Jumping Genes

I found this video interesting because it talks about the effects of transposons, or jumping genes. They use chromosomes of organisms and "jump" between different parts of the genome.  It has been observed that transpons avoid inserting themselves into active genes, allowing their hosts to continue functioning. According to this video, it seems as though transposons are helpful parasites that attempt to "live" longer by allowing the organism in which they inhabit, or their host, to survive. For example, transposons can cells capable of surviving in stressful conditions, such as in cold and salty environments. 98% of DNA of some plants are derived from transposons, which seem to diversify genetic material.

ENCODE Project

The ENCODE, or Encyclopedia of DNA Elements, Project's objective is to aid the biology and medical community by helping them interpret the human genome. It uses several different types of technology to identify all of the functional elements within the human genome. The main purpose is to make all of this information available to public databases for widespread use. This project was launched by the National Human Genome Research Institute to identify all of the regions within the genome that codes for a defined product or a biochemical signature. These signatures can mark important sequences within the genome, such as those for silencers, enhancers, and promoters. The main focus currently is to annotate genes and their RNA transcripts and also regulatory regions for transcription. Click here to access the article that I got my information from. Overall, this project is an important development within bioinformatics and it will be interesting to see how large the database grows.

Transposons and New Discoveries

Transposons are an important topic within our bioinformatics chapter in which short segments of DNA move from one site within a genome to a different site. This article discusses how scientists have re-created a precursor gene to two current human genes. This gene is called Harbringer3_DR and is a transposon. This research could be enlightening to scientists who are attempting to more precisely control where genes incorporate themselves during gene therapy. This particular transposon, Harbringer3_DR, is unique for its ability to insert itself into a genome in a specific manner by recognizing certain DNA sequences.

Transposons typically code for transposase, an enzyme that facilitates transposition, but this transposon also codes for another molecule that resembles a known protein. For this reason, researchers called this molecule Myb-like. The Harbringer3_DR gene exists in other animals, such as zebra fish. Scientists were able to synthesize Harbringer3_DR  using the gene in zebra fish as a template, then placed their constructed gene within a human cell. They were interested to find that the Myb-like protein allowed the transposon to enter the nucleus and brought it within the transposon's tips vicinity. This sparked further interest in discovering how the Myb-like protein and transposase work together to control where the gene is inserted.

In the future, scientists hope to use transposons as vehicles for therapeutic genes that can deliver these genes to specific locations.While inactivated viruses can also be used for this purpose, they are fairly random in their insertion site. Researchers intend to investigate a method of disabling the ability of a transposon to further jump from one location to another after it has been inserted into the desired spot. If this is discovered, there may be a major breakthrough in gene therapy!

Plasmid Cloning Animation

Click here to go to an animation about plasmid cloning. I liked this video because it walks you through the various stages of DNA cloning alongside animations that really clarify the process. It begins with inserting target DNA into a vector, such as a plasmid. It then moves on to the various sites of vectors and how exogenous DNA can be inserted into the vector. I liked how the example used in the animation is the ampicillin-resistance gene, which we discussed in our bacterial transformation lab. The animation goes on to explain how restriction enzymes are used to cleave the vector at specific cloning sites and sticky ends are produced. A recombinant vector, or hybrid vector, is formed and is put into a host cell so that the genes can be cloned. The recombinant plasmid is amplified to produce many copies of it. The animation ends with the long-term effects of this kind of cloning, as multiple daughter cells are formed that have the same recombinant plasmid.

Bioremediation

One of the topics within genetic technology is bioremediation, in which living organisms are used to detoxify environmental pollutants. Basically, microorganisms or plants are used to reduce pollution. A pollutant's structure can be altered so that it is no longer harmful. Enzymes produced by microorganisms can carry out this alteration.

This article is about a species of bacteria than can detoxify contaminated groundwater by removing any uranium that may be present. This species, Geobacter sulfurreducens , gets energy by reducing metal. If you can recall for chemistry, reducing is when a substance gains electrons. This bacteria adds electrons to metals within its environment, including uranium. When uranium is reduced, it becomes less soluble and does not spread as efficiently as it did before, therefore reducing contamination.

