Term 2: Genome Editing Could Correct Genetic Mutations for Future Generations

Anjali Kumar
Source: http://www.sciencedaily.com/releases/2014/12/141215084942.htm
Indiana University, December 15th, 2014

Scientists at Indiana University have discovered a technique for "editing" the genome in sperm-producing adult stem cells. The researchers created an experiment where they created a break in the DNA strands of a mutant gene in mouse cells, then repaired the DNA through a process called homologous recombination, replacing flawed segments with correct ones. This particular study involved spermatogonial stem-cells, which are the foundation for the production of sperm, and therefore, contribute genetic information to the next generation. Repairing an flaws in the cells could prevent mutations from being passed down to future generations. Specially designed enzymes, called zinc finger nucleases and transcription activator-like effector nucleases, were used to create a double strand break in the DNA and bring about the repair of the gene. Modified stem cells were transplanted in sterile mice, and the transplanted cells were able to thrive and grow. However, attempts to breed mice were not successful.


This is relevant to what we have learned in class because we discussed genetic mutations such as substitutions and frameshift mutations, and the effects these mutations have on people and future generations. This experiment is designed to find a way to avoid these mutations, so more people have a better quality of life.

A clear, molecular view of how human color vision evolved

Source: http://www.sciencedaily.com/releases/2014/12/141218210100.htm

By: Emory Health Sciences

Published: December 18, 2014 by ScienceDaily

Summary of the article

The evolution of human vision didn’t happen quickly; it required many genetic mutations in visual pigments spread over millions of years for humans to evolve from ultraviolet vision to violet vision. The speed of evolution depends on how fast the environment changes. The scabbardfish was able to change its vision very quickly because its environment changed very fast, while humans took much longer because their environment changed much slower over time. According to Shozo Yokoyama, a biologist at Emory University, we have now traced all of the evolutionary pathways, going back 90 million years, that led to human color vision.

The first step of studying the adaptive process for vision in humans was estimating and synthesizing ancestral proteins and pigments of a species. Next, experiments were conducted and carried out on them. The technique combines microbiology with theoretical computation, biophysics, quantum chemistry, and genetic engineering.

There are five different classes of “opsin” genes, which encode visual pigments for dim-light and color vision. The opsin genes change and adapt to the environment. When the environment changes, the opsin genes change too. 30 million years ago, our ancestors had evolved four classes of opsin genes, which gave them the ability to see the full-color spectrum of visible light, except for UV (ultraviolet).

After testing ancestral proteins and pigments, researchers identified 5,040 possible pathways for the amino acid changes required to bring about the genetic changes. The researchers did experiments on all 5.040 of them. 80 percent of these pathways stopped in the middle because the mutations blocked water channels that the proteins needed to function.

After conducting even more experiments and were able to identify seven essential genetic mutations that caused the loss of UV vision and developed blue sensitive pigment. Researchers discovered that the mutations had no effect individually, and only changed the pigment when they were all put together in a certain order. This certain order was the order of genetic mutations that gave humans’ ancestors colored vision rather than UV vision.

How this relates to our class:

This article relates to what we have learned in class because it describes how our ancestor evolved to change its vision to the way that humans see now. The article also mentions how natural selection played a part in making all of the ancestors have this advantageous trait after millions of years. Finally, this article talks about how evolution and natural selection relates to the environment. When natural selection occurs, it picks out traits for a species that better suit it for its environment. The faster that the environment changes, the quicker the species will have to adapt. If the environment changes more slowly, then the species will not have to adapt to it as quickly.

Gene Therapy Could Help With Inherited Blindness

Name: Cainwyn Leung
Source: NHS Choices http://www.nhs.uk/news/2014/12December/Pages/Gene-therapy-
               could-help-with-inherited-blindness.aspx
Author: Unknown
Date: 10 December 2014

Summary:
     Retinitis Pigmentosa is a general term for human inherited eye conditions affecting 1 in 4000 people around the world. The conditions cause damage to the light-sensing cells and cone receptors(color-sensing cells) in the retina or even killing the cells. There is no cure for Retinitis Pigmentosa currently, but researchers are developing a new way to aide the inherited eye conditions through gene therapy. The researchers use gene therapy to modify the retinal ganglion cells, which are cells that are not light sensitive normally, to become light sensitive through injecting a chemical into the cell; the effects can last up to nine days. They performed some experiments to see the effects of the modified cells on blind mice, and the mice seemed to regain vision. 

     To genetically modify the retinal ganglion cells, researchers create a receptor protein on the cells' surfaces that can respond to light with the presence of the chemical MAG460. The mice that were used in experiments were genetically engineered so that they would lose both of their photoreceptors, rods, and cones by 90 days, which is mimicking the conditions of Retinitis Pigmentosa in human, and they seem to regain vision after the experiment. However, no experiment is performed on human yet due to the immaturity of the newly developed technology, but researcher believe that the day that this can cure human will not be far giving hope to people with the inherited eye condition.

