Genome Evolution: Flies and Humans

The abstract explains how new research has begun on on the factors that influence the population and evolutionary dynamics of transposable elements (TEs) and TE life cycles. What exactly are transposable elements? To answer that question (that most peeps should know the answer to) they are segments of DNA that can move from one site to another. TEs have sometimes been referred to as "jumping genes" because they are inherently mobile. Genomes have several different qualities when it comes to transposable elements, such as the number of TE copies, the level of TE activity, the diversity of TE families and types, and the proportion of old and young TEs.

The abstract focuses on two well-studied genomes with strikingly different architectures, (humans and Drosophila) which represent two extremes in terms of TE diversity and population dynamics. According to the abstract, researchers argue that there are two possibilities for the answers: (1) the larger population size and consequently more effective selection against new TE insertions due to ectopic recombination in flies compared to humans; and (2) in the faster rate of DNA loss in flies compared to humans leading to much faster removal of fixed TE copies from the fly genome.

Article:

Evolution of genome content: population dynamics of transposable elements in flies and humans.

Mighty-Macho Plants! ...and their Genomes

Yup, you read the title right...props for you haha! Anyways, Researchers at the RIKEN Plant Science Center (PSC) have clarified a key epigenetic mechanism by which an enzyme in the model plant Arabidopsis protects cells from harmful DNA elements. Living cells greatly depend on the proper function of their DNA in order to survive. However, certain DNA elements such as transposons (fragments of DNA that replicate within an organism's genome) disrupt this functioning and disable genes.

Ooh question! How are cells able to defend themselves between such harmful elements? Lets contemplate this question for a few seconds.... Eukaryotic cells have both active and inactive DNA; their inactive DNA become tightly-packed, this is called heterochromatin, and these dense structure serves to repress the expression of nearby gene sequences and protect the genome.

According to earlier research, "heterochromatin silencing" in Arabidopsis involves a key enzyme called HDA6. To further their research, scientists investigated the involvement of HDA6 through two processes: DNA methylation and the modification of histone.

How were researchers able to show whether plants with repressed HDA6 function can silence harmful DNA elements? They found their results through a genome-wide comparison, and discovered that these plants with repressed HDA6 function are not able to silence harmful DNA elements. This is because HDA6 binds directly to transposons and silences their activity through specific histone modifications. Therefore, researchers suggest that this enzyme plays an important role in gene silencing for plants.

(The image above shows Arabidopsis thaliana, a small flowering plant that is widely used as a model organism in plant biology and is also discussed in this article.)

Article:

Discovery of DNA Silencing Mechanism Reveals How Plants Protect Their Genome

Chapter 21: Useful Materials

What exactly is this video about? Well it explains the Human Genome Project (HGP), a research effort to identify and map all human genes. The video takes you inside for a close up look at the complexity of the cell. The HGP officially began on October 1, 1990 and was a 13-year project coordinated by the U.S. Department of Energy and the National Institutes of Health.

There were several goals that the HGP had:

1. To identify all human genes
2. To obtain the DNA sequence of the entire human genome
3. To develop technology for the generation and management of human genome information
4. To analyze the genomes of model organisms
5. To develop programs focused on understanding and addressing the ethical, legal, and social implications of results obtained from the HGP

Overall, I think this video was quite interesting in learning more about the Human Genome Project and scientists' thoughts behind this experiment. Watch it!

I LOVE Gene Cloning!

To be honest, when I first read this article it was a bunch of mumbo jumbo in my mind. I was thinking: what the poop is it talking about??? I also doubt the title is relevant to the article but who cares. But, after reading it a few more time, it made more sense...light bulb moment!

Anyways, the abstract talks about how scientists were using the gene encoding endoxylanase (xynA) from Thermoanaerobacterium saccharolyticum B6A-RI. They cloned and expressed this gene in E. coli. Then xynA encoded a hypothetical 33-amino-acid signal peptide, which corresponded to the N-terminal amino acids. From doing this, there were findings of an open reading frame of 3,471 bp, which corresponds to 1,157 amino acid residues. These results gave xynA gene product a molecular mass of 130 kDa (Dalton).

