Obesity is a rising problem in The United States and its known that obesity affects the immune system. A new study shows that obesity may be affecting our DNA of our immune cells and causing this problem. The branch of genetics that attempts to explain this phenomenon is called epigenetics. Epigenetics is a relatively new area which reveals that things other than the actual DNA sequence can affect you. The study attempts to show a connection between obesity and a change in the DNA called methylation. DNA methylation is what happens when a carbon atom bonded three hydrogen atoms attaches to a specific area on the DNA strand. A group of scientists: Xiaoling Wang, Haidong Zhu, Harold Snieder, Shaoyong Su, David Munn, Gregory Harshfield, Bernard L Maria, Yanbin Dong, Frank Treiber, Bernard Gutin and Huidong Shi; in which they analyzed the leukocyte, or white blood cell, DNA of both obese and lean individuals and determined to what degree certain areas of the DNA were methylated.
In order to do this, seven obese and seven lean individuals were selected and their leukocyte DNA was analyzed using a HumanMethylation27 BeadChip which allows the scientists to determine the degree of methylation on the areas of DNA in question. They broke up the DNA using special enzymes and analyzed the fragments for these methyl groups. What they saw was that obese individuals had increased methylation levels at one gene and decreased methylation levels at another gene. In other words, obese people did in fact have different methylation levels on their DNA. Their DNA was different from those of lean people of the same age. These differences are not in the code, and they can be changed. That’s one of the things that make epigenetics such a big deal. It shows that the DNA sequence is not all that matters, and since we can change these methylation levels, we can affect what proteins a person’s DNA actually codes for. There are some limitations with this study, like the fact that they only used 7 obese people and 7 lean people. This is a very small sample size, and as such it cannot prove anything. What this study does is show the possibility for obesity to affect DNA. To properly understand and categorize and indeed prove that this actually happens, and to determine the connection between the two will require much larger studies to be done with larger sample sizes. This is important because it shows how obesity affects DNA and the immune system. If this process can be completely understood, then there is the possibility that a medication could be found and produced that could counteract this and return the afflicted’s immune system to its normal state. That time is a long ways away, but still the possibility exists.
Friday 25 February 2011
Thursday 17 February 2011
Autism and Mental Retardation Genetics
Autism and Mental Retardation Genetics
Nowadays, there is a very wide range of conditions that fall under the umbrella of declaring someone of having intellectual disabilities. Autism and mental retardation are two of the most prevalent aside from Down’s syndrome. Defining these disabilities can be a bit of a hassle, but there are a few guidelines in which one must follow to determine which is which. Down’s syndrome is caused by a trisomy 21, a third 21st chromosome. In most cases, autism is known as idiopathic, or without a cause. Fragile X syndrome is a condition involving the changes in the X chromosome, or the sex-linked chromosome, which leads to the most common form of inherited mental retardation.
With autism, and the large amount of children born with it, eighty percent of those children had no identifiable cause. Five to ten percent of those children were secondary, and only three percent inherited the chromosomal anomaly.
To be considered mentally retarded, a person must have an IQ below 70 and significant limitations in at least two adaptive skills. Wherever mental retardation is studied, it makes up for about two percent of the population. Unlike autism, mental retardation has a vast amount of causes, almost limitless. Causes range from genetic disorders, metabolic disorders, chromosomal disorders, and others include pre-birth care or lack thereof. However, now there are neonatal screenings that can help predict mental retardation, and point us in the right steps to preventing it. Another way to determine MR (mental retardation) is to have a cytogenetic study done on an individual. A cytogenetic study is a study of the structure and function of a cell, especially focused on the genes. Hopefully with modern advances in technology we can take larger steps in preventing mental retardation.
As of today, we have not put all the pieces together for the involvement of MR. Currently there are more than fifty genes associated with syndromic X-linked mental retardation.
S. Holloway
Nowadays, there is a very wide range of conditions that fall under the umbrella of declaring someone of having intellectual disabilities. Autism and mental retardation are two of the most prevalent aside from Down’s syndrome. Defining these disabilities can be a bit of a hassle, but there are a few guidelines in which one must follow to determine which is which. Down’s syndrome is caused by a trisomy 21, a third 21st chromosome. In most cases, autism is known as idiopathic, or without a cause. Fragile X syndrome is a condition involving the changes in the X chromosome, or the sex-linked chromosome, which leads to the most common form of inherited mental retardation.
With autism, and the large amount of children born with it, eighty percent of those children had no identifiable cause. Five to ten percent of those children were secondary, and only three percent inherited the chromosomal anomaly.