Relevance:
     This article is relevant to the genetic modification topic. In term two, we spent a certain amount of time discussing Genetically Modified Organism, and this article is about genetic modifying cells to cure eye conditions. Although it is not about modifying an organism, but it uses the same techniques in creating GMO. Lastly, this article is also about inherited Retinitis Pigmentosa, which is caused by DNA mutations in gametes so that the condition is inherited.

Revolutionary New Antibiotic Kills Drug-Resistant Germs

Eric Hazen

Source: https://www.livescience.com/49358-new-antibiotic-discovery.html

Author: Bahar Gholipour

Date: January 7, 2015

Summary:

A new antibiotic was discovered by scientists that kills drug-resistant germs when studying strains of bacteria. The scientists tested 10,000 strains of bacteria and isolated compounds that the bacteria produced. These compounds were tested against disease-causing bacteria. One of these compounds is called teixobactin. Teixobactin is effective in treating animals infected with bacterias like Mycobacterium tuberculous, which has strains that are already resistant to drugs making it difficult to treat humans. Teixobactin is still under research and it is not known if it is effective against infections in humans.

Teixobactin works very effectively against drug-resistant pathogens because of its unique way of killing the bacteria. Teixobactin binds to the bacteria’s fat molecules on the cell wall and cause it to break down. Targeting the fat molecules is more effective than targeting protein molecules, which is more commonly used in antibiotics, because the genes that code for the protein molecules can mutate and form resistant against the antibiotic. The bacteria has a more difficult time becoming resistant to the fat molecule targeting drug. It took 30 years for resistances to form when treated with a similar drug, vancomycin.

Relevance:

This article is relevant to our science class because we just finished a unit on molecular genetics and discussed how genes can mutate. These genes can mutate to benefit the organism and make them better suited for the environment around them. When germs mutate to become resistant to antibiotics made by humans a large problem arises; how do we kill these super germs? This question is answered by the antibiotic Teixobactin, which can kill these germs without worry that the germs will mutate again soon and become resistant.

Clear, Molecular View of How Human Color Vision Evolved

"Clear, Molecular View of How Human Color Vision Evolved." FARS News Agency 19 Dec. 2014. Global Issues in Context. Web. 11 Jan. 2015.

Document URL
http://go.galegroup.com/ps/i.do?id=GALE%7CA394445898&v=2.1&u=mlin_m_actonhs&it=r&p=GPS&sw=w&asid=a7652266ad252c6ed79fc45d2f2c5ea4

Summary

It took the ancestors of humans dozens of millions of years to see the rainbow. Just 90 million years ago, our ancestors had a dim vision, seeing UV rays and mainly the color red. They had a bichromatic view of the world. By 30 million years ago, we could see the color blue, but lost our ability to see UV light. This common ancestor lead to gorillas and chimpanzees having the same vision as humans. For some species, the change to blue colored vision came easily. For example, the scabberedfish only needed one mutation to need the change. Our primate ancestors needed seven genetic mutations, in a particular order, to change from UV to blue light. This slow evolution is caused by a lack of environmental change.

There are 5040 ways that the amino acids could have been changed to be able to see blue light. But, 80% of the paths to seeing blue light had non-functioning proteins. This was due to the fact that if one mutation came first, then it would cut off the necessary water supply to the protein. Our ancestors used only one of the remaining 252 pathways to seeing blue light. This lead the researchers to identifying the three amino acid changes that allowed our ancestors to see green.

Relevance

In class we have learned about evolution, and how monkeys and humans share a common ancestor. This article discusses our common ancestor that evolved to see the way we do now. Also, one problem Darwin had with evolution, was the complexity, as he sayed in sixth chapter of On The Origin of Species "To suppose that the eye, with all its inimitable contrivances for adjusting the focus to different distances, for admitting different amounts of light, and for the correction of spherical and chromatic aberration, could have been formed by natural selection, seems, I freely confess, absurd in the highest possible degree." This article states one piece of the puzzle of how our eye evolved to be so complex, and that small changes and simple mutations over millions of years lead to complex changes. This article discusses how over millions of years, natural selection comes into play, causing evolution. It also states that environmental change speeds up evolution. All in all, this article talks about our new unit, and brings up some information from our last unit.

