Chapter 21 Post

Buenos días! This chapter is all about genomes, proteomes, and bioinformatics! 


First of all, let's review/define exactly what these three things are:

• Genome - "the complete genetic composition of a cell or a species"
• Proteome - "the entire complement of proteins that a cell or organism can make"
• Bioinformatics - "a field of study that uses computers to study biological information"

My first useful material is this article from PubMed titled, "Genomics of bacteria and archaea: the emerging dynamic view of the prokaryotic world." As you can tell from the title, it is all about bacteria and archaea genomics. Did you know the first bacterial genome was sequenced in 1995? Did you know the first archaeal genome was sequenced in 1996? Okay, maybe you did, but I didn't! I was born in '95, meaning it was first sequenced the same year as me! 16 years is a considerably long time, but in scientific terms, 16 years is nothing! These are a perfect example of "recent" advances. The article goes on to describe how analysis of hundreds of genomes has enabled scientists to form generalizations on the principles of genome organization and evolution. It mentions the importance of HGT, which stands for horizontal gene transfer. HGT "is a dominant force of prokaryotic evolution." The abstract also describes the mobilome (yes, another "ome"). The mobilome is the total of all mobile genetic elements in a genome, and includes viruses and plasmids. These are all extremely important to HGT.

My next useful material are these videos below from YouTube. The source is MindBites.com, otherwise known as "the dude in the pink shirt." I have used these videos numerous times, and I think the man always explains things in a simple and easy to interpret way. The first video is all about eukaryotic genomes. Unlike prokaryotes, eukaryotic chromosomes typically have a great amount of short repetitive sequences called repetitive DNA sequences. Repetitive sequences can be divided into two categories, moderately repetitive sequences and highly repetitive sequences. Repetitive DNA composes 59% of the genome of humans. That's a lot! Why do eukaryotes have so many of these? The reason is that much of it is derived from transposable elements.

The video above talks about the Human Genome Project. The Human Genome Project was a research effort to identify and map all human genes. In began in 1990 and was mostly finished by 2003. One of the major findings of the project was that humans only have about 35,000 or so genes while fruit flies have 13,600 and round worms have 19,098 genes. People aren't really that "high up" the animal kingdom as we once thought. 

I found another useful material describing the Human Genome Project. This article talks about the Human Genome Project Results. One of the topics mentioned, which we've described in class, is how human beings only differ from one another about 0.1%. So out of our 3.2 billion base pairs of DNA, only 10 million or so are different. The differences in base pairs are called single nucleotide polymophisms. Much more research is needed in SNPs, but the Human Genome Project has given us a great start.

Chapter 20 Post

Hola! This chapter is all about genetic technology. 


One of the really interesting topics is reproductive cloning. Reproductive cloning is defined as "the cloning of a multicellular organism." One of the most famous cloned animals was Dolly. Dolly was a lamb, the first cloned lamb. How did they create Dolly? The video below explains it in a quick, simple, yet informative manner. The first step is extracting the donor sheep's mammary cell and growing it in a tissue culture flask. Then, you have to extract another sheep's unfertilized egg and remove its nucleus. Next, the cells are fused together with electric pulses. The maternal proteins in the egg and the donor nucleus from the mammary cell initiate the development of the egg into an embryo. The embryo is then transferred into a surrogate sheep and pregnancy continues as normal. Then...bam! A lamb is born! It is genetically identical to the donor sheep. Cool, right? Unfortunately, I don't think we'll get to clone sheep in lab, but it's still interesting to learn about it. 

These guys are on the weird side and kind of wacky but they have all the right information. At least it's interesting!


Another really cool topic from this chapter was DNA fingerprinting. The video below shops how DNA fingerprinting works in forensic science. The process described in the video involves gel electrophoresis. Hmm? Wonder what that is? Just kidding! Haha hopefully by now you know this process. PCR should ring a bell too. DNA fingerprinting is done using PCR, amplifying short tandem repeat sequences (STRs). They are short DNA sequences that are repeated many times in a row. DNA appears as a series of bands on a gel. The similarities and differences of the bands show whether the DNA is the same or not. If your sample bands match one of your control bands, you know the DNA is from the same person. Science has contributed extremely to criminal justice!