According to the study, xynA from T. saccharolyticum B6A-RI had strong similarity to genes from family F beta-glycanases. The activity of the cloned endoxylanase had a temperature of 70 degrees C and a pH optimum of 5.5. The cloned endoxylanase A was stable at 75 degrees C for 60 min and displayed a specific activity of 227.4 U/mg of protein on oat spelt xylan (a substrate for the specific assay of endo-1,4-ß-D-xylanase). Therefore, scientists concluded that the cloned xylanase was an endo-acting enzyme, meaning that it contained functions within the cell in which it was produced...ain't that spiffy?

Article:

Gene cloning, sequencing, and biochemical characterization of endoxylanase from Thermoanaerobacterium saccharolyticum B6A-RI.

Humans vs. Sheep....which is easier to clone?

So who wins the fight? Well it has to be none other than....humans! Whoot, whoot! Why? Well because humans are just the best, duh. However, in scientific terms this is because humans and primates, in general, have two active copies of a gene called insulin-like growth factor II receptor (IGF2R). This gene prevents fetal overgrowth, which is a problem that has often hindered efforts to clone animals. This problem is due to the fact that nonprimates have only one functional copy of this gene. Thus resulting in genomic imprinting, which effectively silences the other copy and makes these animals have higher risk of exposure to cancer and cloning-related complications.

Scientists at Duke University used single nucleotide polymorphisms (SNPs), which are distinctive genetic markers, to test for imprinted IGF2R in humans and to "reconstruct the evolutionary history of the imprinted gene." The results showed that there was none found in humans; therefore, indicating that primates lost the imprinted gene around 70 million years ago (geez that is a long time). This study basically showed how humans may have a far less complex cloning process compared to sheep.

While, these researchers are positive about this study, other researchers think that the study is flawed because there might be other genes that contribute to the cloning problems in sheep. According to Ian Wilmut (professor at Roslin Institute who created the cloned sheep named Dolly), "it seems that a little knowledge is a dangerous thing, and the authors have allowed themselves to over-interpret their interesting results." Through the years, their has been countless disputes over gene cloning and stem cell research within the general public, the political spectrum, and the scientific and religious communities. What's your opinion on the cloning controversy? Jk I don't really care...or do I? Share your thoughts anyways. :{)

Article:

Genetic Difference May Make Humans Easier to Clone Than Sheep

Chapter 20: Useful Materials

I thought this video showed a cute way in describing the process of gene cloning, which refers to procedures that lead to the formation of many copies of a particular gene. The video goes through gene cloning step by step.

• Step 1: Obtain a plasmid vector and a DNA fragment: these are your starting materials.
• Step 2: Both the vector and DNA are treated with restriction enzymes that cleave double-stranded DNA molecules produced in over-hanging single-stranded nucleotide tails.
• Step 3: The chromosomal and vector DNA are cut into pieces and linked together; the linkage is catalyzed by DNA ligase.
• Step 4: In order to make multiple copies of this molecule the ligation mix is introduced to E. coli cells during the process of transformation
• Step 5: According to the video, the mixture should be placed on ice and then be exposed to 42 degrees celsius to cause a change in temperature.
• Step 6: The cells are then placed on a plate with growth medium. Only the cells that have required the plasmid resistance for the antibiotic can grow in this type of medium.
• Step 7: The plate should be incubated overnight at 37 degrees celsius.

After all these steps, the results should be that each transformed cell produces a colony of cells. Yay we have now gone through the key steps for molecular cloning!