by Gus Teran

First New Antibiotic in 30 Years

Website URL: http://www.iflscience.com/health-and-medicine/resistance-proof-antibiotic-we-ve-been-waiting
Name: Roy Yoon
Author/Date of Article: Janet Fang, January 8, 2015
Article Summary:
             An international team of scientists led by Kim Lewis of Northeastern University, discovered an antibiotic from soil bacteria. The newly extracted antibiotic from this bacteria  can cause a vast amount of microbes, which can cause diseases to die. No resistance to these new antibiotics has yet been discovered.  Searching for antimicrobial products ,Lewis's team looked at 10,00 compounds which was isolated from the soil which was uncultured. These  compounds were seen as not fit to be cultured, as they could not grow in the experimental conditions of the petri dishes."So Lewis and colleagues developed what they call iChip, which sorts individual bacterial cells into single chambers, and after the device is buried in the ground, several molecules are allowed to diffuse into the iChip" (Fang). Basically, the bacteria "think" that they are living in more natural conditions, so that the bacteria can strive and form colonies. A compound called, teixobactin, causes the cell wall of bacteria to breakdown, and also prevents the synthesis, or forming of the bacterial cell wall. When tested on mice, the teixobactin showed to be deadly to strains of bacteria such as "Staphylococcus aureus, TB-causing Mycobacterium tuberculous, and Clostridium difficile, which causes inflammation of the colon" (Fang). As for concern for antibiotic resistance against the teixobactin, a similar strain of bacteria called vancomycin which functions in similar ways to the teixobactin, took over 30 years for antibiotic resistance to form against it. Lewis's team suggests that it may take even longer for antibiotic resistance to form against the teixobactin.

Article Relevance:
             We have learned about the ongoing issues of antibiotic resistance of bacteria and pesticide resistance of certain organisms. With bacteria evolving and changing constantly through the exchange of genetic material within the bacteria, common antibiotics no longer have effect on certain strains of bacteria and can bring simple infections to extremes. With bacteria using plasmids to share genes for antibiotic resistance, the constantly reproducing bacteria can share these antibiotic resistant  genes with other bacteria. But with Lewis's teams work, there is now a suggested hope that a new type of antibiotic may be effective against these bacteria.

Salt tolerance gene in soybean could save many farms and crops of the future

By Eric Trimble

Summary-

New information found by Australian and Chinese researchers has shed light on increasing the ground-salt tolerance of soybean, and possibly other plants. The lead of the project, University of Adelaide researcher Matthew Gilliham, stresses the importance of the discovery by saying "...many commercial crops are sensitive to soil salinity and this can cause major losses to crop yields... On top of that, the area of salt-affected agricultural land is rapidly increasing and is predicted to double in the next 35 years. The identification of genes that improve crop salt tolerance will be essential to our efforts to improve global food security." And protecting soybeans and their fields certainly is a very important task, as they are currently the fifth most produced crop in the world. After sifting through the genetic sequences of several hundred varieties of soybeans, Dr. Rongxia Guan and Professor Lijuan Qiu of the Institute of Crop Sciences pinpointed what looked like the salt-tolerance gene, and this discovery was later confirmed by researchers at the University of Adelaide. "We initially identified the gene by comparing two commercial cultivars," says Professor Qiu. "We were surprised and pleased to see that this gene also conferred salt tolerance in some other commercial cultivars, old domesticated soybean varieties and even wild soybean." This new information can now be used to selectively breed soybean plants for their salt tolerance, or even find similar genes in different crops such as wheat, says Professor Matthew Gilliham. Scientists can also use genetic markers, to ensure salinity resistance is maintained in different cultivars, or varieties, of the plant. Professor Qiu also found that, "It appears that this gene was lost when breeding new cultivars of soybean in areas without salinity. This has left many new cultivars susceptible to the rapid increases we are currently seeing in soil salinity around the world." Hopefully, work will be put into selectively breeding and future-proofing plants, such as the soybean, against soil salinity.

Relevance-

A large part of the unit of heredity was spent answering the question: how can traits of particular plants and animals be changed over time to help the human population? The answer to that question being — selective breeding. Now that these researchers have found this gene for salt tolerance,they will selectively breed soybean plants that show saline resistance, until they have a plant that can withstand high levels of salt while still producing desirable beans. We also learned how to "tag" specific genes with gene markers, as the scientists in this lab are doing. 

Source- Science Daily- "Salt tolerance gene in soybean found"

Date of Publication- January 9, 2015

Angelman Syndrome: Term 2

Name: Mehak Sikka
Url: http://www.medicinenet.com/angelman_syndrome/article.htm

Angelman syndrome is a genetic condition that is present at birth (congenital). It causes intellectual disability and other features. Other characteristics of Angelman syndrome include distinctive facial features, mental retardation, speech problems and hyperactive behaviour. In most cases, the cause is a missing section (deletion) on the mother’s copy of chromosome 15. Angelman syndrome was once known as ‘happy puppet syndrome’ because of the child’s sunny outlook and jerky movements. It is now called Angelman syndrome after Harry Angelman, the doctor who first investigated the symptoms in 1965. Most diagnoses are made between the ages of three and seven years of age. Estimates vary, but Angelman syndrome is thought to affect one child in every 10,000 to 25,000.   Angelman syndrome may be mistaken for autism because of similar symptoms, including hyperactive behaviour, speech problems and hand flapping. However, a child with Angelman syndrome is highly sociable, unlike a child with autism. It is important that the child is carefully diagnosed, because sometimes Angelman syndrome and autism are both present. There is no cure for Angelman syndrome.  

In our class, during the Unit on molecular genetics, we learned about a few genetic disorders and what can happen when genetic mutations take place in DNA sequences. We learned about chromosomal mutations too. This is how Angel man syndrome relates to what we've learned during Term 2. 