The not as cool type of cloning is gene cloning. This interactive activity explains the process of gene cloning and allows you to make a clone! It explains plasmids, restriction sites, restriction enzymes, and much more! The animations are really good and I thought the activity was really informative. Have fun with gene cloning! If the above link doesn't work, go to this site and click on "view."

Chapter 18 Post

Hello! This chapter is all about the genetics of viruses and bacteria.


First of all, what are viruses? The textbook defines a virus as "a small infectious particle that consists of nucleic acid enclosed in a protein coat." What makes them interesting is that they are non-living, but still have a genome. They are considered non-living because they don't exhibit all seven properties associated with living organisms. Let's review the seven properties:

• Cells and organization - all organisms have an internal order, the simplest unit of organization being the cell
• Energy use and metabolism - all organisms need energy to sustain internal order and metabolism is collectively known as energy used in chemical reactions
• Response to environmental changes - all organisms respond to the environment to aid their survival
• Regulation and homeostasis - all organisms regulate their bodies and exhibit homeostasis, which is maintaining stable internal conditions
• Growth and development - all organisms increase size and/or number of cells and produce a defined set of characteristics
• Reproduction - all organisms must reproduce to sustain life over many generations, and offspring tend to have similar traits to their parents
• Biological evolution - populations of all organisms change over many generations, and evolution is important to promote traits that aid in survival and reproduction

Viruses are not living things for multiple reasons. First of all, viruses are not composed of cells. In addition, viruses cannot solely carry out metabolism, use energy, maintain homeostasis or reproduce. In order for a virus to "reproduce" or replicate, it must be taken up by a living cell.


However, viruses cannot just come along and infect any cell it'd like. It can only infect a cell or species in it's host range. For example, tobacco mosaic virus (TMV) can infect over 150 different species of plants. TMV is considered to have a broad host range. In contrast, some viruses can only infect a single species. Some are even more specific and can infect only a specific cell type in a species!


What's the structure of a virus, you ask? They're about 20 to 400 nanometers in diameter. That's considered relatively small, because most bacterium are 1,000 nanometers in diameter. All viruses have a protein coat called a capsid that encompasses a genome that consists of one or more molecules of nucleic acid. They're composed of protein subunits called capsomers. There are a bunch of shapes capsids can be, including helical and polyhedral. The structure of the tobacco mosaic virus (TMV) is helical, as shown below.

The structure of a virus with a helical capsid.

An additional capsid shape I mentioned was polyhedral and below is what that looks like.

The structure of a virus with a polyhedral capsid.

If you look at the virus with a polyhedral capsid (above), you can see a labeled structure called an envelope. Many viruses that infect animal cells have viral envelopes that enclose the capsid. It is comprised of a lipid bilayer that is derived from the host cell's plasma membrane and is embedded with virally encoded spike glycomers.


Spike glycomers aren't there for decoration, they help viruses bind to the surface of a host cell. Bacteriophages (viruses that infect bacteria) tend to have complex protein coats and accessory structures used for anchoring the virus onto a host cell and inserting the viral nucleic acid.


The genetic material of a virus is called a viral genome. Some viruses have nucleic acid of DNA and others have RNA. The genome can be linear or circular, depending on the virus. Some viruses have multiple copies of the genome. Genome sizes vary greatly, from a few thousand nucleotides to over a hundred thousand nucleotides in length. The extra nucleotides encode for extra genes, which in turn encrypt for many proteins involved in virus structure. 


Viruses are a great example of structure = function. Every component and detail of a virus has a specific function.


Although viruses aren't living organisms, they exhibit a "viral reproductive cycle" which is the expression of viral genes over a series of steps that result in the production of new viruses. Scientists have determined there to be five/six general steps to the viral life cycle, although each virus is unique and the steps vary among different types of viruses.


The video below describes HIV virus infection and replication. HIV stands for human immunodeficiency virus and is the virus that caused AIDS in humans. There were many videos of HIV replication on YouTube, but I found the one below to be the best.

