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.
Mr. Hohn's Period 1 Media Blog
Due Dates and Topics for Quarter 2: Post Media, Summary, and Relevance by 1/12. Questions of classmates made in comments by 1/14. Answers to Questions posted in comments by 1/16. Early completion is HIGHLY recommended.
Wednesday, January 14, 2015
Sunday, January 11, 2015
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.
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
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.
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
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