Lettuce Pills May Help Treat Haemophilia

Source URL: http://www.scientificamerican.com/article/lettuce-pills-you-heard-that-right-may-help-treat-haemophilia/
Name: Lee Dong
Author and Date of Article: Elie Dolgin, Dec. 16 2014

Article Summary:
            In humans, there are two common forms of Haemophilia, a disorder that impairs the body's ability to clot blood.The second most common form of Haemophilia, Haemophilia B, is when the body has a natural lack of Factor IX, a protein that helps the coagulation or clotting of the blood. However, when 5% of humans with Haemophilia B are treated with a replacement coagulation proteins, the body mistakes the foreign therapy proteins as dangerous and develops an antibody that fights the protein. This problem is even worse with the most common form of Haemophilia, Haemophilia A, when the body lacks the protein Factor VIII. 30% of humans suffering from Haemophilia A start to produce antibodies to therapy proteins of Factor VIII. In fact, if the therapy continues with both forms of Haemophilia when there is an antibody produced by the body, life-threatening allergic reactions like anaphylaxis can occur.
           A treatment developed by scientists partially solves this by very frequently inserting the proteins needed to lower antibody resistance to them. However, this has a success rate of only 75% and is not only time-consuming but very expensive. But with the genetic engineering of lettuce cells to contain chloroplasts producing Factor IX and VIII, one can avoid the production of antibodies for the foreign proteins before the therapy even starts to insert them into the human body. Although this lettuce-cell powder does not prevent the failure of clotting blood by themselves, it prevents antibodies from forming so effective proteins can be inserted without immune resistance.

Article Significance:
            The mentioned article is very relevant to two focuses that the Honors Biology curriculum has touched in the span of the ongoing year: genetics and GMOs. Haemophilia is a sex-linked trait, occuring on the X chromosome. Thus, males are more susceptible to Haemophilia because they only have one X chromosome, thus if the gene for Haemophilia is inherited from that X chromosome, the male will have Haemophilia. Since this is treated by genetically modified lettuce chloroplasts, this also would cover the mini-unit on GMOs. The lettuce cells that had been used did not initially contain anything that produced Factor IX or Factor VIII, all genes of which were shot into the lettuce cells via gene gun or a bacteria plasmid infection. Thus, the lettuce cells are considered GMO, and are used in this case for medicine. Relating to the class debate regarding the use of GMOs in present-day society, this could be used as supporting data as to why GMOs can be beneficial, finding a way to regulate haemophilia in both a more convenient and cost-effective method.

Conditional reprogramming leads to breakthroughs on the cancer front

  Source: http://www.npr.org/blogs/health/2015/01/07/372691919/a-bed-of-mouse-cells-helps-human-cells-thrive-in-the-lab
  Author: Richard Harris
  Date: January 7, 2015

       In Georgetown University Medical Center, Dr. Richard Schlegel and his group found a way to keep human cells alive in the lab, using a technique called conditional reprogramming.  This technique works by placing a layer of living mice cells that are unable to grow, underneath the living human cells.  For reasons still unknown to Dr. Schlegel, the mice cells keep the human cells alive in the lab without issue.  This is a instrumental breakthrough, as previously, it was very difficult to keep human cells alive in the lab.  In addition, when they were kept alive, they often were not biologically similar to similar cells found in the body. 
       Dr. Schlegel and his group have grown over 30 types of cancer cells with this technique.  On these cells, they now have the ability to test different medications and vaccines, not only the medications specifically prescribed for cancer.  While testing a variety of different medications on cervical cancer cells, Dr. Schlegel noted that a common drug used to treat malaria also killed cervical cancer cells.  Working with Dr. Connie Trimble and her team at Johns Hopkins University School of Medicine, Dr. Schlegel is now running clinical trials with this drug.  There is hope that the drug will be able to help treat women with cervical cancer that do not have access to life-saving surgery. 

       This research relates to our class as we discussed cancer in our unit on cells.  It offers an alternative method to eradicate cancer cells to the ways we discussed in class.  Also, the mice cells act as a medium for the human cells, providing them with nutrients that they need to survive.  We discussed the topic of bacteria mediums in our unit on molecular genetics. 

