogram process occurs by introducing additional copies of the TGIF2 gene found on chromosome 2 of mice which reprograms the liver cells to take on an unspecialized state and stimulates the development of liver cells into pancreatic beta cells.

Although this study was not done on humans, progress and a new discovery has been made. This research brings genetic therapy for human diabetic patients a step closer for a cure. This is amazing research since so many lives are restricted by this disease. With the continuous study of the TGIF2 gene a cure may be within the near future.

The interesting part of this discovery for me that leaves me with a few questions is with the introduction of an increased amount of a certain gene would this lead to other mutations and to what degree? Would the mutations if any influence the degree to which other genes are expressed?
https://www.sciencedaily.com/releases/2017/02/170213083736.htm
http://www.genecards.org/cgi-bin/carddisp.pl?gene=TGIF2

Why we sleep?

Of all the articles I have posted, this by far is the most interesting to me, because it is a topic in which I have high interest in? I came across an article which covers some hypothesis that seems credible and logical to me, on why we sleep. For years numerous of hypothesis were proposed on why we sleep but it isn't until now, scientist have propose an hypothesis that compliments common sense. The article reveals that we sleep to forget things--as the memory bank can only store a certain amount thus, when we sleep we forget something in order to make space to learn new things. https://www.nytimes.com/2017/02/02/science/sleep-memory-brain-forgetting.html?rref=collection%2Fsectioncollection%2Fscience&action=click&contentCollection=science&region=rank&module=package&version=highlights&contentPlacement=9&pgtype=sectionfront

http://www.sleepreviewmag.com/2017/02/purpose-sleep-forget-scientists-say/

TB Gene Controlling Mutation

Anyone that watches the news, knows it's common to hear about the next new "superbug" or the next new big bad bacteria with high mortality rate such as the recent zika virus or swine flu outbreak. But behind the scenes geneticist have been working hard to find new breakthroughs concerning bacteria and pathogens. 

Scientist from Centro Nacional de Biotecnologia in Madrid and University of Sussex in Brighton have discovered a new gene referred to as NucS which has a large influence on whether or not mutations develop within the superbug, Mycobacterium tuberculosis. Tuberculosis (TB) is responsible for commonly affecting the lungs and can cause ailment in other areas of the body as well. The main problem concerning TB is its ability to mutate which results in becoming resistant to antibiotics. 

The NucS genes produces a specific protein, and this protein is able to repair the genome of TB, thus preventing mutation. If mutation of TB can be controlled or prevented this could allow more time for the development of new antibiotics and also slowing the rate of evolution of this bacteria. 

In my opinion this is amazing on how far science has come and far it can go. With the constant analysis of genes within bacteria and pathogens this could lead to a better understanding on how antibiotic-resistance starts in different strains of bacterium other than TB

https://www.sciencedaily.com/releases/2017/01/170127113019.htm. 

http://chelorg.com/2017/01/28/scientists-have-figured-out-why-tb-did-not-destroy-all-of-humanity/

Having Twins is in Your Genes

For a while, scientists have known that it was highly likely to give birth to twins being a twin themselves, but nobody really knew why.  After conducting studies and collecting data from over 2,000 woman who gave birth to fraternal twins, a number of researchers from multiple countries collectively found two different genes that increased the likelihood of having twins.  Scientists searched for what are called single nucleotide polymorphisms, or SNPs.  The first one they found was linked to a hormone that regulates the release of eggs from the ovaries.  If levels are too high, multiple eggs could be released, resulting in the birth of fraternal twins or other multiple births.  The second gene found, which is still somewhat of a mystery, relates how the ovaries respond to the hormone that regulates egg release.  Not much is known about the gene, but researchers believe it could relate to why some mothers respond better to in vitro fertilization.  I find this type of research fascinating since I am a twin myself.  Knowing that there is another set of twins in my family always made me wonder if it really is true that having twins is linked to genetics, so finding this article was reassuring.

http://www.sciencemag.org/news/2016/04/having-fraternal-twins-your-genes-and-your-hormones