The video talks about all of the stages of the HIV viral life cycle. These include attachment, entry, integration, synthesis, viral assembly and release. The first step is infecting a suitable host cell. There needs to be certain receptors on the cell surface for HIV to enter the host cell. The receptors interact with protein complexes in the viral envelope. Then the video shows a cool animation of entry which is difficult to describe, but you'll see it. 


In addition, the video talks about all of the key enzymes used in the process, including reverse transcriptase. Reverse transcriptase looks really complex and cool in the video! But the most awesome is integrase! It cleaves a dinucleotide from each 3' end of the DNA, creating two "sticky ends." It then transfers the DNA into the cell nucleus, integrating it. The genome the has HIV's genetic information. It looks really cool in the video! The video goes on to describe the other steps leading up to the virus exiting the cell. Also, the video talks about the effect of drugs on the HIV virus (on a molecular level). I don't know why, but I thought the sound of the inhibitors were really cool, kind of like a drum. This was an overall very helpful video because of the good information and great visuals.


Another virus that the book (and I) have mentioned is the tobacco mosaic virus, abbreviated TMV. This article from Scientific American is titled, "Tobacco Plant Transformed into Plague Vaccine Factory." TMV was the first virus to be discovered. It infects plant species and causes "mosaic-like patterns in which normal-colored patches are interspersed with light green or yellowish patches on the leaves." Tobacco mosaic virus almost never kills the plant it infects but does damage leaves, flowers, and fruit.

A plant infected with tobacco mosaic virus (TMV).

The article describes how the tobacco plant and TMV knowledge has helped scientists make vaccines. The "plague" or "black death" of the Middle Ages was one of the worst diseases in human history. To prevent any such catastrophe from occuring again, researchers used tobacco plants to make plague vaccines. Charles Arntzen and others at Arizona State University injected tobacco plants with TMV to make plague antigens. They're proteins known as F1, V and a combination of the two. The three "modified viruses" penetrated the plants and produced antigens. Arntzen and his colleagues had "a full crop of tobacco leaves filled with vaccine" in only 10 days! 


They then tested the vaccines on guinea pigs exposed to Yersinia pestis, the bacteria responsible for airborne plague. All of the guinea pigs not vaccinated died within a week, but 60% of the vaccinated guinea pigs survived (the ones who died lived longer than a week)! The V antigen was concluded to be the best because 75% of V antigen vaccinated guinea pigs survived. This vaccine could be imperative to human survival if the plague were to ever resurface.


All we've been talking about are viruses so far, but don't think I've forgotten about bacteria!


One of the topics we've discussed in class is horizontal gene transfer, something bacteria can do, but humans can't. This article from PubMed is titled, "Adaptive horizontal transfer of a bacteria gene to an invasive insect pest of coffee." Horizontal gene transfer is defined by the book as, "a process in which an organism incorporates genetic material from another organism without being the offspring of that organism. Horizontal gene transfer among animals is very rare, but possible. The HhMAN1 gene from the coffee berry borer beetle expresses horizontal gene transfer. The beetle is a pest that destroys coffee beans. HhMAN1 encrypts a mannanase (any enzyme that catalyzes the hydrolysis of mannans), "representing a class of glycosyl hydrolases that has not previously been reported in insects." So how did they get there? HhMAN1 horizontal gene transfer probably is because of intensive agricultural practices. This is validated by the fact that closely related species don't colonize coffee beans.

An illustration of Hypothenemus hampei (the coffee berry borer beetle). I would have uploaded a real picture, but trust me, they are disgusting looking! 

That's all for my chapter 18 post! Sorry for it being kind of on the long side.

Chapter 16 Post

Hola! This chapter is all about simple patterns of inheritance. We all know about Gregor Mendel (aka the father of genetics) and his basic pea plant experiments, so I won't waste any time talking about that.


I found the section about sex determination pretty interesting. Humans have either two X chromosomes (if you're female) or one X and one Y chromosome (if you're male). But this isn't the case for all animals! How and why are sex chromosomes different? This article does a great job of explaining everything. Hermann Henking first studied wasp sperm cells in 1891. He observed that some cells had 12 chromosomes and other had only 11. He also noticed that the 12th chromosome acted different than the other 11. Puzzled, Henking called the 12th chromosome the "X element" because of its "unknown nature." 


