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#65 Jan 29, 2013
DNA Methylation and Histones

Although patterns of DNA methylation appear to be relatively stable in somatic cells, patterns of histone methylation can change rapidly during the course of the cell cycle. Despite this difference, several studies have indicated that DNA methylation and histone methylation at certain positions are connected. For instance, results of immunoprecipitation studies using human cells suggest that DNA methylation and histone methylation work together during replication to ensure that specific methylation patterns are passed on to progeny cells (Sarraf & Stancheva, 2004). Indeed, evidence has been presented that in some organisms, such as Neurospora crassa (Tamaru & Selker, 2001) and Arabidopsis thaliana (Jackson et al., 2002), H3-K9 methylation (methylation of a specific lysine residue in the histone H3) is required in order for DNA methylation to take place. However, exceptions have been observed in which the relationship is reversed. In one study, for example, H3 methylation was reduced at a tumor suppressor gene in cells deficient in DNA methyltransferase (Martin & Zhang, 2005).

In an interestingly coordinated process, proteins that bind to methylated DNA also form complexes with the proteins involved in deacetylation of histones. Therefore, when DNA is methylated, nearby histones are deacetylated, resulting in compounded inhibitory effects on transcription. Likewise, demethylated DNA does not attract deacetylating enzymes to the histones, allowing them to remain acetylated and more mobile, thus promoting transcription.

In most cases, methylation of DNA is a fairly long-term, stable conversion, but in some cases, such as in germ cells, when silencing of imprinted genes must be reversed, demethylation can take place to allow for "epigenetic reprogramming." The exact mechanisms for demethylation are not entirely understood; however, it appears that this process may be mediated by the removal of amino groups by DNA deaminases (Morgan et al., 2004). After deamination, the DNA has a mismatch and is repaired, causing it to become demethylated. In fact, studies using inhibitors of one DNMT enzyme showed that this enzyme was involved in not only DNA methylation, but also in the removal of amino groups.

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#66 Jan 29, 2013
DNA Methylation and Disease

Given the critical role of DNA methylation in gene expression and cell differentiation, it seems obvious that errors in methylation could give rise to a number of devastating consequences, including various diseases. Indeed, medical scientists are currently studying the connections between methylation abnormalities and diseases such as cancer, lupus, muscular dystrophy, and a range of birth defects that appear to be caused by defective imprinting mechanisms (Robertson, 2005). The results of these studies will be invaluable for treating these disorders, as well as for understanding and preventing complications that can arise during embryonic development due to abnormalities in X-chromosome methylation and gene imprinting.

To date, a large amount of research on DNA methylation and disease has focused on cancer and tumor suppressor genes. Tumor suppressor genes are often silenced in cancer cells due to hypermethylation. In contrast, the genomes of cancer cells have been shown to be hypomethylated overall when compared to normal cells, with the exception of hypermethylation events at genes involved in cell cycle regulation, tumor cell invasion, DNA repair, and others events in which silencing propagates metastasis (Figure 1; Robertson, 2005). In fact, in certain cancers, such as that of the colon, hypermethylation is detectable early and might serve as a biomarker for the disease.

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References and Recommended Reading

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Jackson, J., et al. Control of CpNpG DNA methylation by the kryptonite histone H3 methyltransferase. Nature 416, 556560 (2002) doi:10.1038/nature731 (link to article)

Jones, P. A., & Taylor, S. M. Cellular differentiation, cytidine analogs, and DNA methylation. Cell 20, 8593 (1980)

Martin, C., & Zhang, Y. The diverse functions of histone lysine methylation. Nature Reviews Molecular Cell Biology 6, 838849 (2005) doi:10.1038/nrm1761 (link to article)

McGhee, J. D., & Ginder, G. D. Specific DNA methylation sites in the vicinity of the chicken beta-globin genes. Nature 280, 419420 (1979)(link to article)

Morgan, H., et al. Activation-induced cytidine deaminase deaminates 5-methylcytosine in DNA and is expressed in pluripotent tissues. Journal of Biological Chemistry 279, 5235352360 (2004) doi:10.1074/jbc.M407695200