Researchers are attempting to discover how this species is able to remove uranium. They strongly believe that the pilli of these bacteria plays an important role in this process. Without pilli, this species reduces uranium in the environment within its cell envelope, which is fatal to the cell. When pilli are present, the bacteria are able to survive the process since it is occurring farther away from the cell and the pilli also increase the surface area at which electron transfer can take place.

Research into the ability of the pilli to conduct electricity and transfer electrons to power the bacteria may help scientists understand more about bioremediation. There is also a possibility of producing non-living devices that can perform the same type of function as these bacteria if enough research is conducted into how the bacteria function. It is also possible that this species can be manipulated to remove other radioactive isotopes of elements, such as plutonium. Overall, research into bioremediation could be very beneficial to the environment.

Rapid PCR

So...this might be my shortest blog post until now. Well, here goes. Do you recall our GMO experiment in which we had to use polymerase chain reactions, or PCR? And do you remember how the thermal cycling involved meant that we would not be able to retrieve our results the day of, and the lab was split between two weeks? Well, it is possible that PCR can be sped up so that it is completed under three minutes!

To brush up, polymerase chain reactions make many, many copies of a specific DNA sequence (as specified by the primers used in the reaction). This amplification allows scientists (or us) to perform genetic tests on these sequences for various purposes. This article states that PCR amplification can be completed in as little time as two minutes and eighteen seconds. Basically, a rapid thermal cycler was created in which the sample's temperature is altered 45 degrees Celsius every second. 30 cycles of PCR can be completed within this time. DNA amplification enzymes, such as polymerases, that are able to work under these conditions were also discovered.

The ability to almost instantly amplify genes could be extremely beneficial to the medical community specifically in addition to the scientific community as a whole.

HIV Life Cycle Video

This video shows the life cycle of HIV, which we know is a retrovirus. This video displays the entire life cycle, starting from attachment and moving on to entry, integration, synthesis of viral components, viral assembly, and release. I really liked the visuals in this video and felt that they enhanced the understanding of the life cycle of HIV. While the video did not explicitly state where each step started and stopped, I was able to track the various stages. There was also some interesting extra information in the video, such as how the virus uses GP120 surface glycoprotein to attach to a CD4 membrane protein as well as its corecepotor. The video then proceeds to explain how the viral envelope and the cell membrane fuse and allow the capsid to enter the cytosol. Overall, I felt that this video included all the information about the life cycle of a retrovirus that is present in the book and also added on to it by including extra information that is specific to HIV.

Bacterial Conjugation

As we learned in class, gene transfer in bacteria can occur through transformation, transduction, and conjugation. In this post, I will be focusing on conjugation. In conjugation, there is direct contact between the donor cell and the recipient cell through which a strand of DNA is transferred. See the picture below for a visual of how conjugation occurs. It has been found that conjugative plasmids contain genes that are resistant to several types of antibiotics. Therefore, if resistance to a particular antibiotic is selected, resistance to other types of antibiotics will be simultaneously selected. Plasmids involved in gene transfer also code for conjugative pilli that facilitates the transfer of DNA by binding to the recipient cell from the donor cell. At the end of conjugation, both cells have the plasmid that was transferred.



According to my article, this is the main method of the transfer of antibiotic resistance between bacteria. It may be useful to develop a method of preventing conjugation in order to prevent the development of bacteria that are resistant to multiple antibiotics. Several decades ago, it was found that filamentous bacteriophages are capable of preventing conjugation. Further investigation showed that this was accomplished by closing up the conjugation pilus (or sex pilus). This is mainly mediated by g3p, a phage protein within the phage coat that seems to lower conjugation rates. These results indicate that certain proteins from the phage can be used to slow down antibiotic resistance in bacterial cells.

Click here to view the abstract of the article I used and click here to view the full article.

To Share and Share Alike

This chapter in biology has been all about the genetics of viruses and bacteria. One of the topics that we covered in class was horizontal gene transfer, in which genetic information is trasnferred between bacterial cells. This leads to increased genetic variation. I found the picture below to be helpful in understanding the difference between horizontal and vertical gene transfer.