Henking found that the "X element" couldn't be found in female grasshoppers and hypothesized that the "X element" must help determine the sex of insects. Over ten years later, Nettie Stevens studied numerous beetle species and their inheritance patterns. She also hypothesized that chromosomes had something to do with sex.


Besides the XX-XY system that we have, there are also the XX-XO and ZZ-ZW systems! 


XX-XO system

• Found in insects such as crickets and grasshoppers
• Females carry two X chromosomes (XX) and produce gametes with X chromosomes
• Males carry only one X chromosome (XO) and produce some gametes with X chromosomes, some gametes without sex chromosomes
• The number of X chromosomes determines maleness

ZZ-ZW system

• Found in birds, snakes and some insects
• Females carry the mismatched chromosome pair (ZW) 
• Males carry the identical pair (ZZ)
• Similar to humans' XX-XY system, except that females have the mismatched pair

The picture above shows the Punnett Squares of different sex determination patterns

Another topic in this chapter I found interesting were sex linked genes. The X chromosome of humans is a lot bigger than the Y chromosome. The X chromosome carries over 1000 genes while the Y chromosome carries less than 100 genes. That's a huge difference! It helps to explain why many genes are found on the X chromosome but not on the Y. These genes are called X-linked genes. The book mentioned Morgan's crosses of Drosophila melogaster and I decided to go on PubMed to research this more in-depth. This article describes how eye color mutants contribute to our knowledge of enzymatic pathways and vesicular transport. It also mentions the studies of mutations aiding organogenesis. In case you didn't know, organogenesis is the development and production of the organs of a plant or animal.

The eye (particularly of the Drosophila melanogaster) has one of the greatest experimental fields and phenotypes. The fly eye is comprised of unit-eyes called ommatidia. I looked it up, and each omnatidium has photoreceptor cells, in addition to support cells and pigment cells. Omnatidium structure is very complex, and any minor mutations will physically appear on the ommatidium. Studying eye mutants helps scientists to further understand signal transduction, cell polarity and programmed cell death.  Drosophila melanogaster is a great experimental system because of its multiple identifying genes.

One section of the chapter that I had to spend a little extra time studying was pedigree analysis. Pedigree analysis involves looking at a pedigree for a specific trait and analyzing it for multiple generations of a family. It takes some time and practice to understand a pedigree, but once you understand a few concepts, everything is a piece of cake!

The video above gives some great pedigree analysis practice. And if you look in the bottom corner, something may look familiar. Screencast-O-Matic! Haha I guess other people do use it. The lady in this video takes you step-by-step at looking at different pedigrees. What was great about this video is it starts really basic, and doesn't show a giant confusing pedigree. It only shows small pedigree sections, so you won't get confused. It also talks about the difference between autosomal and sex-linked traits on a pedigree. While doing the ConnectPlus homework, I had to determine the types of traits shown on different pedigrees. After reading the book, I wasn't sure which was which. But after watching this video, I understood the concept. It is a little on the long side, but it's a good quality video. Even if you understand pedigrees well, I would still recommend watching it because it's wonderful practice.

That's all for this chapter's post! 

Chapter 15 Post

Hello! Mysterious person, I'm Emily. Oh wait, you already knew that, silly me. Welcome to my blog, if you've never seen it before. It's called, "Em Fu The Science Guru!" Get it, like Bill Nye the Science Guy? I know what you're thinking, I'm a loser. But the truth is, I was trying to be creative, and at the time, it seemed like a catchy name. To be honest, I still really like it, no matter what anyone else says. After you read my blog post, you can check out my fishy (you can feed them!), or my scientific links, or my favorite scientific quote, if you'd like. But that's optional, you can if you have free time. So I think that's enough of an introduction to my blog. Now I will actually begin with the biology.