P.S. Didn't you love the guys accent? ...I sure did. :{)

This video explains how scientists obtain a genetic fingerprint at Guy's Hospital in London, England. It shows how a researcher is using an automatic DNA extractor to produce a high purity DNA fragment from a blood sample. Basically, the rest of the video explains how these researchers use gel electrophoresis to produce the needed genetic fingerprint. Why might this be important, you may ask? To answer that question, DNA fingerprinting has gained acceptance as a precise method of identification. Also it is commonly used in forensics by helping provide evidence in a criminal case. Therefore, DNA fingerprinting can be very helpful during these times of identity theft, terrorism, and the TV criminology craze.

Sperm Impaired by HIV-infection... *tear, tear*

The abstract of this article explains how researchers conducted a perspective study on HIV-infected patients. The reason for this experiment was because couples who were serodiscordant (couples with on partner HIV positive and the other HIV negative), had a human immunodeficiency virus type 1 (HIV-1)-infected man, who was most likely on highly active antiretroviral therapy (HAART). The semen alterations are caused by the HIV-1 infection and the antiretroviral drugs. These couples wanted to achieve safe conception by requesting assisted reproductive technology (ART). Therefore, the goal of this study is to investigate the semen parameters in HIV-1-infected patients with and without HAART and to compare their sperm characteristics with those of healthy men.

The experiment:

• The study consisted of 226 men, who attended the university fertility center of Mannheim between May 1996 and July 2003.
• The patients were divided into three groups:
• HIV-infected men taking antiretroviral therapy.
• HIV-infected patients who did not take antiretroviral therapy until now.
• Control group with 93 men consulting our fertility center together with their wives because of tubal sterility.
• Semen samples were examined with regard to ejaculate volume, sperm concentration, motility, and morphology.

The results of this conducted research was that it showed major differences between the ejaculate of HIV-infected and non-infected men. The HIV-infected men as a whole had a lower ejaculate volume compared to the control group. The group with HIV-infection with HAART also had a less slow progressive and more abnormally shaped spermatozoa (motile sperm cell) compared with the control group. Overall, the differences between the groups with and without HAART were not that significant. The spermiogram, which is a microscopic examination of a sample of sperm, was negatively altered in HIV-infected men, especially in men with HARRT, when compared to the control group. This means that the ejaculate volume significantly changed through the course of they study.

I just realized I didn't add any quirky remarks in this post, well until now...oops!

Article:

HIV-infection and modern antiretroviral therapy impair sperm quality.

Bacteria Transfer Genes without Sex???

Sketchy title right ^^??? Well it might be exactly what you are thinking ;{). The article is basically about how bacteria are able to adapt to fast changing conditions, in the absence of sex. The answer to this phenomenon is yup, you guessed it: gene transfer!

The beginning of the article talks about how "oceans are highly dynamic habitats." When an oil spill occurs it makes a bunch of liters of hydrocarbons available to eat. "Without sex—and many bacteria don't have sex thank you very much—it's harder for marine microbes to mix it up and achieve the genetic diversity that's key to population success." In order to quickly adapt, horizontal gene transfer (HGT) occurs. Horizontal gene transfer is the primary reason for bacterial antibiotic resistance.

(The image above is microbe called Rhodobacter capsulatus, which can release packets of genetic material that allow them to swap genetic code.)

Next the article explains how Lauren McDaniel, a marine biologist of the University of South Florida and her colleagues tested the gene transfer abilities of nine alphaproteobacteria. Whoa, lets stop for a second because you might be just as confused as I am...what the poop is alphaproteobacteria? To answer that question, alphaproteobacteria is a class of bacteria included in the phylum "Proteobacteria." This specific type of bacteria have gene transfer agents (GTAs) or, "little genetic escape pods" according to McDaniel.