Robertson, K. DNA methylation and human disease. Nature Reviews Genetics 6, 597610 (2005) doi:10.1038/nrg1655 (link to article)

Sarraf, S., & Stancheva, I. Methyl-CpG binding protein MBD1 couples histone H3 methylation at lysine 9 by SETDB1 to DNA replication and chromatin assembly. Molecular Cell 15, 595605 (2004) doi:10.1016/j.molcel.2004.06.0 43

Suzuki, M., & Bird, A. DNA methylation landscapes: Provocative insights from epigenomics. Nature Reviews Genetics 9, 465476 (2008) doi:10.1038/nrg2341 (link to article)

Tamaru, H., & Selker, E. A histone H3 methyltransferase controls DNA methylation in Neurospora crassa. Nature 414, 277283 (2001) doi:10.1038/35104508 (link to article)

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#68 Jan 29, 2013
Explore This Topic It's afterall a learning site.

Consequences of Gene Regulation .Atavism: Embryology, Development and Evolution.
Epistasis: Gene Interaction and the Phenotypic Expression of Complex Diseases Like Alzheimer's.
Gene Interaction and Disease.
Genetic Control of Aging and Life Span.
Genetic Diagnosis: DNA Microarrays and Cancer.
Genetic Imprinting and X Inactivation.
Genetic Regulation of Cancer.

Imprinting and Genetic Disease: Angelman, Prader-Willi and Beckwith-Weidemann Syndromes.
Obesity, Epigenetics, and Gene Regulation.
..Gene Responses to Environment .Environment Controls Gene Expression: Sex Determination and the Onset of Genetic Disorders.
Environmental Cues Like Hypoxia Can Trigger Gene Expression and Cancer Development.
Environmental Factors Like Viral Infections Play a Role in the Onset of Complex Diseases.
Environmental Influences on Gene Expression.
Environmental Mutagens, Cell Signalling and DNA Repair.

Gene Expression Regulates Cell Differentiation.
Genes, Smoking, and Lung Cancer.
Obesity, Epigenetics, and Gene Regulation.
The Complexity of Gene Expression, Protein Interaction, and Cell Differentiation.

..Regulation of Transcription .Gene Expression Regulates Cell Differentiation.
Negative Transcription Regulation in Prokaryotes.
Operons and Prokaryotic Gene Regulation.
Positive Transcription Control: The Glucose Effect.
Regulation of Transcription and Gene Expression in Eukaryotes.
The Role of Methylation in Gene Expression.
Transcription Factors and Transcriptional Control in Eukaryotic Cells.

..Transcription Factors .Do Transcription Factors Actually Bind DNA? DNA Footprinting and Gel Shift Assays.
Gene Expression Regulates Cell Differentiation.
Genetic Signaling: Transcription Factor Cascades and Segmentation.
Gradient-Based DNA Transcription Control in Animals.
Hox Genes in Development: The Hox Code.
The Complexity of Gene Expression, Protein Interaction, and Cell Differentiation.
Transcription Factors and Transcriptional Control in Eukaryotic Cells.
..

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#69 Jan 29, 2013
cont.

From DNA to Protein .

Discovering the Relationship Between DNA and Protein Production.
DNA Transcription.
Nucleic Acids to Amino Acids: DNA Specifies Protein.
Reading the Genetic Code.
Simultaneous Gene Transcription and Translation in Bacteria.
Translation: DNA to mRNA to Protein.

..Organization of Chromatin .

Chromatin Remodeling and DNase 1 Sensitivity.
Chromatin Remodeling in Eukaryotes.
Examining Histone Modifications with Chromatin Immunoprecipitation and Quantitative PCR.
The Complexity of Gene Expression, Protein Interaction, and Cell Differentiation.
The Role of Methylation in Gene Expression.

..RNA

mRNA: History of Functional Investigation.
RNA Functions.
RNA Transcription by RNA Polymerase: Prokaryotes vs Eukaryotes.
Small Non-coding RNA and Gene Expression.
The Role of Ribosomes in Protein Synthesis.