This article talks about two adults, uncle and niece, who have partial trisomy 8 and partial monosomy 21. This is due to a familial balanced translocation on their 8 and 21 chromosomes. A translocation is when one segment of a chromosome becomes attached to a different chromosome. There's two types of translocations:

• Simple translocation - when only one segment of a chromosome moves to a different one)
• Reciprocal translocation - two different chromosomes exchange pieces

Fluorescence in situ hybridisation (aka FISH) was used to specifically see the chromosomal breakpoints in a more accurate manner. The first patient reviewed (the uncle) had mild mental retardation and facial dysmophism, while the niece's symptoms were much more severe. She had severe epilepsy, however, she did not have the facial dysmorphism. Why? When the data was compared to other trisomy 8 cases, it was found that the phenotype of partial trisomy 8p was a lot more "variable." This means that the phenotypes are unpredictable, explaining why the uncle and niece had different symptoms. It's very unfortunate that translocations for these individuals caused mental retardation. 

This video talks all about mitosis, meiosis and sexual reproduction. It's from KhanAcademy, one of my favorite resources. Their videos are always really helpful. We all know about how a zygote is formed, all that basic stuff. One thing that I really loved was how he explained how zygotes actually become people. Most textbooks don't really go into that, so I found this really helpful. In addition, the speaker explained the basics of mitosis/meiosis in a very clear manner. He also talked about the topic of differentiation, which is how a zygote becomes a complex system of cells that make up our body! 


Genetic mutations are also explained by the speaker. Mutations seem really complicated, and don't get me wrong, they are! However, he talks about mutations in a way that makes everything seem so simple. I was so incredibly impressed by this video that I watched two more, linked below.


All About Mitosis
All About Meiosis

My next useful material is this animation that talks about the cell cycle. I liked all the useful facts it gave. Did you know it takes 10 hours to replicate all of the nuclear DNA in your body? I didn't know that. And one thing that was really cool was the apoptosis animation. The author, Barbara did a great job explaining everything. After the G1 phase, one of the identical daughter cells exits the cell cycle to become a specialized cell, and the other stays in the bone marrow (hello stem cell!) to go through the cell cycle again.


I also loved the simplicity of this animation. It isn't incredibly long, but you will get a lot of "aha" moments.

Chapter 14 Post

Hello! Mysterious person, I'm Emily. Oh wait, you already knew that, silly me. Welcome to my blog, if you've never seen it before. It's called, "Em Fu The Science Guru!" Get it, like Bill Nye the Science Guy? I know what you're thinking, I'm a loser. But the truth is, I was trying to be creative, and at the time, it seemed like a catchy name. To be honest, I still really like it, no matter what anyone else says. After you read my blog post, you can check out my fishy (you can feed them!), or my scientific links, or my favorite scientific quote, if you'd like. But that's optional, you can if you have free time. So I think that's enough of an introduction to my blog. Now I will actually begin with the biology, sigh. I'll try to make this as entertaining as I can for you.

So the title to this chapter is "Mutation, DNA Repair, and Cancer." Not too many know this, but I'm fascinated by cancer, and might even pursue oncology one day. Also, I love blood! No, not in a creepy vampire kind of way, but in a biological way. Learning about blood was one of my favorite parts of A&P, I found it really cool. Hematology and oncology are closely related, most doctors who pursue one of these specialities end up specializing in both. It's kind of like the relationship between Gynecology and Obstetrics. Most of the doctors in this field are OBGYNs. I would love to study hematology further, but most likely this would also involve going into oncology. Luckily, I have a great interest in oncology, and actually enjoyed this chapter.

Heading back to biology, the first section was all about mutations. Mutations are often associated with cancer, and are often seen as bad. However, mutations are a natural part of life, and contribute to evolution. So they can be good, and are actually necessary for a species to survive. There are a few different types of mutations, all causing different effects of polypeptides. It's super easy to get them confused, but I found Table 14.1 in the book to be really helpful. I'd suggest checking it out for quick review before an exam. Just so you know, this isn't one of my official useful materials. I just wanted to mention it, so you could check it out if you hadn't before.