Now that we got that confusion out of the way, once they completed their research, McDaniel and her team found that these packets were absorbed by their fellow bacteria and incorporated into their own genetic code. "These particles were able to transfer genes from a donor strain to wild-type bacterial strains as well as natural populations," McDaniel explains. When they observed the bacteria they noticed that the bacteria were transferring genes to not only their own species but also to other closely related bacteria and genera. Not only were they able to transfer genes from different species, they were also able to do it hundreds of millions of times more frequently than previously estimated for other methods of gene transfer.

To be honest, that is quite cool (haha I'm such a nerd). Anyways according to molecular biologist Ford Doolittle of Dalhousie University, the overall impact of this type of gene transfer may be limited. Why you may ask? Well given that the DNA fragments transferred were quite short in length, only being 500 to 1,000 base pairs long. However, HGT is an effective weapon in the bacterial evolutionary supply and is responsible for many of the genes present in today's microbes not only in bacteria, but also the ocean, which can be viewed as a "bit of a microbial DNA soup." Ewww DNA soup.

Article:

Horizontal Gene Transfer: Bacteria Transmit Genetic Code without Sex

Chapter 18: Useful Materials

This video shows a brief overview of what occurs during bacterial conjugation. It talks about how plasmids (small circular piece of DNA fond naturally in many strains of bacteria) carry genes that code for antibiotic resistance. During conjugation, DNA from a plasmid can be transferred from one bacterial cell to another through pilli, which allows the exchange for genetic material.

Then.....

cue the mood music!

Next the video shows how one bacterial cell can transfer DNA to another bacterial cell. As long as the donor and recipient cell are in close contact, conjugation can occur. I thought this part was quite funny, not because it is showing how the bacterial cells are interacting with each other, but because of the mood music. The bacterial cells are trying to get it in...literally (haha I'm so funny)!

Although this video may not be as entertaining as the first one, it does provide very useful material on HIV replication. The video explains how HIV 1 replication is a multi-stage process, with each step being crucial to successful replication. Therefore, this can be a potential target of antiretroviral drugs. Overall, the expression of viral genes is called the viral reproductive cycle, resulting in the production of new viral genes or in this case, HIV.

VAR-MD...what is it???

Wait, I can totes guess what you are thinking right now: "what is VAR-MD?" I know I am a mind reader but shh don't tell people. Haha anyways, from reading the abstract of this article I learned that researchers have developed a new software tool called VAR-MD. The reason for this creation is because it is now an easier way to analyze variants generated by exome sequencing of families with rare Mendelian disease.

Now that we know why it was developed... you are probably wondering: "what exactly does this software tool do?"

To answer that question, VAR-MD analyzes the DNA sequence variants produced by human exome sequencing. VAR-MD generates a ranked list of variants using predicted pathogenicity (the ability of a pathogen to produce an infectious disease in an organism), Mendelian inheritance models, genotype quality and population variant frequency data.

Researchers tested VAR-MD by using two previously solved data sets and one unsolved data set. In the solved cases, the correct variant was listed at the top of VAR-MD's variant ranking. In the unsolved case, the correct variant was highly ranked allowing for subsequent identification and validation. It was concluded that, with the use of family-based, annotated next generation sequencing data, VAR-MD has the potential to enhance mutation identification. Due to the development of VAR-MD, scientist predict that as the reference databases, such as dbSNP and HGMD, continue to improve, software performance will advance as well. Ain't that neat?!

Article:

VAR-MD: A tool to analyze whole exome/genome variants in small human pedigrees with Mendelian inheritance.

Yay! Green Pea Seed Gene is Identified..whoot, whoot!

This is article is about how researches have discovered another gene that was manipulated by none other than Austrian monk, Gregor Mendel. If you do not know who Gregor Mendel is...well then you probably have not taken a biology class or you are just stupid. Anyways, Gregor Mendel was the first person to trace the characteristics of successive generations of a living thing. Mendel demonstrated that the inheritance of certain traits in pea plants follows particular patterns (laws of Mendelian inheritance). He took pea plants that vary in traits (height, color, shape, etc.) and counted the proportions of these traits in several generations of pea plants. Mendel concluded that these features must derive from genes, which he discovered were randomly divided between offspring.