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#70 Jan 29, 2013
Same site library:

Editor(s): Bob Moss
"The importance of deoxyribonucleic acid (DNA) within living cells is undisputed" (Watson & Crick, 1953). This opening sentence of James Watson and Francis Crick's second major paper, published shortly after the announcement of their proposed structure for the genetic material, has proven to be an understatement. Today, it is readily apparent that Watson and Crick's breakthrough set off a firestorm of discovery and innovation that has continued for over 50 years.

The material in this topic room describes the science surrounding the structure and function of DNA. Here, you will find information on the chemical structure of DNA; details about the organization of DNA into chromosomes, genes, and gene families; and data regarding important categories of sequences within DNA, such as introns, exons, promoters, telomeres, and centromeres.

As pointed out by Watson and Crick, the structure of DNA is central to its function, namely its duplication and its expression of the information contained in its nucleotide sequence. Thus, this topic room explores both functions, taking a close look at the processes of DNA replication, transcription, and translation.

Changes in the DNA sequence lead to most of the genetic disorders that affect humans and other organisms. Learning how these "mutations" cause disease allows investigators to more accurately diagnose and treat various disorders. Furthermore, researchers' ability to manipulate the genetic sequence has given rise to a new set of powerful technologies and industries that are collectively known as biotechnology. Such advances and techniques are also explored in depth throughout this room.
.More .Close

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#71 Jan 29, 2013
shareClose .Digg.MySpace.Connotea.Part of the Topic.Genetics Other Topics.Cell Biology.Scientific Communication.Career Planning.Ecology.Earth Systems.Soil, Agriculture, and Agricultural Biotechnology.Environmental Ethics.Biological Anthropology.. Explore This Topic.Applications in Biotechnology

.Genetically Modified Organisms (GMOs): Transgenic Crops and Recombinant DNA Technology.
Recombinant DNA Technology and Transgenic Animals.
The Biotechnology Revolution: PCR and the Use of Reverse Transcriptase to Clone Expressed Genes.

..Gene Copies .Copy Number Variation.
Copy Number Variation and Genetic Disease.
Copy Number Variation and Human Disease.
DNA Deletion and Duplication and the Associated Genetic Disorders.
Tandem Repeats and Morphological Variation.
..Transcription & Translation .DNA Transcription.
RNA Transcription by RNA Polymerase: Prokaryotes vs Eukaryotes.
Translation: DNA to mRNA to Protein.
What is a Gene? Colinearity and Transcription Units.

..Discovery of Genetic Material .Barbara McClintock and the Discovery of Jumping Genes (Transposons).
Discovery of DNA as the Hereditary Material using Streptococcus pneumoniae.
Discovery of DNA Structure and Function: Watson and Crick.
Isolating Hereditary Material: Frederick Griffith, Oswald Avery, Alfred Hershey, and Martha Chase.

..Jumping Genes .Barbara McClintock and the Discovery of Jumping Genes (Transposons).
Functions and Utility of Alu Jumping Genes.
Transposons, or Jumping Genes: Not Junk DNA?.
Transposons: The Jumping Genes.

..DNA Replication .DNA Damage & Repair: Mechanisms for Maintaining DNA Integrity.
DNA Replication and Causes of Mutation.
Genetic Mutation.
Genetic Mutation.
Major Molecular Events of DNA Replication.
Semi-Conservative DNA Replication: Meselson and Stahl.

..RNA .Chemical Structure of RNA.
Eukaryotic Genome Complexity.
Genome Packaging in Prokaryotes: the Circular Chromosome of E. coli.
Restriction Enzymes.
RNA Functions.
RNA Splicing: Introns, Exons and Spliceosome.
RNA Transcription by RNA Polymerase: Prokaryotes vs Eukaryotes.
What is a Gene? Colinearity and Transcription Units.
....