CRE Germs Pose A Threat On Human Health As We Know It

Devon Lukas
Source: http://www.cdc.gov/media/dpk/2013/dpk-vs-hai.html
Author/Publication: N.a./ CDC, February 28, 2014

CRE, short for Carbapenem-Resistant Enterobacteriaceae, are a group of germs that are resistant to pretty much all antibiotics known in medicine today. CRE infections are bacterial infections that are spread by human to human contact. CRE infections occur almost always in a hospital or in someone who is getting a lot of medical care. Though CRE is not actually that common, there are two unusual traits to it that gets health departments worried. The first is its resistance. Two types of CRE bacteria are the KPC and NDM enzymes that break down carbapenems, therefore, the infection is very hard to treat. Even some of the strongest drugs, called carbapenems, cannot fight the CRE germs. Due to this, a CRE bloodstream infection kills 1 in every 2 people that it infects.
The second is CRE's spreadability. CRE can actually transfer its resistance to antibiotics into other bacteria. Medical people are not only worried about the spread of CRE and it becoming a more common and untreatable infection, but also about it causing other bacteria to become antibiotic-resistant. About 4% of the 4,000 US hospitals, and about 18% of the 200 US long-term acute care hospitals had at least one CRE infected patient, and at least one infection has been reported in 42 of our states. Medical facilities are doing all they can to prevent the spread of this worrisome and untreatable infection, including the "Detect and Protect" approach, and only prescribing antibiotics when absolutely necessary.

The CRE crisis directly relates Mr. Hohn's Biology class's study on the evolution of antibiotic-resistance in bacteria, but also to our study of GMO's. CRE gaining resistance works through evolution. When antibiotics are used to treat infections and diseases, they are meant to kill off or slow the bacteria causing the problem. But the antibiotic causes selection within the bacteria, just like natural selection in animals, so that the bacteria evolves to fit an environment in which antibiotics are there. The antibiotic at first kills off most of the bacteria, but the ones resistant through a mutation, different gene, etc., survive and reproduce, making the resistance normal in that bacteria specie. Antibiotics used for something minor can also start the evolution process in other bacteria that is not even related to the minor issue. This is what medical officials found is happening with the CRE. Antibiotics used for a cold don't actually help the cold at all, and add to the resistance of much more dangerous bacterias already living in our bodies like the CRE. This is why they are trying to cut down on antibiotic prescription.
In our GMO unit, we talked about pesticide resistance becoming a problem for farmers. E. coli, which was in some of the GMO crops, is a type of CRE. The "superbugs and super weeds" that resulted from that became resistant to pesticides used to kill them and protect the crops, much like how the bacterial infection becomes resistant to antibiotics.

“Survival of the Most Productive” Tactic Boosts Output of Engineered Bacteria

Source: http://www.genengnews.com/gen-news-highlights/survival-of-the-most-productive-tactic-boosts-output-of-engineered-bacteria/81250755/

By: researchers at the Wyss Institute led by geneticist George Church, Ph.D.

Published: Dec 31, 2014

Summary

Scientists at Wyss Institute are using negative selection to engineer bacteria to be more productive.  They bred the bacteria to produce an industrially-valued chemical output in quantities 22 to 36 times more than previously possible.  Billions of cells were evaluated in order to identify the rare cells with the high production phenotypes.  Once they are selected, they are forced to reproduce and the process starts again.  Multiple rounds of evolution were run to enrich the population of the most productive cells.  This results in the engineering of the cell’s central metabolic pathways, allowing the microbes to have superior pathway designs.  Chemical production and ability to evaluate the cells allows the researchers to harness evolution.  They hope to apply the methods used to improve production of more useful compounds.

Relevance

This article is relevant to what we are learning in Honors Biology by relating to 14.3 artificial selection, or selective breeding.  The scientists here are evaluating the bacteria and selectively breeding the bacteria that have the desired traits.  They also remove “cheater cells (non-producers)” as they go along with the breeding.  By doing this over and over again they are changing the gene pool in the bacteria population, leading to the perfect bacterium that is desired by the creator which is similar to what we are studying in class. 

New class of antibiotic found in dirt could prove resistant to resistance

Source: http://www.washingtonpost.com/news/speaking-of-science/wp/2015/01/07/new-class-of-antibiotic-found-in-dirt-could-prove-resistant-to-resistance/

By: Rachel Feltman

Published: January 7, 2015 by The Washington Post

Summary

Bacteria have been evolving to resist antibiotics quicker than we can form new treatments.  When an antibiotic is put into use, the bacteria get accustomed to its effects and, eventually, become resistant to it.  However, a new antibiotic has been found with a unique way of stopping proliferation which may be able to put an end to these resistant bacteria.  This new antibiotic was discovered by a Northeastern University professor, Kim Lewis, when experimenting with a sample of dirt in a field in Maine.  Lewis and his coworkers placed soil between two semi-permeable membranes, making the soil microbes grow like the laboratory conditions were a natural environment.  A Teixobactin, a specific chemical compound, was identified by the experiment.  It destroyed drug-resistant TB and MRSA in the cells of mice.  The antibiotic performed this action with the bacteria neither gaining any resistance nor killing the mice. The mice that were infected with the MRSA and given pneumonia did not show any notable side effects either.  This new type of antibiotic aims at the building blocks of the bacteria’s cell wall, not at the proteins inside like most antibiotics do.  Teixobactin binds two lipids that are essential in cell wall production, so if one of the lipids grows a resistance, the other could still be attacked.  This tactic was successfully tested, but there is no compound in existence that bacteria will never grow resistant to.  However, Teixobactin will definitely take much longer for the bacteria to counter.