After 141 years of research (geez louise that is a long time!), the gene that they uncovered was specifically the controlled the color of his peas'

seeds. This is the third gene they identified out of the seven genes Medel used in his experiment...so there are quite a few that remain a mystery. Hold up, you are probs asking: "how the poop did scientists discover this gene?" Well to answer that question, researchers identified the sequence of a gene common to several plant species; this gene was used to break down a green pigment molecule, eventually finding out that it matches Mendel's gene.

Researchers have also been trying to locate the sequence of a gene called staygreen (sgr) in the meadow grass, Festuca pratensis, in hopes of determining the sequence Mendel's gene for seed color. The team compared genetic markers specific to the sgr region of the grass's chromosome with the markers

on the corresponding portion of the rice genome, which contained 30 potential genes in that area, including one similar to other pigment-metabolizing proteins. Rice? Porque? They used rice because it is genetic similar to Festuca. Anyways, researchers picked out the location of the pea sgr sequence from pea plants that varied in their seed color in order to find out if it was equivalent to Mendel's gene. Sure enough, the pea version of sgr was always found in the same tiny part of the chromosome as Mendel's seed color gene. Now that scientist have the specific gene, they can begin their studies to figure out exactly what its functions are.

(Image on top right: Picture of Gregor Mendel, who is remembered as the "father of genetics" today.)

(Image on bottom left: A monohybrid cross example of Mendel's pea plant experiment. He crossed two yellow pea plants, both of which were heterozygous dominant, and they produced 3/4 yellow peas and 1/4 green peas.)

Article:

Gene Behind Mendel's Green Pea Seeds Finally Identified

Chapter 16: Useful Materials

When I found this video I thought it was the cutest thing ever! So I thought I would share it with you. Basically, this video talks about how genes carry down traits through family members. It gives several example of different types of traits, such as gender and blood type. The video also talks about how some traits are inherited from just one parent, while others are a mixture of both parents. Most traits are influenced by not just one but many genes, which combine with one another to form a single trait... isn't that neat?! Anyways, I think you should watch this video because it is just too cute!

This animation (CLICK HERE) shows an example of a Punnett square. What is a Punnett square, you ask? Well a Punnett square is a diagram that is used to predict an outcome of a particular cross or breeding experiment. What I like about this animation is that it gives several example of how to use a Punnett square. It also makes you decide what the genotype and phenotype of the Punnett square is. This animation was quite helpful and if you ever need help in understanding how a Punnett square works, I advise you to check out this animation!

Spo11 Catalyzing Meiosis-Specific DNA!

From reading the title, you might be just as confused as I was when I first read this article. But not to fear! Your confusion will hopefully be cleared up by the end of this post (cross your fingers!). Now on to the important stuff...the abstract of this article is from PubMed talks about Spo11, which is a protein involved in double-strand breaks (DSBs). DSB initiates meiotic recombination in S. cerevisiae, a species of yeast that is used in numerous biological studies.

Lets pause for a second and ponder what meiotic recombination might mean...done pondering? Well meiotic recombination is a genetic recombination process by which a molecule of nucleic acid (usually DNA, but can also be RNA) is broken and then joined to a different one. Meiotic recombination in eukaryotes facilitates chromosomal crossover. The crossover process leads to offspring's having different combinations of genes from those of their parents, and can occasionally produce new chimeric alleles (artificially constructed gene).

Spo11 is one of several proteins required for DSB formation, and was identified when DSB, in certain mutants, would covalently attach to it. Spo11 is strongly involved in these findings as "the catalytic subunit of the meiotic DNA cleavage activity." Why is this important? Well because these findings are the "first identification of a biochemical function for any of the gene products involved in DSB formation." Therefore, not only are these findings important, but they also have clear, supporting evidence that the mechanism of meiotic recombination initiation is evolutionarily preserved.