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#72 Jan 29, 2013
Functions and Utility of Alu Jumping Genes
By: Leslie A. Pray, Ph.D. 2008 Nature Education Citation: Pray, L.(2008) Functions and utility of Alu jumping genes. Nature Education 1

(1)....Alu elements have long been considered "junk" DNA--or, even worse, "selfish" DNA. Turns out, these prolific transposons are much more useful than originally thought.
1Introduction.2Short Interspersed Elements (SINEs): The Alu Example .3Transposable Elements Are More Than Just Jumping Genes.4Evidence of Alu Jumps in the Genome Serve as Important Genetic Markers 4.1Use of Alu Elements in Molecular Biology .4.2Use of Alu Elements in Evolutionary Biology .4.3Uses of Alu Elements in Forensic Science ..5Summary .6References and Recommended Reading.

Alu elements are a type of "jumping gene," or transposable element (TE), that exists only in primates. Like all TEs, they are discrete DNA sequences that move, or "jump," from one place on the genome to another, sometimes inserting copies of themselves directly into the middle of protein-coding genes. Although Alu elements have long been considered "junk" DNA, scientists are beginning to question whether these elements might serve important biological functions after all. While much remains to be discovered about the role of these prolific transposons, researchers now recognize that Alu elements are major players in human evolution, as well as useful tools for molecular genetic and forensic applications.
Short Interspersed Elements (SINEs): The Alu Example

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#73 Jan 29, 2013

Alu elements are highly repetitive DNA sequences that can be classified as SINEs (short interspersed elements), which are themselves a type of "nonautonomous" retrotransposon.(Retrotranspos ons are TEs that move about the genome via an RNA intermediary.) An Alu element is transcribed into messenger RNA by RNA polymerase and then converted into a double-stranded DNA molecule by reverse transcriptase. The new double-stranded DNA molecule is then inserted into a new location in the genome. Because they are nonautonomous, like all SINEs, Alu elements don't have the genetic capacity to produce DNA copies of themselves or to integrate into new chromosomal locations. For those activities, they rely on another type of transposon, called L1. Most Alu elements are approximately 300 base pairs long, with considerable sequence variation.

Alu elements frequently duplicate when they jump, and scientists estimate that the human genome acquires one new Alu insert in approximately every 200 births. In other words, the number of Alu elements in the human population (and in other primate populations) tends to increase over time. Alu TEs are believed to have emerged in primates around 65 million years ago. Today, they are the most abundant type of human TE, making up an amazing 10% of the (diploid) human genome. Thus, in a mere 65 million years, these transposons have gone from zero to about 1 million copies per cell! Indeed, part of what makes Alu elements so important is that they are found in nearly every human (and other primate) gene. These elements are spread throughout the genome and occur at varying densities in different loci.

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#74 Jan 29, 2013
Transposable Elements Are More Than Just Jumping Genes

The fact that other nonprimate mammals function quite well without Alu elements confirms that these elements are not required for the basic function of cellular processes. Yet, because primate genomes have so many Alu elements, many biologists speculate that these TEs may have played an important role in our species' evolution, and that nature may have taken advantage of these elements in some way, such as by putting them to work in generating new proteins. This conflicts with the long-held belief that all transposable elements are just "junk," existing for no purpose other than self-replication.

Figure 1: Schematic model for exonization of an Alu element..(A) Alu is inserted into introns of primate genes by retrotransposition.(B) During the course of evolution, mutations within pseudo-splice sites in the intronic Alu activate these sites (black arrows). Mutations changing splicing regulatory elements are also possible (green arrow).(C) Following these mutations, part of the Alu sequence is recognized as a new exon ("exonized"), and spliced into the transcript. Typically, the Alu-containing transcript is the minor splice form, as in most cases the created splice sites are weak. Most exonizations involve the antisense orientation of the Alu sequence, presumably because of the preceding long poly-T that serves as a strong poly-pyrimidine tract necessary for the 3' recognition.
Sorek, R. RNA (2007), 13:1603-1608. Published by Cold Spring Harbor Laboratory Press. Copyright 2007 RNA Society.
Although they have yet to gather much data to support their arguments, scientists have hypothesized various roles for Alu elements, such as stimulation of protein translation, particularly under stressful cellular circumstances; this hypothesis is rooted in the fact that many Alu RNAs are expressed during times of stress. However, the hypothesis attracting the most attention of late is the one stating that Alu elements may have served an important evolutionary role by contributing to the formation of new genes or gene combinations, or perhaps by adding new functionality to already-existing genes through a process known as exonization (Sela et al., 2007).