The mutation type that fascinated me the most were frameshift mutations. They produce a completely different amino acid sequence because the reading frame is shifted over, changing the entire sequence downstream. When reading the book, I literally said, "whoa!," aloud. It's amazing how one addition/deletion of a single base can do so much. I decided to look into frameshift mutations as one of my useful materials. This article is titled, "Immunogenic peptides generated by frameshift mutations in DNA mismatch repair-deficient cancer cells." The authors wrote it in a very clear manner, unlike some PubMed articles that are impossible to comprehend. I'm sure you know what I'm talking about. The article states that the loss of DNA mismatch repair functions contribute to approximately 15% of human tumors. In cancer cells, there's an insertion or deletion at microsatellites. Microsatellites are repeating sequences of base pairs of DNA. Any mutations in coding microsatellites can be very bad, because genes can lose their function! Oh no! Frameshift mutations like these have been found recently. The authors found a "broad but comprehensive set of frameshift peptides that might be combined in a multivalent vaccine for MSI+ cancers." MSI stands for microsatellite instability, in case you were wondering. They identified and examined mutations in different genes, and found mutations that seemed similar to those found in cancer. Their research hopefully has brought us closer to finding a vaccine to MSI cancers. MSI cancers seem really interesting, and they connect frameshift mutations back to real-life. This article proved that frameshift mutations are incredibly dangerous and make a big difference.

After learning all about the consequences of mutations, I realized how vital DNA repair was! DNA repair allows us to live our lives by minimizing the occurence of mutations. One type of DNA repair is nucleotide excision repair (NER). I didn't understand it at first because the book's definition was a long run on sentence. After reading it a few times I understood it, but couldn't exactly picture it in my head. So I looked it up and found this diagram that does a pretty good job of illustrating all of the information. The book also had a diagram (showing NER in E. coli), but I understood this one a lot better. The illustrations could be better, but the point got across well. First, the damaged DNA gets distorted. Then, an enzyme complex finds the distortion and separate the DNA. Single-stranded binding proteins help to stabilize the strands and both sides are cleaved by an enzyme. Lastly, the damaged part is taken away and the empty space is filled by DNAP and sealed by DNA ligase. This diagram helped me realize that NER is actually quite simple after all!


The last section of the book was all about cancer! One topic I found quite interesting were types of cancer caused by viruses. The book specifically talked about the Rous sarcoma virus (RSV), and I decided to look more into it. This article gave a detailed description of RSV. RSV was the first virus shown to be able to cause cancer, called an oncogenic virus. A tumor from this virus is called a sarcoma, which is a connective tissue tumor. It's considered to be a retrovirus, it's genes are encoded in RNA instead of DNA, like HIV. RSV has four genes: gag encodes the capsid protein, pol encodes the reverse transcriptase protein, env encodes the envelope protein, and src which encodes a tyrosine kinase. Src is what makes RSV oncogenic, although it is not understood very well. As the article states, "the expression of this gene in some way...is able to transform cells in culture." A study was conducted on cells infected with RSV and it was found that they are temperature-sensitive, meaning that temperature changes can activate or denature the encoded protein, reversibly. In addition to it being a viral gene, it is also a proto-oncogene, called c-src. This is found in vertebrates and invertebrates, including humans! Ours in on chromosome 20, by the way. C-src has probably not changed much since the start of evolution because of how widely its found. Fortunately, Peyton Rous, the man who discovered RSV was awarded a nobel prize for his work, at the age of 87.


Thanks so much for reading by blog! I apologize for the length, but I hope you enjoyed reading it! 

Chapter 13 Post

Hello everyone! Long time no blog! This week's chapter is titled Gene Regulation. It focuses on regulation of transcription in bacteria, regulation of transcription in eukaryotes, and regulation of RNA processing and translation in eukaryotes.


This article from PubMed is about lac operon induction in Escherichia coli, a systematic comparison of IPTG and TMG induction and influence of the transacetylase LacA. The most frequently used expression systems in bacteria are based on the Escherichia coli lac promoter. Moreover, lac operon elements are used today in systems and synthetic biology. In a handful of cases the inducers IPTG or TMG are used. Here the author reported a comparison of lac promoter induction by TMG and IPTG which focuses on the aspects inducer uptake, population heterogeneity and a potential influence of the transacetylase, LacA. They provided induction curves in E. coli LJ110 and in isogenic lacY and lacA mutant strains and they showed that both inducers are substrates of the lactose permease at low inducer concentrations but can also enter cells independently of lactose permease if present at higher concentrations. Using a gfp reporter strain they compared TMG and IPTG induction at a single cell level and showed that bimodal induction with IPTG occurred at approximately ten-fold lower concentrations than with TMG. In addition, they observed that lac operon induction is influenced by the transacetylase, LacA. By comparing two Plac-gfp reporter strains with and without a lacA deletion they could show that in the lacA(+) strain the fluorescence level decreased after few hours while the fluorescence further increased in the lacA(-) strain. The results showed that through the activity of LacA the IPTG concentration can be reduced below an inducing threshold concentration, an influence that should be considered if low inducer amounts are used.