Article:

Meiosis-specific DNA double-strand breaks are catalyzed by Spo11, a member of a widely conserved protein family.

A New Discovery in Mitosis??? (drumroll...)

I am guessing that you all want to know what the new discovery is right? Well there is no discovery.....................haha just kidding; I fooled you for a second didn't I? Well researchers from The George Washington University Medical Center, have discovered something that could possibly "revolutionize the way scientists think about key aspects of cellular lifecycle." It can also offer new opportunities for cancer researchers to help reduce the progression of cancer. This new discovery can shed some light into the understanding of mitotic cell division.

What is mitotic cell division, you may ask? Well mitosis is the process by which a eukaryotic cell separates the chromosomes in its cell nucleus into two identical sets, resulting in the production of two daughter cells from a single parent cell. According to Rakesh Kumar, Ph.D., chair of the GW Department of Biochemistry and Molecular Biology, "this represents a crucial moment when the division of genetic material is still equally distributed. An even exchange is critical for stable genetic changes." Therefore, if something were to go wrong during cell division, such as chromosomal mutations (deletions, duplications, inversions, and translocations), it could lead to an unequal production of abnormal cells and quite possibly result in cancer.

Researchers from the GW Department of Biochemistry and Molecular Biology may have discovered a missing link about the protein, Arpc 1b, which acts as an activator as well as a substrate for Aurora A, "an enzyme which plays a central role in cellular reproduction in normal cells but is over-expressed in several cancers." The missing link found is the role that Arpc 1b plays in beginning the cell cycle and how the process is kept in balance.

Not only is this finding beneficial in keeping the cell cycle in harmony, it may also offer a potential target for pharmaceutical therapy. You might be asking, how can this happen? Well researchers discovered that Arpc1b promotes tumorigenic properties of breast cancer cells when it is over-expressed. With this new discovery, researchers hope to uncover a way to suppress Arpc 1b activity in cancer cells, in order to have this important biological event kept in pristine balance.

Article:

Missing Link in Cell Mitosis Discovered: The Role of Protein in Controlling Cell Division Unveiled

Chapter 15: Useful Materials

When I first found this video, I knew that I just had to post it! This video describes the phases of mitosis through the song, "I Got a Feeling" by the Black Eyed Peas. The song explains all the phase of mitosis (interphase, prophase, metaphase, anaphase, telophase, and cytokinesis) and what happens during each phase. I think it is a catchy tune and it is just too cute! Seriously, words cannot describe it's cuteness (haha yup, thats right, I'm calling a song cute...deal with it). Anyways, I recommend that you should listen to this awesome song because you just might learn a little something about mitosis.

What the Fudge Are Tumor Supressor Genes???

Although the abstract for this article is super short, I shall attempt to expand this paragraph as much as possible. The abstract does not explain much; but it does talk about the mutation of tumor suppressor genes and tumor suppressor proteins. For those of you reading this post that are pulling your hair out and screaming, "what the fudge are tumor suppressor genes" at your computer screen, allow me to take you out of your misery. Tumor suppressor genes, when normal, encodes a protein that helps prevent cancerous growth. However if tumor suppressor genes are mutated, their normal function is eliminated and cancer may occur.

The main thing that the abstract explains for tumor suppressor gene mutation is that the mutation is "thought to contribute to tumor growth by inactivating proteins that normally act to limit cell proliferation." For example, a tumor suppressor gene is like the brake pedal on a car. It normally keeps the cell from dividing too quickly, just as a brake keeps a car from going too fast. When something goes wrong with the gene, such as a mutation, cell division can get out of control.

There are several tumor suppressor proteins, but only two of them (p53 and pRb) are understood thoroughly enough in detail. Both of these proteins have a common role in the events of transcription and phosphorylation that are required for a cell to pass from the G1 to S phase.