The Thin Gene

In the article "The Thin Gene" Abby Solomon is discussed and her genetic disorder. Solomon is 5"10 and only weighs 99 pounds. Solomon neonatal progeroid syndrome, a condition that results from damage to the FBN1 gene. This gene causes Solomon to get hungry every hour and she begins to starve if she does not eat. She dreams about food and enjoys food but she get full very quick. Even though she thinks about food all the time she still gets full very quick and still ends up consuming less calories then a normal women her age. This mutation also "mangles noses and eyes and destroys the layer of fat under the skin so that even teenagers look middle-aged. It also interferes with the body’s ability to make a hormone called asprosin, which regulates blood sugar". Dr. Chopra of Baylor college of medicine started doing research on Abby's disorder. Dr. Chopra said that this disorder is not like a normal eating disorder, this disorder causes Abby to snack a few times every hour in order to not pass out. Abby is a great opportunity for Dr. Chopra to do research on this gene and find out what causes it. As mentioned before the hormone asprosin, which is a blood circulating hormone; asprosin deficiency keeps Abby on the brink of starvation. Dr. Chopra got to thinking that if a deficiency in asprosin causes starvation in a sense then it could help people with obesity. They tested this on mice , and found that it can reverse insulin resistance and weight gain. I found all of this very interesting and I do think it could be a great break through to help people with obesity and diabetes. When asked if she wishes she was different Abby said she would not change anything about herself because this is a chance to get to find what is wrong with her and hopefully help others.

 

ADAM9 Gene Helped Monkeys Survive

Snub-nosed monkeys are a small part of the monkey species that are found living in low oxygen environments. The monkeys are found in areas that are thousands of feet about sea level. Scientists found that the ADAM9 gene actually has helped these monkeys live in an area that does not have much oxygen. The ADAM9 gene has also been found in different animals such as chickens, but they have their own versions of the gene. Scientists also found that because of such small populations of this monkey, they are less diverse then other monkeys in the world.

I found this article interesting because this gene is not found in all monkeys. Only specific animals have this gene, and it is even cooler because it helps them to survive. This gene was also found in an extinct species of human relatives. It makes me wonder if they have done any studies on people who live in Colorado compared to New Orleans. It would seem that people who are used to living in higher altitudes quite possibly could have this gene.

Blonde Genes,Do You Want Them?

Even people that are related and look exactly alike possess a very vast range of genetic variations in their DNA, genes that are responsible for how their body will develop, or responds to outer stimuli. Some of these different variants are known as single nucleotide polymorphisms (SNPs). The chemical units that make up DNA are represented by the letters A,T,C, and G. Although most people may carry a C at a specific place in their DNA, some might have a T instead. There have been millions of SNPs discovered in people's DNA. Some of them may be linked to increasing the chances of getting a certain disease. However, others may affect height or a person's appearance.

Previous research has linked a specific SNP with blonde hair in European people. Now Kingsley's group has provided proof that the SNP that induced blonde hair lies within a piece of DNA that is known as an enhancer. Enhancers are pieces of stretched DNA that behave somewhat like light switches, which allows the gene to turn on under certain conditions. They are located far far away from genes, It is like a light switch in England controlling a bulb in California. Although there is quite some distance, they still have the ability to control the gene's activity.

Kingsley's team genetically modified mice to carry the blonde enhancer. As expected, mice carrying that DNA change began to develop light-colored fur coats compared to the mice with another type of that enhancer. This new enhancer has the ability to control the action of a gene that was already known for affecting hair color. This can ultimately lead to less pigment production in the hair follicles, which will lead to lighter hair. This cannot affect eye or skin color.

I believe this is a great opportunity for those people who have an issue with their hair color. If they do not want their kids to have that hair color, this can be a way out for them.

Beagles Linked with Human Gene Deficiency

In this article, researchers found that DNA in beagles are linked to social disorders in people. There are five genes in a beagle, which are linked to their social behavior. Four out of the five genes have been found in humans who has social disabilities such as schizophrenia, autism, and aggression. A specific gene, SEZ6L, was the specific gene observed when researching the beagles. What researchers found was that even though in humans these genes make them socially awkward, it is actually beneficial for the beagles.

The researchers performed an experiment. There were three different treats under three glass plates. (One under each plate). The last plate was screwed in, making it impossible for the dog to get. The dog at first thought getting the treats was easy, considering the first two treats were eaten within seconds of trying to get them. It seemed that when the beagle tried to get the third treat and could not, he looked to the human in the room for help. Showing some social skills other animals such as wolves would not show. Some researchers are unsure of how accurate this in only because the experiment was done in beagles and not other dog breeds. Further experiments with different breeds should be done. Here is more about the experiment.

I found this article so interesting because it reminds me of my dog. Trooper, my dog, is very social. When he needs me, he lets me know. He constantly brings his ball to me, puts it on my lap and makes these noises until I do something about it. It is not a cry and it is not a bark, its like he is trying to tell me what to do. He does this anytime he needs something and its actually very convenient. On the other hand, my two other dogs are not so vocal. It makes me wonder if these are coincidences or if there is a gene only in specific breeds.