Relevance

This article is relevant to unit 6 because the unit mentions the ability of bacteria to adapt to new antibiotics in 14.5 and how it has cause the evolution of antibiotic-resistant populations.  This article is all about trying to solve that predicament by using a different technique, targeting the cell wall and not the protein.  This article talks about how we can try to stop bacteria from constantly counteracting our antibiotics, and how we might be able to slow it, but all compounds can be, eventually, resisted by bacteria.  This shows that the problem of antibiotic-resistant bacteria will never be completely solved, but it can, and hopefully, will be decelerated by Teixobactin.

Evolution of Color in the Red Devil Ciclid

Lily Friedman
Source: http://www.sciencedaily.com/releases/2015/01/150109093727.htm
By: Monash UniversityPublished: January 9th, 2015


Summary: 
When individuals from the same species come in different colors, why doesn’t one color eventually replace the others through natural selection? The Journal of Evolutionary Biology has studied a species of Central American freshwater fish, called the red devil cichlid, to see how different colors are maintained. This species comes in two colors; dark and gold. The gold color is genetically dominant, but the dark color is much more common. When the researchers filmed the red devil cichlids over both dark and light surfaces, they saw that the dark fish could alter its brightness to match the surface it was on, but the gold fish could not. This extra layer of camouflage helps hide the dark colored fish from predators, so they are more fit to survive in their environment. This study is being used to answer the big question of how and why do variants of the same animal exist in nature.


Relevance: 
This is an example of natural selection, because even though the gold color is dominant, the dark color is more common. The dark colored fish are likely to be able to hide from predators, and survive long enough to have offspring and pass of their dark-colored gene. The gold fish are more likely to be eaten by predators, and not pass on their genes to the next generation, which is why the dark color is more common. Eventually, the species could evolve to have only dark colored fish because of this natural selection.

Scientists look to genomes to uncover mystery of bowhead whale's longevity

Source: http://www.mankatofreepress.com/news/state_national_news/scientists-look-to-genomes-to-uncover-mystery-of-bowhead-whale/article_cd2ddec8-b8ea-5d8e-9d92-1bbfbc2fe5a7.html

By: Deborah Netburn Los Angeles Times (TNS)

Summary: The bowhead whale is the longest living mammal on Earth, a lifespan up to 200 years, and scientist are trying to figure out how. This week, researchers at the University of Liverpool made the genome of bowhead wahle public in order to encourage other scientist to look for clues in its DNA. By looking at its genome, and comparing it with other species with shorter life spans, they may be able to identify some of the genetic pathways involved in its long life span. Magalhaes, the lead author in a study examining the whale's genome, has discovered some changes in the bowhead's genes related to cell cycle, DNA repair, cancer and aging. He believes these changes help the bowhead resist age-related diseases. The reaserches also noted that the whale has more than 1,000 times more cells than humans, but don't have an increase cancer risk, suggesting they have adaptations allowing them to suppress cancer more effectively than other animals. 

Relevance: This article is relevant to the evolution unit. It is relevant because, the bowhead whale had to at one time split from the path of other whales. Natural selection most likley happened, and the whales able to live longer became the species they are today.

Cameron Kassm  
    

New Antibiotic is Potent Killer of Suprebugs

Source: http://www.techtimes.com/articles/25211/20150108/new-antibiotic-potent-killer-superbugs.htm
By: James Maynard
Published: January 8th, 2015 8:09 am

Summary:

Scientists in the pharmaceutical field have recently discovered a new antibiotic that could help fight superbugs: bacteria that have become resistant to antibiotics. Antibiotics are medicines that kill or slow the growth of bacteria. Since penicillin was first discovered by a scientist as a way to kill bacteria, it had been used throughout the world to help people fight diseases and infections. However, certain types of bacteria evolved over time to penicillin and other drugs. It was then useless to fight bacteria that were already resistant with antibiotics. Now with the discovery of Texiobactin, bacteria that have become immune to antibiotics can now be killed. This is a leading breakthrough, because "Methicillin-resistant Staphylococcus aureus" a form of staph infection has become immune to the antibiotic and causes many people to fall terribly ill. Texiobactin prevents the cell walls of bacteria from forming by binding on two types of lipids. When the Texibactim attaches to the cell wall, it tears the wall. After this, the bacteria will die. Finding alternative antibiotics can become difficult, because if some bacteria were to survive after the antibiotic was applied, then the antibiotic is useless. It becomes harder to find new antibiotics, because a lot of them have caused antibiotic-resistant bacteria, and there are limited amounts of antibiotics. 

Relevance: 

This article is mostly relevant to unit 6 (the current unit.) It talks about antibiotics which in 14.5. In the reading, it talks about what antibiotics are and how bacteria has evolved in such a way that it has become resistant to antibiotic. The implications this has on people fighting against life threatening infections like tuberculosis is serious since certain strains have adapted to be resistance all antibiotics. It also relates to 14.1 where natural selection comes into place. When the a certain strain of bacteria is presented with a drug, the bacteria which can tolerate it will be more suitable to the environment than other ones. It would then pass on this trait to its offspring and eventually the strain would become immune. 