To be considered mentally retarded, a person must have an IQ below 70 and significant limitations in at least two adaptive skills. Wherever mental retardation is studied, it makes up for about two percent of the population. Unlike autism, mental retardation has a vast amount of causes, almost limitless. Causes range from genetic disorders, metabolic disorders, chromosomal disorders, and others include pre-birth care or lack thereof. However, now there are neonatal screenings that can help predict mental retardation, and point us in the right steps to preventing it. Another way to determine MR (mental retardation) is to have a cytogenetic study done on an individual. A cytogenetic study is a study of the structure and function of a cell, especially focused on the genes. Hopefully with modern advances in technology we can take larger steps in preventing mental retardation.
As of today, we have not put all the pieces together for the involvement of MR. Currently there are more than fifty genes associated with syndromic X-linked mental retardation.
S. Holloway
Monday 14 February 2011
Gene Idenification for Anxiety Disorders Via Mice
There are a range of anxiety disorders: generalized anxiety disorder (GAD), panic disorder, social phobia, agoraphobia and others. In humans, identifying genes that predispose people to anxiety is difficult. Because of this, mice have been studied to identify genes to in turn look for in humans. In the study “An Association Analysis of Murine Anxiety Genes in Humans Implicates Novel Candidate Genes for Anxiety Disorders,” 17 genes were identified through studying seven brain regions with gene expression profiling. And variations in 13 of these genes were tested as candidate genes in a study that examined the link between genes and human anxiety disorders. A population-based Finnish study was conducted with 321 patients and 653 control subjects, 30 years of age and older.
To select which of these genes were associated with anxiety, the 13 candidate genes were examined against 139 genes that differentiate by only a single nucleotide known as single nucleotide polymorphisms. After identifying associating genes 69 more single nucleotide polymorphisms were selected from these. The combined 208 single nucleotide polymorphisms were genotyped and eight were chosen to be studied at length. The eight were chosen because they either had two or more markers in the gene had a high probability in allele-based association tests or there was a great probability of a haplotype - an allele combination on a chromosome- associated with it.
Six genes that were found to be correlated to anxiety in mice were also found to do the same in humans: ALAD, CDH2, DYNLL2, EPB41L4A, PSAP and PTGDS. The most significant associations were between ALAD and social phobia, DYNLL2 and GAD and PSAP and panic disorder. However ALAD was also shown to correlate to phobic anxieties, CDH2 to social phobia, DYNLL2 and PTGDS to GAD, EPB41L4A was shown to correlate with several anxiety disorders but most significantly with GAD and PSAP was shown to be associated with panic disorder.
This article was interesting because to be able to pinpoint a gene or a set of genes that controls anxiety is astounding. Everyone has some sort of anxiety, and some anxiety is good and actually required for dealing with situations in life. It is needed to function. But for people who have one or more anxiety disorders it is difficult to deal with. Using mice to figure out what genes to look for in humans is resourceful. This research is locating the genes that cause anxiety and has the potential in the future to allow researchers to figure out how to manipulate the genes to alleviate major anxiety symptoms.
Hollie
To select which of these genes were associated with anxiety, the 13 candidate genes were examined against 139 genes that differentiate by only a single nucleotide known as single nucleotide polymorphisms. After identifying associating genes 69 more single nucleotide polymorphisms were selected from these. The combined 208 single nucleotide polymorphisms were genotyped and eight were chosen to be studied at length. The eight were chosen because they either had two or more markers in the gene had a high probability in allele-based association tests or there was a great probability of a haplotype - an allele combination on a chromosome- associated with it.
Six genes that were found to be correlated to anxiety in mice were also found to do the same in humans: ALAD, CDH2, DYNLL2, EPB41L4A, PSAP and PTGDS. The most significant associations were between ALAD and social phobia, DYNLL2 and GAD and PSAP and panic disorder. However ALAD was also shown to correlate to phobic anxieties, CDH2 to social phobia, DYNLL2 and PTGDS to GAD, EPB41L4A was shown to correlate with several anxiety disorders but most significantly with GAD and PSAP was shown to be associated with panic disorder.
This article was interesting because to be able to pinpoint a gene or a set of genes that controls anxiety is astounding. Everyone has some sort of anxiety, and some anxiety is good and actually required for dealing with situations in life. It is needed to function. But for people who have one or more anxiety disorders it is difficult to deal with. Using mice to figure out what genes to look for in humans is resourceful. This research is locating the genes that cause anxiety and has the potential in the future to allow researchers to figure out how to manipulate the genes to alleviate major anxiety symptoms.