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#75 Jan 29, 2013
Exonization is the creation of a new exon from an Alu-containing (or any TE-containing) intron.(i.e., they are "spliced" out). The process of exonization is illustrated in Figure 1. First, the Alu TE is inserted into an intron of a gene. Initially, the Alu is spliced out of the mRNA as part of the intron. Over time (as many as several million years), however, mutations accumulate, leading to the formation of active splice sites on either end of the Alu element, and the Alu TE is thus eventually recognized as an exon, at least in some molecules of mRNA.

Scientists have reported thousands of Alu exonization events among primates. In humans, for example, Alu TEs are responsible for an estimated 62% of all new exons (Zhang & Chasin, 2006). This raises an important question: How could the insertion of so many new exons into vital genes not be detrimental? As Rotem Sorek of the Lawrence Berkeley National Laboratory in California, explains, "The answer lies in alternative splicing" (Sorek, 2007). With alternative splicing, some initial RNA transcripts that contain a new exon arising from Alu are spliced to include the new exon in the final mRNA, while other identical transcripts are spliced differently, thereby removing the Alu exon. As a result, some transcripts lack the new exon and produce the same "old" protein, while others produce entirely new proteins or protein variants. Some of these new proteins might be deleterious; others might be selectively neutral (neither harmful nor beneficial to the organism or cell); and some could very well be beneficial, thereby giving an organism (or a cell or gene) a selective edge while not eliminating the "old" protein altogether.

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#76 Jan 29, 2013
Scientists are only beginning to explore this possibility, and a few observations do seem to support the idea. For instance, not only do newly born exons undergo alternative splicing more frequently than old exons, but, according to Sorek (2007), almost all exonized Alu elements in the human genome are alternatively spliced. Therefore, even though the original transcript with the newly exonized Alu element is intact and could encode potentially deleterious RNA and protein products, alternative splicing leads to the production of multiple transcripts, multiple mRNAs, and, ultimately, multiple proteins. In fact, some scientists speculate that Alu elements have played a key role in the evolution of the primate brain, and that all of the protein possibilities afforded by Alu movement and exonization have contributed to the complexity of human neuronal circuitry and "higher-order" cognition (e.g., rational thought)(Mattick & Mehler, 2008).

On the other hand, scientists have associated some individual Alu insertions with human disease. The simple insertion of an Alu TE in the wrong place can often wreak molecular havoc. For example, in 1991, researchers discovered a case of neurofibromatosis caused by an Alu sequence inserted in an intron of the NF1 gene (Wallace et al., 1991). The presence of the Alu sequence caused a splicing error, which in turn caused one of the exons to be left out of the transcribed mRNA, thereby leading to a shift in the reading frame and production of an abnormal protein. Since then, researchers have reported a growing number of Alu-disease associations in disorders ranging from hemophilia to breast cancer. According to one estimate, about 0.4% of all human genetic disorders are caused by or associated with Alu TEs. In many cases, it is not clear whether the association is causal (i.e., whether the Alu insertion actually causes the disease), but the lack of any other noticeable mutation often leads researchers to suspect that it is.

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#77 Jan 29, 2013
Evidence of Alu Jumps in the Genome Serve as Important Genetic Markers

Regardless of what they do to the genome (and the cell and organism) when they jump, Alu TEs have, at the very least, served science well. Today, molecular biologists use Alu TEs as research tools, evolutionary biologists use them to resolve questions about primate systematics and human history, and forensic investigators use then to home in on possible perpetrators of unsolved crimes.
Use of Alu Elements in Molecular Biology

Figure 2: Using Alu sequences to detect oncogenes..Scientists in Robert Weinberg's laboratory in the late 1970s and early 1980s used DNA from tumor cell lines to transform mouse fibroblasts (NIH-3T3 cells). They then isolated the transforming gene (a mutant oncogene) using the Alu sequences that 'went along for the ride.