This article, titled, Clock Genes Might Control the Sleep We Need, focuses on Clock genes, which are long known to regulate our circadian rhythms, and also give clues to what makes sleep so persistent. Sleep is the one thing we can’t cheat. We lose it in our busy lives but yet our brains, surprisingly keep score – and force payback as soon as we lie down. And if it’s big, we sleep in, sometimes missing important activities. A clue has emerged from new research published in BioMed Central Neuroscience. Researchers have found that the expression of genes called “clock genes” are highly correlated with the need for sleep. It’s shown that clock genes regulate our 24-hour circadian rhythm – but researchers say these genes also appear to control the persistence of sleep. Researchers studied some mice that need a lot of sleep and those who need little sleep. They found that for mice the expression of clock genes increased the longer an animal stayed awake, and decreased when the animal was in recovery sleep.

The video above talks about the lac operon. It's a good animation about the process. As I was researching videos on YouTube, I was questioning the validity and trustworthiness of some videos. I ended choosing this one partly because it came from a textbook. Also, the animations are good and the information is detailed and clear. I like that the text is displayed at the side because reading information, in addition to hearing it, helps me learn better. I would suggest watching this video.

Chapter 12 Post

Hello! This chapter is all about gene expression at the molecular level. One of the major focuses of this chapter is transcription and translation. The following video helped me out a lot by explaining these processes in a clear and concise manner. It's very easy to get transcription and translation confused, and the video does a great job comparing and contrasting the two. He also used a smart pad with a powerpoint presentation, kind of like Dr. Weber, so I found that cool. The guy also uses some outside animations that were quite helpful. I would suggest watching the video for a quick refresh of transcription and translation.

Another focus of the chapter was The Genetic Code. I found this topic very interesting and decided to look it up. All I found was pretty much what the book said, it's history and boring stuff. But then I found this article that had the word "new" in it, so it sounded interesting. I always like to read about advancements to things. This article from PubMed talks about adding new chemistries to the genetic code. The advancement of new orthogonal aminoacyl-tRNA synthetase/tRNA pairs has lead to the addition of about 70 unnatural amino acids (UAAs) to the genetic codes of Escherichia coli, yeast, and mammalian cells. These UAAs signify a range of structures and function not found in the canonical 20 amino acids and thus provide new chances to generate proteins with enhanced or novel properties and probes of protein function and structure.

An additional topic of the chapter was RNA splicing. The following video talks about the process of removing introns after RNA transcription. It's less than 2 minutes long, but still manages to provide important details. The visuals, which look rather old, are actually good with the explanation. The lady has a very pleasant and clear voice, compared to the monotone male voice we usually hear in most animation. I would suggest watching the video because it's really worth the 1:39 you have to put in.

That's my last post for this semester! Have an amazing winter break, everyone!

Chapter 11 Post

So this chapter is all about nucleic acid structure, DNA replication and chromosome structure. I was delighted when I found out we were moving on to a new unit of the book, genetics! Prior to this year I hadn't really been exposed to genetics too much in depth, so I was excited to explore this topic. 

My first useful material is this game from the official site of the Nobel Prize, Nobelprize.org. And did I mention it’s a game?! Oh wait- I did. If you like animations and visual learning, I would suggest trying out the game. It lets you first make copies of a double-stranded DNA molecule by matching base pairs to each strand. When you’re done, you have to read about different organisms and determine which organism the DNA belongs to. But be careful! If you match incorrectly or determine the wrong organism, you’ll lose a ton of points. 

A screenshot from the game.