According to my article, it was originally thought that horizontal gene transfer in bacterial cells only occurred in certain situations, such as in the presence of strong antibiotics. In actuality, prokaryotes (which include bacteria and archaea) are able to receive genes rather frequently either through a bridge or a virus. This can even occur when the two prokaryotes transferring genes are from different species. Researchers have found that 88 to 98% percent of new genes in bacteria come from horizontal gene transfer. The genes that are transferred are usually next to genes that are not similar in function. Genes that evolve within a bacteria are often located near genes that serve similar functions. The study shows that the majority of new DNA in bacteria comes from horizontal gene transfer. It has also been observed that newly transferred DNA usually stay longer within the genome and evolve more efficiently. Overall, horizontal gene transfer allows prokaryotes to evolve quickly to fit a new environment. This is also the cause of rapid development of antibiotic resistance in bacteria.

To access the article from which I retrieved my information, click here.

Dihybrid Crosses Video

Embarrassing as it might be to admit, I forgot how to do dihybrid crosses between freshmen year and now. I did not find the book to be particularly helpful in explaining this, so I found this video:

He uses traits in mice, the grasshopper phenotype and the prune phenotype, to set up a cross. I particularly liked how he explained what happened if the genes were linked (on the same chromosome) and if they were independently assorted. I also liked how he used the pictures of chromosomes to really explain how these crosses occur, very similar to what Dr. Weber did in class. Later on in the video, he goes through what happens when two genes are linked, using a CSP (craniofacial and skeletal malfunction) phenotype that is on the same chromosome as the grasshopper phenotype. He uses the appropriate terminology throughout the video and I appreciated his use of the terms "parental" and "recombinant". Sometimes, Youtube video makers are rather incompetent when it comes to terminology, but thankfully he is not! He also briefly touches on the probability aspects of dihybrid crosses. I also learned something new when at the end of the video he talked about map units and what they measure. The last think I liked about his explanation was how he explained the proper way to write the genotype of the mouse, with regards to the linkages of the genes.

Diseases for Darwinism

This article discusses Huntington's disease, what causes it, and the other effects that having this disease can have besides the classic symptoms. Huntington's disease is a neurological disorder that destroys neurons in certain regions of the brain. This causes the patient to have difficulty controlling movements. This can lead to various cognitive and emotional problem. This disease occurs due to a mutation that leads to the abnormal elongation of a gene known as huntingtin. The length of this gene becomes problematic when it exceeds past a certain extent and the length has an impact on the severity of symptoms.

Animals with this type of mutation only develop Huntington's when they make p53 (the tumor suppressor we learned about in Chapter 14!). Studies at Tufts University have found that people with Huntington's disease are less likely to have cancer and have more children than the average person. It is possible that increased p53 plays a role in these "side effects" of Huntington's. This is because, as we have previously learned, p53 regulates cell division and helps prevent cancers. The article goes on to talk a little bit more about p53 and its link to Huntington's. However, I want to get more into the material that is related to Chapter 16. As we know, Chapter 16 is about simple patterns of inheritance. As we have also learned in class, Huntington's disease is autosomal dominant. Look at this nifty picture to see how this disease is passed down generations:

The mutated gene is located on an autosomal (non-sex) chromosome and a person needs only one copy of the mutated gene for them to express the disease. As you can see in the picture above, the father is heterozygous for Huntington's but expresses the disease since it is dominant. Because he has children with a normal woman, 50% of his kids are unaffected while the other 50% are affected. I retrieved this infromation from here. If you are curious about Huntington's this site is extremely reliable and has a brief overview of the disease as well as detailed explanations.

The information in the previous paragraph is mostly review (since we have discussed the autosomal dominant nature of Huntington's in class), and I would also like to discuss another aspect of the Scientific American article that relates to our current chapter. A biologist at Tufts, Philip Starks, who has been studying p53 and Huntington's (as mentioned before) suspects that Huntington's is an example of antagonistic pleiotropy. Pleiotropy is when a mutation in a single gene results in multiple effects on the individual's phenotype. There are several forms of pleiotropy. One is when a single gene expression can alter cell function in more than one way. Another is when different cell types express a gene within a multicellular organism. Finally, one gene may be expressed at different phases of development. Check out pg. 343 in our biology textbook for even more information regarding pleiotropy. Starks believes that Huntington's may be pleiotropic because the same protein that results in the debilitating symptoms of Huntington's may also be responsible for making Huntington's patients more reproductively successful.