Petunias Preventing Self-Fertilization

By Celine Qi


Summary:
The Institute of Evolutionary Biology and Environmental Studies at the University of Zurich have discovered evidence that many plant species are able to recognize self and non-self pollen. These plants also have the ability to reject pollen. This ability of the plants allows them to avoid inbreeding, which may result in genetic defects appearing in their offspring. Plants are able to recognize pollen made by themselves because of a molecular mechanism called "self-incompatibility", or "SI". The one-to-one self-recognition evolved from plants and animals and is when a single male protein is able to identify a single female protein; this can prompt a pollen rejection response to occur. Petunias do not use one male and one female protein for the one-to-one recognition but instead involve multiple proteins; eighteen male proteins identify forty female proteins. 

S-genes, proteins which are coded by self-incompatibility genes, are a part of the self-recognition process. The direct interaction between the male SLF proteins (S-locus F-box) and the female S-RNases (S-ribonucleases) is extremely complicated in petunias. This mechanism in the flowers exhibits evolutionary patterns that are similar to the immune defense systems in animals, including humans. Studying this procedure enables the understanding of how such a complex system evolved and how it is managed at the cellular level. This information also benefits plant breeders.

Relevance:
This article relates to the curriculum's study of Heredity. In this unit, breeding between plants, specifically Mendel's pea plants, were studied. Gregor Mendel allowed his plants to self-pollinate, producing identical offspring. Pea plants are self-fertilizing plants, where the pollen of one plant, the male sex cells fertilize the eggs, the female sex cells, of the same plant. However, for petunias, these flowers did not allow themselves to inbreed. This is because its forty female proteins were toxic to the plants own pollen. As a result, the plants could not fertilize themselves. In the unit of Molecular Genetics, disorders were studied and relate to the genetic defects that can show up in the petunias' offspring through inbreeding. This would have resulted in weaker, more sickly plants because they would have had an increased risk of being affected by harmful traits.


Source: http://www.sciencedaily.com/releases/2015/01/150108084447.htm
Date of Publication: January 8th, 2015

Orangutans crack consonants and vowels to shed new light on the evolution of human speech

Alissa Kong

Source: http://phys.org/news/2015-01-orangutans-consonants-vowels-evolution-human.html

Date Published: January 9, 2015

Summary:

In the past, we have always assumed that great apes, a very close ancestor of humans, seem to not be able to modify and learn new calls. This prompted us to question how humans evolved and developed the spoken language if our ancestors had trouble with developing new verbal skills.

A recent study done by Liverpool John Moores University and Pongo Foundation have discovered new calls from orangutans, a species which is part of the great apes, which show important similarities to the human spoken languages that may have been the origin of the many languages we speak today. Adriano Lameira led the study and explained that the new calls orangutans can learn are made from the quick opening-and-closing of the lips, which is very similar to the motions of our lips when we are talking. Furthermore, the one of the orangutan’s calls was very much like human consonants and another was like human vowels. This may have eventually led to what we call vowels and consonants today in our respective languages.

This study ultimately shows that our original thinking that great apes lack the capability to learn new calls was incorrect and that our languages today may have developed from the calls of our close ancestor, the great apes.

Relevance:

This article relates to the evolution unit that we are currently studying. In that unit, we learned about some of the ancestors of humans and how the species of today evolved, or changed from their ancestors. This particular article is about how humans evolved from the great apes and how we potentially could have taken the spoken calls from our close ancestors and changed them into our own various languages of today.

Genetic drift causes more flu cases

Source: http://www.forbes.com/sites/davidkroll/2014/12/31/get-your-flu-shot-anyway-despite-genetic-drift/
by David Kroll
Published 31 Dec, 2014

The flu has always been a problem. There seems like there are new types every year: swine, avian, type A, etc. This is all because of genetic drift. The flu virus mutates, and over time becomes a new strain. The new strain can be a bit different than it's ancestor, or a lot different. This will determine the vaccine's effectiveness. If the new strain gets too far different from its ancestor, there will have to be a new vaccine made for the specific flu strain. The fact is that most of the flu cases in people that are vaccinated are because there are many more unknown flu strains out there that don't have vaccines. So, while it's still worth it to get your flu shot, just keep in mind that it doesn't make you invincible.

Relevance:
This article relates to our studies in class because we have been learning about genetic drift. Genetic drift is the random microevolution of organisms due to mutations and dominant & recessive alleles.