Hollie
Thursday 10 February 2011
Reversed Island Syndrome - Evolution and Genetics at Work
Island Syndrome is a well known change in genetic patterns that occurs as a species evolves on an isolated island habitat. This change can happen to birds blown out to sea by storms or to small mammals and reptiles that float out on debris. Island Syndrome occurs because, on most islands, the species that landed has escaped its main predators, and islands typically have enough resources to support a high, stable population. Therefore, this syndrome is characterized by an increase in energy allocation to growth, as opposed to reproduction, since mates are guaranteed to be plentiful. Organisms grow bigger, live longer, and are less aggressive because resources are easy to find, meaning there is little competition within the species.
However, rarely, this stability is not always present on isolated islands, and the new species will either find another strong predator, limited resources, or a harsh climate, all of which can create high fluctuations in the population density. This is the case with the Licosa Island Wall Lizard (Podarcis sicula klemmeri) found on Licosa Island off the coast of Italy, which was studied by members of the Department of Earth Science and the Department of Structural and Functional Biology in the University of Naples. This lizard was a recent descendent of the Italian Wall Lizard (Podarcis sicula) and had recorded population density swings of up to 40%. This means that the total numbers of lizards on the island can drop by nearly half, from year to year. The members of the research team theorized an opposing hypothesis for the Island Syndrome in situations where population density is highly variable, which they called Reversed Island Syndrome (RIS). It was thought that this syndrome would be characterized by higher reproductive energy demands, since the survival of a mate at any one time would not be as secure. One of the most distinct traits of the Licosa Lizard was its bright blue color, which the team traced back to a gene that controls a specific set of traits that could theoretically be involved in the behavioral patterns of RIS. The physical and behavioral traits coded for by this gene were as follows: more aggressive behavior, extreme sexual dimorphism (difference in body size), and high sexual competition.
All of these behaviors were found in the Licosa Lizards, both when observed on the island and when they were raised in captivity. Through many series of tests and observations, it was clear that the large majority of these traits were much more apparent in the Licosa Island Lizards than in their mainland relatives. It was also apparent that many of these traits were driven by the fact that the Licosa Lizards expended much more energy on reproduction; for example, Licosa females are much smaller than Licosa males and mainland lizards because they put more energy into developing their eggs and young. Since these behaviors were characteristic of RIS, a wider survey of other research was done, and it appears that other reptile species that could possibly be influenced by RIS are often a black or blue color, meaning that the specific pigmentation gene could be a co-factor for RIS.
This does not mean, however, that all of the traits specified, such as coloring, must be present in order for RIS to be in effect. In addition, even though a reptile has a specific coloring it may not be under the influence of RIS. Instead the main driving force behind the presence of RIS within an island population is a highly variable population density and the possibility of a lack of mates at any one time that can trigger a selection for more sexually aggressive characteristics. This study has been one of the first steps for confirming this hypothesis and its result are an influential step towards confirming the effects of RIS on reptiles and other species.
~Written By: Rachel Taupier
However, rarely, this stability is not always present on isolated islands, and the new species will either find another strong predator, limited resources, or a harsh climate, all of which can create high fluctuations in the population density. This is the case with the Licosa Island Wall Lizard (Podarcis sicula klemmeri) found on Licosa Island off the coast of Italy, which was studied by members of the Department of Earth Science and the Department of Structural and Functional Biology in the University of Naples. This lizard was a recent descendent of the Italian Wall Lizard (Podarcis sicula) and had recorded population density swings of up to 40%. This means that the total numbers of lizards on the island can drop by nearly half, from year to year. The members of the research team theorized an opposing hypothesis for the Island Syndrome in situations where population density is highly variable, which they called Reversed Island Syndrome (RIS). It was thought that this syndrome would be characterized by higher reproductive energy demands, since the survival of a mate at any one time would not be as secure. One of the most distinct traits of the Licosa Lizard was its bright blue color, which the team traced back to a gene that controls a specific set of traits that could theoretically be involved in the behavioral patterns of RIS. The physical and behavioral traits coded for by this gene were as follows: more aggressive behavior, extreme sexual dimorphism (difference in body size), and high sexual competition.
All of these behaviors were found in the Licosa Lizards, both when observed on the island and when they were raised in captivity. Through many series of tests and observations, it was clear that the large majority of these traits were much more apparent in the Licosa Island Lizards than in their mainland relatives. It was also apparent that many of these traits were driven by the fact that the Licosa Lizards expended much more energy on reproduction; for example, Licosa females are much smaller than Licosa males and mainland lizards because they put more energy into developing their eggs and young. Since these behaviors were characteristic of RIS, a wider survey of other research was done, and it appears that other reptile species that could possibly be influenced by RIS are often a black or blue color, meaning that the specific pigmentation gene could be a co-factor for RIS.