Gene Therapy and X-Linked SCID

In class this week, we learned about various patterns of inheritance. These included simple Mendelian inhertiance, incomplete dominance, codominace, sex-influenced inheritance, and X-linked inheritance. For this blog post, I am focusing on the last of these types of inheritance patterns.

X-linked severe combined immunodeficiency, or SCID, is a disease that causes people to not have functioning immune systems, leaving them susceptible to life-threatening infections. This disease results from a lack of T cells and natural killer cells as well as nonfunctional B lymhocytes (remember these from A&P?). Children with this disease are usually diagnosed to the recurrence of infections despite normal treatment. The final diagnosis of X-SCID is done by checking lymphocyte counts, lymphocyte functionality tests, and testing of the molecular genes. The best treatment for SCID is a bone marrow transplant from a genetically matched sibling. In the absence of such a sibling, unmatched donors are often recruited to donate bone marrow although these transplants are only about 70 percent successful.

As seen in the name of the disease, the inheritance of this condition is X-linked. This condition is more likely to occur in males, since they only have one X chromosome. Therefore, there is no recessive or dominant involved in their inheritance. In a female, it is possible to have recessive X-linked conditions that are not expressed due to the presence of normal genes on the other X chromosome. This is not an option for males, since they have an X chromosome and a Y chromosome. If a mother is a carrier for this disease, the chance of her transmitting this gene is 50%. Males who have SCID can only pass this gene on to their daughters, and not their sons. As we know from what we learned in class, this is because an X chromosome is contributed to daughters while a Y chromosome is contributed to sons. It is possibly for prenatal testing to be conducted on women to determine if they are carriers for this disease.

Feel free to read this article, from which I retrieved my information, to understand more about this disease. I mainly attempted to focus on the information that was relevant to our current chapter of patterns of inheritance.

Meiosis Video

I found this video useful because ever since freshmen year, I have had difficulty differentiating what to call "chromosomes", "sister chromatids", and "homologous chromosomes". Even Ms. Patil couldn't understand why I couldn't understand meiosis properly! And when Dr. Weber explained it, I understood it for about 5 minutes before once again I was confused. In a way, watching this brief video on meiosis helped me figure out these terms. While it does not go in depth, the video hits all the major points of meiosis. It goes from interphase through the second cytokinesis. It even mentions crossing over and how it occurs. My only complaint is that it does not mention how errors might occur during meiosis. Of course, one can always refer to my previous blog post for that!

As a quick addition, I would like you to view this image:

Typical Sexual Cycle for Humans	Typical Sexual Cycle for Protists
and Other Animals

Diploid Phase       Haploid Phase


that I retrieved from here. While its just a simple image, it clarified my confusion over what diploid-dominant and haploid-dominant species were. For some reason, the description in the book was somewhat confusing to me. Here, the image on the left displays the cell cycle of a diploid-dominant species while the image on the right displays the cell cycle of a haploi-dominant species.

Surprises in Cell Division

As promised, this summary as well as this article are shorter than those of my previous post. So, without further ado...

A research group at the California Institute of Technology has been able to capture the first three-dimensional image of cell whose nucleus is dividing in high resolution. A new method of cell slicing and imaging were used that allowed for the image to be obtained. While conventional electron microscopy involves much handling of the specimen prior to viewing, a technique called electron cryptomography, or ECT, was used trap the specimen in a more native manner, encasing it in a thin layer of ice. A limitation is that ECTs require the sample to be 500 nanometers thick at the most. The smallest known eukaryote was used and even that needed to be sliced carefully using a machine and a diamond knife.

Now that we know why what the researchers at CalTech did allowed them to capture the image while others previously could not, let's move on to the cell division aspect of this. I will refrain from going in depth regarding how mitosis works, as we discussed this quite thoroughly in class. During metaphase, the sister chromatids line up at the center of the nucleus, where they are held by microtubules in the form of a mitotic spindle. In most fungi, plants, and animals, more than one microtubule attach to each chromosome prior to the separation of the chromosome sets. In the image taken by the researchers at CalTech, a cell with 20 chromosomes is present, but only 10, somewhat incomplete microtubules were found. I was quite surprised when I read this because in all the pictures in our bio books and the pictures we drew in class, there was at least one kinetechore microtubule per sister chromatid set.
This is sort of how I have always pictured mitotic metaphase:

Note that I pictured it with one microtubule per sister chromatids

This leads to the question of how the sister chromatids separated. The researchers hypothesized that perhaps the chromosomes bundled up so that they could be separated by a fewer number of microtubules. Further studies using this slicing and imaging technique might lead to new discoveries in several kinds of cells, including human cells.