(The image above is the cell cycle with the checkpoint proteins: cyclin and cyclin-dependent protein kinases (cdks))

Lets start with p53, (or protein 53) which is responsible for proteins that can either repair damaged cells, or cause damaged cells to die, a process called apoptosis. When the gene is not working due to a mutation, these proteins that repair cells or eliminate damaged cells are not produced, and abnormal cells are allowed to divide and grow. A mutation in the p53 gene (located on chromosome 17) is the most common mutation found in cancer cells, and is present in over 50% of cancers.

Now lets think about pRb, (or retinoblastoma protein) which functions to prevent excessive cell growth by inhibiting cell cycle progression until a cell is ready to divide. pRb is part of a category of tumor suppressor genes that encodes proteins that are negative regulators or inhibitors of cell division. The Rb protein negatively controls a regulatory transcription factor called E2F that activates genes required for cell cycle progression from G1 ro S phase. The binding of Rb proteina and E2F inhibits its activity and prevents cell division.

Hopefully that thoroughly explained tumor suppressor genes and its functions. If you are still unsure about the role of tumor suppressor genes, think of my analogy I said earlier in this post. A tumor suppressor gene is like a brake pedal: tumor suppressor gene regulates cell division just like how a brake pedal regulates the speed of a car! (Hehe I probs can guess what you are thinking..."Serina why are you just so clever?")

Article:

Tumor suppressor genes

Gene Mutation: Beneficial or Detrimental?

Did you read the title of this post? Well you should have, if not go read it now (do it...you won't)! Anyways, from reading the title, you might be asking yourself: how can gene mutation can be beneficial? Usually when people think of mutations, they relate it to being harmful to the body because gene mutations are changes in the DNA structure that can alter a particular gene.

Well this article gives an example of how gene mutation can be somewhat helpful. In Berlin, a baby was born with bulging thighs and biceps that were credited to a unique beneficial genetic event. Now you could be asking yourself: how is this mutation beneficial? According to the article, the mutation was advantageous in the short run because the child able to lift seven-pound dumbbells with arms extended. I am not sure how scientists seem to think that this ability is beneficial to the child. Is he going to enter a weight lifting competition? Although this capability may seem profitable now, the child's future is still a mystery. Dr. McNally states that, "the boy is still very young and that problems could occur later in his life."

It was discovered that the child had a mutation in the gene that produces a protein called myostatin. And me, being the clueless airhead that I am, did not know what myostatin was... good job Serina! So I googled the word (thank god for google...the lifesaver for many of my problems). According to MedicineNet.com, myostatin is: "growth factor that regulates the size of muscles beginning in early embryonic development and continuing throughout life." Due to the abnormal amount of this protein in the child's body, researchers have concerns that his heart muscle could be damaged. Even though the child's cardiovascular system is fine at the moment, you can never be too sure about how it will be in following years.

After some thinking, this is not what I would call a "beneficial" mutation. Why? Well lets examine the main reason... does anyone know what will happen to the child as he grows? Most likely, the answer is NO (unless you're a psychic) because the child's future is unsure; no one is positive of how his life will unfold. Therefore, the child's gene mutation may seem advantageous now, but that could change at any moment; whether it be tomorrow, next week, or next year.

Article:

Gene Mutation Makes Tot Stronger

Chapter 14: Useful Materials

This video is from the brilliant Khan Academy. In this video, Sal explains the basics of cancer and how it is the by-product of broken DNA replication. He also explains how cancer can occur. Cancer is a disease of multicellular organisms characterized by uncontrolled cell division. It is one of the tope leading cause of death in humans!

Whenever I need to study definitions or key points, I always turn to Quizlet (CLICK HERE)! As I've mentioned before, this website has been a life saver on numerous occasions. It basically has all the needed terms and references from the chapter in the book! Therefore, this site is worth visiting for some easy studying techniques.

DNA methylation and cancer (*gasp*)...