This does not mean, however, that all of the traits specified, such as coloring, must be present in order for RIS to be in effect. In addition, even though a reptile has a specific coloring it may not be under the influence of RIS. Instead the main driving force behind the presence of RIS within an island population is a highly variable population density and the possibility of a lack of mates at any one time that can trigger a selection for more sexually aggressive characteristics. This study has been one of the first steps for confirming this hypothesis and its result are an influential step towards confirming the effects of RIS on reptiles and other species.
~Written By: Rachel Taupier
Friday 4 February 2011
Genetically Altered Tobacco Could Smoke Other Non-food Crops as Biofuel
The article I chose to write about is called “Genetically Altered Tobacco Could Smoke Other Non-food Crops as Biofuel”. I found the article on scientific American Genetic Engineering Feed. This article is about tobacco being genetically modified so it can be used as an alternative fuel source. Tobacco is a crop, which is grown in warm climates all over the world. In the United States it is mainly grown in Virginia, Kentucky, and central Tennessee. When grown for energy production instead of smoking, it can create a large amount of inexpensive biomass (plant materials used as fuel) more efficiently than any other agricultural crop.
The tobacco plant produces very oily seeds, which the biofuel oil is extracted from and unfortunately they do not produce large numbers of them. So far scientist at Thomas Jefferson University in Philadelphia in the Biotechnology Foundation Laboratories have discovered two genes that control oil production, Lec2 (the leafy cotyledon 2 gene) and DGAT (the diacyglycerol acytranderase gene). After genetically modifying Lec2 and DGAT to be over expressed, more oil from the plants seeds and leaves can be accumulated. After being genetically modified the plant went from producing 1.7% - 4% increasing to about 6.8%. In many cases, 20 times the standard amount has been produced.
Dr Viaceslav Andrianov, Ph.D, professor of Cancer Biology at Jefferson Medical College of Thomas Jefferson University states “Tobacco is very attractive as a biofuel because the idea is to use plants that aren’t used in food production. Tobacco represents an attractive and promising energy plant platform and could also serve as a model for the utilization for other high biomass plants for biofuel production”.
I have become very interested in this idea of using tobacco oil to create ethanol. After researching this topic I found that scientist were able to get 100 miles per one gallon of this fuel. Another great thing about this is that there is an immense amount of food grade protein that can be extracted from the sludge remaining after the ethanol is produced. Fraction-1 protein is a tasteless, odorless, crystalline substance that can be extracted from tobacco, and it is a complete protein. The protein would be equivalent to eating beef and it would basically be free food. The protein would be paid for by the ethanol produced from the tobacco biomass. I believe this is a very good start on the “Go Green” idea.
Josh
The tobacco plant produces very oily seeds, which the biofuel oil is extracted from and unfortunately they do not produce large numbers of them. So far scientist at Thomas Jefferson University in Philadelphia in the Biotechnology Foundation Laboratories have discovered two genes that control oil production, Lec2 (the leafy cotyledon 2 gene) and DGAT (the diacyglycerol acytranderase gene). After genetically modifying Lec2 and DGAT to be over expressed, more oil from the plants seeds and leaves can be accumulated. After being genetically modified the plant went from producing 1.7% - 4% increasing to about 6.8%. In many cases, 20 times the standard amount has been produced.
Dr Viaceslav Andrianov, Ph.D, professor of Cancer Biology at Jefferson Medical College of Thomas Jefferson University states “Tobacco is very attractive as a biofuel because the idea is to use plants that aren’t used in food production. Tobacco represents an attractive and promising energy plant platform and could also serve as a model for the utilization for other high biomass plants for biofuel production”.
I have become very interested in this idea of using tobacco oil to create ethanol. After researching this topic I found that scientist were able to get 100 miles per one gallon of this fuel. Another great thing about this is that there is an immense amount of food grade protein that can be extracted from the sludge remaining after the ethanol is produced. Fraction-1 protein is a tasteless, odorless, crystalline substance that can be extracted from tobacco, and it is a complete protein. The protein would be equivalent to eating beef and it would basically be free food. The protein would be paid for by the ethanol produced from the tobacco biomass. I believe this is a very good start on the “Go Green” idea.
Josh
Subscribe to:
Posts (Atom)