The top image shows multiple microtubules per set while the bottom picture show the bundling of chromosomes idea that fits with the information found in the study

Click here to view the article.

Human Aneuploidy

In Chapter 15, we learned about mitosis, meiosis, and the eukaryotic cell cycle. One of the topics covered is how variation in chromosome numbers and chromosome set numbers can occur. These changes can have significant consequences. Aneuploidy is one form of chromosome number variation in which there is a change in how many particular chromosomes there are. Therefore, the sum of the chromosomes could be a number that is not a multiple of a set. Aneuploidy can lead to congential birth defects as well as miscarriage. Most aneuploidy occurs due to errors in maternal meiosis I, and increased maternal age has an impact on error rates. The term nondisjunction is used frequently during this article. In case you did not know, nondisjunction is when chromosomes fail to separate properly during cell division.

Aneuploidy is both "the leading cause of miscarriage" and "the leading cause of congential birth defects and mental retardation". Research has been conducted on whether or not particular meiotic defects can be connected to aneuploidy or infertility. Most studies have involved males, which is mostly irrelevant to the understanding of human aneuploidy. Pairing of chromosomes, synapsis, and recombination need to be observed as they occur in fetal ovarian tissue. This can be challenging, particularly because there are years separating when the cells are in prophase and when they divide. Studies have been conducted on female oocytes instead to determine if chromosomes are already "set-up to mal-segregate" at the appropriate time. Several groups have concluded that in human oocytes there are high levels of defects during synapsis. This is not enough information to conclude that these defects during prophase relate to human aneuploidy. It needs to be determined whether or not chromosomes that are known to exhibit nondisjunction are also more prone to defects in synapsis and recombination.

A type of aneuploidy that you have most likely heard of before is trisomy, or trisomy 21 in particular. This is also known as Down syndrome.

Recent studies on mice have attempted to recreate the nondisjunctional meisosis and recombinational defects that are present in humans. The oocytes of the offspring of two closely related mice were analyzed and it was discovered that meiotic nondisjunction increased due to disturbance in recombination. In another study, it was discovered that oocyte chiasmata are located closer to the telomeres when maternal age is higher than the norm. This caused the connections between homologous chromosomes to be lost more frequently. Mutations also play a role in improper segregation. Research in these areas has supported the idea that abnormalities during prophase (particularly during synapsis, recomination, and cohesion of sister chromatids) can cause errors during chromosome segregation. Extensive research has also been conducted on pre-disposing factors, such as environment and even in a chemical used during the manufacturing of plastics and resin.

A helpful image displaying aneuploidy caused  by nondisjuncton

The molecular background of meiotic nondisjunction has yet to be discovered, as are the reasons behind the increases in nondisjunction with increasing age. In order for this to occur, in vitro studies need to be used on meiosis, but we first have to produce gametes from stem cells. The collaboration between stem cell researchers and aneuploidy researchers may be beneficial. By looking at both fields, scientists may be able to generate in vitro systems that are capable of producing genetically normal eggs while also discovering why meiosis in human females is frequently faulty.

Click here to see where I found this resource. Click here to access the full article. Thanks for reading this unusually long article. I will make sure to make my next two posts a bit shorter to compensate!

Nucleotide Excision Repair

While we were talking about the types of repair in class, I was having difficulty picturing how the repair worked. This animation goes through the process of nucleotide excision repair, starting from when base damage is recognized and the multiprotein NER complex forms. Next, helicase unwinds the DNA and the complete complex is created. Afterwards, exonucleases cut the DNA and the fragment is excised. A repair synthesis complex is formed and new DNA is synthesized, which ligase binds to original DNA. After this, DNA returns to its normal configuration. Even though this is only a short animation, I found it useful just to help me picture how nucleotide excision repair worked.