Lets start off with the basics...what is DNA methylation? As if you don't already know?!? DNA methylation is the biological process by which a methyl group, which is an organic functional group with the formula CH3, is added to DNA nucleotide. Through DNA methylation, a methyl group can be attached to a carbon atom on cytosine or to a nitrogen atom on adenine. The addition of a methyl group to these nucleotides can serve many important biological purposes, such as suppressing potentially harmful viral genetic information that is present in the human genome.

Now that we understand the fundamental info, I can explain what the article is about. Basically, this article talks about DNA methylation and how cancer can be involved in the process.

The enzyme involved in this process is DNA methyltransferase, which catalyzes the transfer of a methyl group from S-adenosyl-methionine to cytosine residues to form 5-methylcytosine, a modified base that is found mostly at CpG sites in the genome. CpG islands are found near promoters in vertebrates and plants. In different types of tumors, abnormal or accidental methylation of CpG islands in the promoter region has been observed for many cancer-related genes resulting in the silencing of their expression. However, the reason why abnormal hypermethylation takes place is not known. The genes involved include tumor suppressor genes, genes that suppress metastasis and angiogenesis, and genes that repair DNA suggesting that epigenetics plays an important role in tumorigenesis.

Article:

DNA methylation and cancer

New Discovery of Gene Regulation in Mammals!

As you may have read from the title this article talks about a new type of gene regulation. Researchers at the University of California, Santa Cruz (UCSC), have discovered a type of gene regulation never before observed in mammals. The UCSC researchers discovered a ribozyme (RNA enzyme or catalytic RNA) that controls the activity of an important family of genes in several different species. A ribozyme is an RNA molecule that catalyzes a chemical reaction.

A newly discovered role for the hammerhead ribozyme was found embedded within certain genes in mice, rats, horses, platypuses, and other mammals as well. The genes are involved in the immune response and bone metabolism. Monika Martick, a UCSC postdoctoral researcher and first author of the Nature paper says, "the unique thing about these ribozymes is that they control the expression of the genes they're embedded in."

In the genes studied by Martick and coauthor Lucas Horan, a graduate student in molecular, cell, and developmental biology at UCSC, the messenger RNA contains sequences that assemble to form an active hammerhead ribozyme. The hammerhead ribozyme is able to divide itself in two because it is a self-cleaving molecule. By preventing protein translation, this self-cleaving action in the messenger RNAs effectively turns off the genes. Most likely, another mechanism exists to turn on the genes by stopping the self-cleaving action of the ribozyme. However, the UCSC researchers are still searching for such a mechanism, but they assume it is out there, somewhere.

Article:

New Mode Of Gene Regulation Discovered In Mammals

Chapter 13: Useful Materials

As always I love posting videos from Mr. Anderson because he explains stuff so well. It's like having a personal teacher at your finger tips! Anyways, this video is about the regulation of genes in both prokaryotes and eukaryotes. He also talks about operons, which are clusters of genes under transcriptional control of one promoter in bacterial cells. Another thing he explains is the importance of transcription factors in eukaryotic gene expression. Overall, this video is quite helpful...but I mean lets be honest, all of his videos are helpful (am I right or am I right?).

This video is a NDSU Virtual Cell Animation that talks about lac operon. Is it just me or do these videos creep you out too? The music at the beginning of each video is quite creepy and mysterious. But I'm not here to talk about creepy music, I'm here to talk about this awesome video. The video explains lac operon, which is an operon required for the transport and metabolism of lactose in Escherichia coli and some other bacteria. It consists of three adjacent structural genes, lacZ, lacY and lacA. The lac operon is regulated by several factors including the availability of glucose and of lactose. If lactose is absent, the gene is turned off; if lactose is present, the gene is turned on. In the absence of lactose, a repressor protein (made by the lacI gene) binds to the operator region upstream of the lacZ, lacY and lacA genes and prevents the lactose utilization gene from being transcribed.