In molecular biology, the fact that Alu elements are widely dispersed throughout the primate genome but absent in other animals makes these elements a useful tool for identifying human DNA sequences that have been inserted into cells of other animals in what are known as marker-rescue experiments. A classic Alu marker-rescue experiment was the 1982 discovery of the first human oncogene by Robert Weinberg and his trainee Chiaho Shih (Shih & Weinberg, 1982). Knowing that human genes can be associated with Alu sequences, the researchers suspected that if they were to transfer a human oncogene into a mouse cell, the oncogene would most likely take some Alu sequences along for the ride. Thus, Weinberg and Shih isolated DNA from a human bladder cancer cell and added it to some mouse cells growing in culture. Many of the mouse cells took up different pieces of this human DNA and added it to their own DNA. In fact, a small number of the mouse cells took up the human oncogene (i.e., the mutated gene responsible for transforming the normal bladder cell into a cancer cell). These particular mouse cells were transformed, becoming visibly different from their counterparts that had not taken up the oncogenic DNA (Figure 2). Moreover, when injected into mice, these cells could form tumors.

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#78 Jan 29, 2013
Upon observing this sort of tumor formation, Weinberg and Shih were faced with the challenge of finding the lone human oncogene in the middle of billions of base pairs of mouse DNA. Luckily, Alu elements provided the answer. Weinberg and Shih isolated DNA from the newly transformed (i.e., cancerous) mouse cells and added it to other mouse cells growing in culture, again transforming a few of these cells. The scientists did this repeatedly, and after each round, they removed a small sample of DNA for use in a Southern blot analysis, tracking the number of copies of Alu elements to measure how much human DNA remained in the mouse cells. Because the mouse genome does not have Alu sequences naturally, the sequences that the researchers found in the transformed cells could be inferred to be associated with the mutated human gene. The scientists ended these serial "transfections" only when the Southern blot analysis revealed a single band of Aluthat is, only one small region of the original human DNA remained, and, presumably, this region contained the oncogene.(Because this small region had been initially isolated from a human tumor cell and was associated with tumor formation in every generation of mouse cells, it was reasonable to conclude that whatever region of human DNA remained contained the oncogene.) Weinberg and Shih then probed this remaining bit of DNA with various other DNA sequences known to cause cancer (all from animal viruses) to identify the specific oncogene.

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#79 Jan 29, 2013
Use of Alu Elements in Evolutionary Biology

In evolutionary biology, scientists take advantage of some key features of Alu elements that set them apart as genetic polymorphic loci (i.e., DNA sequences that vary within the population) and make them ideal for answering certain types of questions about genetic ancestry and relatedness. For example, the probability that two different Alu elements will insert independently in the same place is practically zero. Moreover, most Alu elements, once inserted, are rarely removed. Combined, these facts mean that two individuals who share the same Alu sequence in the same spot on the genome most likely had a common ancestor who had that same Alu sequence in that same spot in his or her genome. In contrast, with other types of loci, it is often difficult to know whether two individuals share the same genetic marker because they acquired it from a common ancestor or developed the change independently by chance.

Thus, scientists have used Alu element analyses to confirm, for example, that flying lemurs are not part of the order Primata, because Alu elements have been detected in all primates tested but not in flying lemurs (Xing et al., 2007). Alu elements have also been used in attempts to resolve what is known as the "trichotomy problem": the evolutionary relationship among humans, chimpanzees, and gorillas.
In one study, the distribution of more than 100 different Alu elements suggested that humans and chimpanzees are a sister clade and that gorillas are the out-group (Salem et al., 2003). In other words, this study suggests that humans are more closely related to chimpanzees than to gorillas.

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#80 Jan 29, 2013
Uses of Alu Elements in Forensic Science

In forensics, Alu elements can be used to determine the geographical ancestry of a DNA sample, such as whether it originated from sub-Saharan African, Western European, Indian, or East Asian "stock." While these may seem like broad categories, having this kind of "continental" information can help investigators further refine their analyses (i.e., the identification of unknown samples) by using only those markers known to yield useful information for a particular population group. As Ray et al.(2005) explain, "The inference of an individual's geographic ancestry or origin can be critical in narrowing the field of potential suspects in a criminal investigation."