While searching Youtube for actually useful material, I came across this:

Basically, this song is terrible but I found that it actually had accurate information on p53 and its actions as a tumor suppressor gene. The song explains how p53 can respond to genetic mutations and why it is important for the maintenance of "genome integrity". It also connects the topic to cancer, and how defects in p53 can lead to disease. So...just remember that "to keep your genome mutation free is the concentrated passion of p53!"
P.S. I may have posted this because its sorta stuck in my head now in all of its suckishness and I figured that I ought to inflict its damage upon someone else. I am such a philanthropist!

Secrets of a Salty Survivor

Well, one article on cancer is more than enough for me. An important part of our chapter was learning about DNA repair. DNA repair is necessary to minimize damage caused by mutations. There were several methods of DNA repair that we discussed in class, including direct repair, nucleotide excision repair, and methyl-directed mismatch repair. In this article, the author talks about a microbe called Halobacterium (pictured below) from the Dead Sea that has a highly developed DNA repair system.

Research into this topic can potentially help protect astronauts from DNA damage that results from interplanetary space radiation. As we learned in class, DNA molecules are sensitive to radiation. According to a researcher studying Halobacterium, her research group fragmented the bacteria's DNA completely through radiation only to find that it had reassembled its chromosome to working condition in several hours. Um, whoa!

Naturally, Halobacteria live in the extremely salty conditions of the Dead Sea (which is actually a lake), where most sea life would find inhospitable. This is because the salt causes the DNA to become damaged and even die in normal organisms because the extreme saltiness would lead to the same lesions as those created by exposure to radiation. In a series of experiments funded by NASA, researchers subjected this bacteria to the most dangerous form of UV radiation, and 80% of the bacteria survived while other bacteria, such as E. coli, would have been completely obliterated.

Each dot represents a gene while the color of each dot represents the level of activity

A DNA microarray (pictured above) was created to fully picture the response of Halobacteria to radiation. In response to radiation, a set of pre-created repair enzymes quickly began to repair the DNA, after which more repair enzymes were produced. This bacteria has several DNA repair mechanisms, some of which are similar to plant, animal, Archaeal, and other bacterial repair methods. 

Studies such as these can help researchers determine how DNA repair functions in humans and how it could possible by enhanced.

Tumor-Suppressor Protein Helps Keep Breast-Cancer Protein at Bay

In Chapter 14, we have been learning about mutation, DNA repair, cancer, and the possible interconnection of the three. One of our topics was tumor-suppressor proteins, which code for proteins that fix DNA damage and down-regulate cell division, acting as inhibitors. This article talks about a protein coded for by a tumor-suppressor protein called BRCA1. This protein by keep ovarian and breast cancer at bay be preventing the transcription of repetitive DNA segments. It has long been known that there is a connection between defective BRCA1 and breast and ovarian cancer.

Researchers have been attempting to discover how BRCA1 could play a role in ceasing the cancerous activities of cells. A study was conducted by a research group on mice that lack the BRCA1 gene. They found the expected defects with DNA repair and cell cycle regulation in association with a non-functioning BRCA1 gene. In addition, they found that these cells are scarce in heterochromatic centers, which are areas of compacted, untranscribed DNA located by a chromosome's centromere. Rather, these areas were highly active and produced "satellite repeats", which are many RNA transcripts. BRCA1 proteins in normal cells keep these areas untranscribed by tagging histones with ubiquitin. When this was artificially added, the cells were able to recover.

Therefore, it was determined that BRCA1 proteins prevent genomic instability. It still remains to be discovered why BRCA1 is so specific to breast and ovarian cancer. Further research has shown that satellite repeats can be found in many types of tumor tissues, and there are most likely several factors that contribute to the inability to maintain heterochromatin. Studies also have yet to determine why people with a defective BRCA1 gene are more likely to get cancer initially, while it now know why tumors develop after BRCA1 becomes defective.

Useful Materials for Chapter 13

I liked the video above because  it describes gene regulation in both prokaryotic and eukaryotic cells. The visual displays were highly beneficial to the understanding of the processes he speaks about. I particularly liked that the video references both the lac operon and the trp operon, both of which we discussed in class. The pictures were very clear, and helped me understand the topic better. Both negative and positive controls are discussed, and overall the video is thorough, clear, and concise. At only 10 minutes in length, it is certainly worth watching if anyone is having difficulty understanding some of the more general concepts regarding gene regulation.