Fragile Bones: From Hunter-Gatherers to Farmers

Source: http://www.sciencedaily.com/releases/2014/12/141222165033.htm

by Timothy M. Ryan and Colin N. Shaw

Published December 22nd, 2014

Evolutionary biologists have recently discovered that the human skeleton has become much lighter and more fragile since the switch from hunting-gathering to farming. According to new research 7000 years ago the human bone was almost as strong as the modern orangutan; 6000 years later bone mass had decreased by about 20%. Researchers have been hypothesizing on why this shift occurred. It could possibly be due to a new diet, as with the shift to farming came a less diverse choice of foods. After running more experiments with the fossils this theory was eventually decided against as well as the theory that there was a separate change in body size.  Rather they think that the change is due to the change in amount of exercise, which would mirror research suggesting that bone health is more dependent on exercise than a calcium rich diet.  On that note the future of bone health and human fitness looks even more grim. “There's seven million years of hominid evolution geared towards action and physical activity for survival, but it's only in the last say 50 to 100 years that we've been so sedentary -- dangerously so," says Dr Colin Shaw, an evolutionary biologist at the University of Cambridge. And he’s right; these days TVs, phones, and computers, all derail from our once very active lifestyle. Next, Shaw’s research team is looking to find correlations between the agility of marathon runners and the structure of their bones.

This article exemplifies the process of natural selection and evolution, and is very relevant to our evolution unit. As learned in class, genetic changes are largely affected by differences in the environment. One of these genetic changes was a decrease in bone mass.

Stem Cells Make Insulin, Restore Retinas

Summary:
Embryonic stem cells were first cultured in labs over 30 years ago and their high healing potential. These cells can differentiate into many different types of tissues and ultimately regenerate organs and heal diseases. Two groups led by Robert Lanza, chief scientist at Advanced Cell Technology, and Douglas Melton of Harvard University announced advances in the stem cell field in October. The groups manipulated human embryonic stem cells into pancreatic cells and transplanted them into diabetic mice. The cells produced insulin and healed the mice in 10 days. Before human trials, the next step is to prevent rejection of the foreign cells by the body.

Their therapeutic target are eyes failing from macular degeneration. They produced a tissue called retinal pigment epithelium, or RPE. They injected the RPE cells into one eye of each 18 patients, half with age-related macular degeneration and half with Stargardt's macular dystrophy. Each subject was followed for an average of two years. Not only were there no harmful effects from the RPE cells, but most patients showed improvement. 10 patients showed improvement in vision and 7 patients' eyesight has stabilized. Although there is some controversy over harming human embryos, Lanza and Melton managed to make tissues similar to RPE from adult cells which they hope will satisfy those who oppose the experiment.

Relevance:
This article relates to the unit on Molecular Genetics. In that unit, we learned about embryonic stem cells. Stem cells are undifferentiated and have the potential to form any type of somatic cell. The human embryo around 7 days after fertilization is a blastocyst, or a hollow ball of about 100 cells with embryonic cells in the center. These cells are the embryonic cells used to make RPE cells in the experiment expressed in the article. This experiment also mentions patients with Stargadt's macular dystrophy, a genetic eye disorder that causes progressive vision loss. This relates to the genetic mutations we learned in the Molecular Genetics unit. This inheritable eye disorder is caused by a mutation in the ABCA4 or ELOVL gene which code for the instructions making proteins that are found in light-sensing cells in the retina.

Daisy Yin
Source: http://discovermagazine.com/2015/Jany-feb/12-stem-cells
Tuesday, December 30, 2014
Jeff Wheelwright

Genetic Mutations in Whales Lead to Longer Life Spans

Name: Ceallagh Hanlon

Source: Live Science: 

http://www.livescience.com/49320-bowhead-whale-genome-sequenced.html

Date: 1/5/15

Author: Becky Oskin

Summary:

Recently, scientists have been looking at the genomes of whales for clues pertaining to their long life spans. Specifically, mutations in the genome of the bowhead whale offer interesting data. Scientists have found that these whales live for around 200 years due to beneficial mutations. For example, bowhead whales have a gene called ERCC1. Researchers have found that a mutation (the specific type is unclear) in this gene helps repair damaged DNA. This could conceivably protect against cancer by stopping cancerous cells from replicating too quickly. Other mutations that contribute to the long life span of whales include a duplication in a gene linked with DNA replication and cell growth called PCNA. Scientists think the duplication of part of this gene could slow aging and lead to longer life spans. In addition to investigating the effects of these mutations on live spans, scientists also looked at the way the whales genes are expressed in their major organs such as the liver, brain, and heart. Researchers have been able to study the genomes of whales by using the tissue of whales killed by whalers in Alaska and Greenland.

Biologist Joao Pedro de Magalhaes, who is also an expert in aging science, plans to investigate these mutations further. He hopes that these whales may provide the key to prolonging the length of a human life, perhaps by genetic modification.

Relevance:

Our study of molecular genetics is closely related to this article. We learned about different types of mutations, specifically relating to genes and on the chromosomal level, and the possible effects they have on the organism. This study investigates the effects of genetic mutations like duplications, particularly the positive effects they have on the organism. Additionally, this study can relate to our study of evolution. These whales have evolved to have longer life spans which suggests that these mutations are inherited. Because bowhead whales live an average of 200 years, it is evident that the mutations occur frequently in the gene pool.