Summary
Although biologists have been using Alu elements as a research tool for more than a quarter of a century, they are just beginning to collect and interpret data on the potential regulatory and developmental roles of Alu SINEs in humans and other primates. Originally considered "junk" genes, Alu TEs are now believed to be evolutionary contributors. Scientists speculate that the generation of new protein types, stimulation of protein translation, and creation of new gene combinations may all be affected by the presence of Alu elements. Additionally, because they are restricted to primates, Alu elements provide scientists with an interesting test case for general TE functioning and may lead to a better understanding of both the beneficial and deleterious effects of gene jumping within the genomes of numerous species.

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References and Recommended Reading

Deininger, P. L., & Batzer, M. A. Alu repeats and human disease. Molecular Genetics and Metabolism 67, 183193 (1999)

Mattick, J. S., & Mehler, M. F. RNA editing, DNA recoding, and the evolution of human cognition. Trends in Neurosciences 31, 227233 (2008)

Ray, D. A., et al. Inference of human geographic origins using Alu insertion polymorphisms. Forensic Science International 153, 117124 (2005)

Salem, A. H., et al. Alu elements and hominid phylogenetics. Proceedings of the National Academy of Sciences 100, 1278712791 (2003)

Sela, N., et al. Comparative analysis of transposed element insertion within human and mouse genomes reveals Alu's unique role in shaping the human transcriptome. Genome Biology 8, R127 (2007) doi:10.1186/gb-2007-8-6-r127

Shih, C., & Weinberg, R. A. Isolation of a transforming sequence from a human bladder carcinoma cell line. Cell 29, 161169 (1982)

Sorek, R. The birth of new exons: Mechanisms and evolutionary consequences. RNA 13, 16031608 (2007)

Wallace, M. R., et al. A de novo Alu insertion results in neurofibromatosis type 1. Nature 353, 864866 (1991)(link to article)

Xing, J., et al. Mobile elements in primate and human evolution. Yearbook of Physical Anthropology 50, 219 (2007)

Zhang, X. H., & Chasin, L. H. Comparison of multiple vertebrate genomes reveals the birth and evolution of human exons. Proceedings of the National Academy of Sciences 103, 1342713432 (2006)

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#82 Jan 31, 2013
regards to Dogen:
http://www.topix.com/forum/news/evolution/TFA...

testtube protein/enzyme design

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#83 Jan 31, 2013

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http://arvix.org/pdf/physics/9708026.pdf
5 pages
Boolean logic applied to a non competive surrounding.

I.o.w. do mutations (phenotype) also occur in a neutral setting.

Neutral Mutations and Punctuated Equilibrium in Evolving Genetic Networks. 1998
Stefan Bornholdt and Kim Sneppen.

quote
Let us briefly discuss the meaning of the stasis times
and punctuations observed here. According to the definition
of our model, we quantify the waiting time in terms
of the number of times mutant networks are exposed to
new environments before a neutral mutation occurs that
fulfills continuity. Thus they are not to be confused with
the neutral evolution introduced by Kimura [3] which
leads to waiting times consisting of a number of neutral
mutations. The genetic networks are formally defining a
species and the length of the waiting times indicates
the genetic flexibility of a species.
Associating the interconnectedness of the networks
with the genetic flexibility of real organisms one may
attempt to understand a puzzling decomposition of lifetimes
of species in the fossil record. First it was noted by
Van Valen [16] that each group of closely related species
has exponentially distributed lifetimes. Second, an analysis
of the overall distribution of genera lifetimes, tabulated
by Raup and Sepkoski [17], showed that this is
rather distributed as / 1/t2 [19] for genera lifetimes exceeding
10 million years. It is tempting to speculate
that groups of closely related species are associated to
the same genetic flexibility, and thus evolve, and eventually
get extinct, with a frequency given by this genetic
flexibility. This would explain the exponential distribution
of Van Valens. Averaging over all genetic flexibilities
is then an average over different characteristic lifetimes,
and our simplified evolution scenario demonstrates how
such an averaging can give an overall 1/t2 distribution.
The obtained 1/t2 scaling may be an inherent part of
our neutral evolution scenario [18].

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