Click here for a link to vocabulary words on prokaryotic gene regulation. It may help you remember some terms found in this chapter if you are a person who uses flashcards as a learning tool.


If you are having difficulty understanding the trp operon, which is perfectly understandable, click here to access a tutorial on the subject. It includes images, animations, and a quiz at the end to ensure that anyone can  benefit from using the tutorial. The animation is step-through as well as narrated, and may help you understand the topic if the book simply is not doing it for you.

The Role of Methylation in Gene Expression

There are several methods of controlling gene expression in eukaryotes, of which methylation is one. This is a tool in epigenetics that allows cells to "turn off" genes. Epigenetics is the control of genes by factors not related to an individual's DNA sequence. These types of tools determine what proteins are ultimately translated and function. Preserving chromosome stability, genomic imprinting, and embryonic development all involve DNA methylation, and errors in methylation have been linked to several serious human diseases. Early experiments with 5-azacytidine, which inhibits DNA methyltransferase enzymes, allowed scientists to investigate how DNA methylation impacts cell differentiation and gene expression.


DNA methyltransferase enzymes convert the cytosine bases of eukaryotic DNA to 5-methylcytosine. This cytosine is located next to a guanine nucleotide. DNA methylation's exact role in gene expression is currently unknown, although it is possible that it blocks promoters to which transcription factors would otherwise bind. Methylation of promoters has been linked to low or no transcription. There are differences in methylation levels in different tissue types as well as between normal and cancerous cells. 


Histone methylation patterns have been found to change dramatically through the cell cycle. Some studies have shown that DNA and histone methylation are connected, such as in studies that show DNA and histone  methylation working together to ensure that proper methylation patterns are passed on to daughter cells during translation. Sometimes, when DNA is methylated, deacetylation occurs in nearby histones. This allows for a stronger inhibition of transcription. Similarly, DNA that is not methylated does not attract deacetylation enzymes to nearby histone proteins. Methylation is generally a long-term process, but it can also allow for "epigenetic reprogramming".





Research is currently being conducted into the connection between methylation errors and diseases, including lupus, cancer, and muscular dystrophy. Tumor suppressor genes have been found to be silenced in cancer cells due to hypermethylation. Overall, methylation rates in cancer cells are much higher than in normal cells. In certain cancers, hypermethylation can be a marker for diagnosing cancer, as it may be detectable in early stages of the cancers.


Click here for the link to the article from which I retrieved my information. 

Octopi Respond to Environment Through RNA Editing

To start off with, the most commonly accepted plural form of the word "octopus" turns out to be "octopuses". "Octopi" and "octopedes" have also been used as plural forms, but they are more objectionable. In my blog, I will be referring to more than one octopus as octopi simply because I think it sounds better, no matter how objectionable the term may be. And also because I can.



Genetic mutations are responsible for the existence of complex creatures. The complexity of creatures can also be attributed to RNA editing, in which enzymes are altered without impacting organisms' genetic blueprints. RNA editing has allowed organisms to regulate essential functions, including the development and function of nervous systems. Octopi have provided evidence suggesting that this type of editing has allowed them to adjust to external, environmental changes in addition to internal changes. Researchers have investigated how this editing has allowed octopi to live in warm and cold bodies of water. These editing tools have helped them acclimate to different environments.


Cephalopods have been seen doing much RNA editing. Different processes can be fine-tuned in different organisms with the same genetic makeup. Since octopi are cold-blooded, temperature differences can have an impact on neural pathways. Nervous system communication is dependent on neural firings. These firings are started by sodium-ion channels and stopped by potassium-ion channels. Both of these channels slow down in cold temperatures, with the potassium-ion channels slowing significantly more than sodium-ion channels. RNA editing plays a role here, as one Antarctic octopus's editing locations allowed for an increase in the rate of the potassium channel closing. This allowed for the channels to become closer in rate. Other species of octopi, such as those living in Arctic and tropical waters, have also displayed RNA editing.


There is more than one response to the environment that requires RNA editing, and it certainly does not stop with temperature regulation. Scientists have discovered about 100 editing sites in just eight mRNAs. They are also editing the RNA that edits, allowing for greater diversity in enzymes that edit.


Click here to access the article from which I retrieved my information.