This game was a great break from usual learning out of a text book. Interactivity is my most successful way of learning, so I actually did learn a lot from this game. It was also fun too, so that was an added bonus. If you have some free time I’d recommend playing this game.

Next I found this video that explains telomere replication. When reading the book I understood the structure and function of telomeres, but I didn’t exactly get the replication process. This video does a good job explaining the entire process and integrating exactly what telomerase does. The book had very nicely drawn visuals, which I’ll credit it for, but seeing this as an animation made this seem much simpler and easier. I liked how the nucleotides were all colored to show which regions were the genes and which regions were the telomeres. In addition, this video is from a biology textbook, it’s not just some random video. It’s only two minutes long, and it pretty much summarizes what the book says in 6 long paragraphs.



Being on the topic of telomeres, I decided to read more about it online and stumbled across this PubMed article. The article talks about telomere length in cardiovascular disease and how telomeres play a role in aging. Atherosclerosis is an age-related disease that involves different types of leukocytes. Telomere dysfunction has been connected in aging and senescence. Shorter leukocyte telomere length (LTL) has been verified to predict cardiovascular disease and mortality. The article overviews telomere biology and telomere dynamics of different leukocyte populations. In addition, the article talks about pitfalls in the methodology of LTL quantification and how telomere length can be implemented as an individual biomarker for cardiovascular aging. It’s actually really interesting how big of a role telomeres play in our lives.

Chapter 9 Post

This chapter focuses on cell communication. Cell communication is defined as the process through which cells can detect and respond to signals in their environment. Cell communication is vital to our survival and involves an extraordinary diversity of signaling molecules and cellular proteins that are devoted to this process.


I actually find cell communication very interesting. This video shows an animation of cell communication. It was very well made and its explained very clearly. The major concept of cell communication is shown in a way that relates what we're learning to real life. Without cell communication, we wouldn't be here. Every bodily function relies on a myriad of signals from cell communication.

Apoptosis is programmed cell death. This article talks about leptin-deficient mice that are obese and infertile. The author believed dysfunctions of the ovaries were related to leptin-deficiency. Different mice with homozygote, heterozygote, or wild-type were obtained for analysis. The results were that compared with control ovaries with corpora lutea, ob/ob ovaries lacked corpora lutea, follicular atresia was at a higher rate; lipid droplets accumulated in follicle cells and in the oocyte with damaged mitochondria; the basement membrane of follicles was thickened. LOX-1 and CD36 expressions were comparable for all three groups. Ob/ob ovaries showed significantly higher levels of TLR4 and cleaved caspase-3 than the ones from the control groups. The high LC3-II/I ratio in the WT and ob/+ ovaries was related to the presence of corpora lutea. The StAR protein was lower in the ob/ob ovaries signifying reduced steroidogenesis. The conclusions were excessive lipid storage causes disorders of ovarian function in ob/ob mice. The local lipid overload leads to advanced follicular atresia with apoptosis and defect steroidogenesis. They suggest that the changes in lipid metabolism lead to increased oxidative stress and thereby, they are an important reason of anovulation and infertility.

This video shows signal transduction. It does a pretty good job of explaining everything and how its works. It gets relatively into detail without over analyzing signal transduction. It was sweet, simple, and got to the point.

 

Chapter 7 Post

This chapter covers cellular respiration and fermentation. Cellular respiration is a process by which living cells obtain energy from organic molecules and release waste products. Fermentation is the breakdown of organic molecules to harness energy without any net oxidation (that is, without any removal of electrons). 

One of the major focuses of this chapter is glycolysis. In glycolysis, glucose (a six carbon atom compound) is broken down to two pyruvate molecules (with three carbons each), producing a net gain of two ATP molecules and two NADH molecules. The two ATP are made by substrate-level phosphorylation, which happens when an enzyme directly transfers a phosphate from an organic molecule to ADP. Glycolysis occurs in the cytosol in eukaryotes. Initially, I found glycolysis a bit confusing. The ten steps can be overwhelming, but once I grasped the concept, it wasn't so bad. This animation explains all of the steps of glycolysis in a clear and concise manner. I found it much easier to learn glycolysis through animations than through pictures. Instead of just displaying the before and after, the animation demonstrated the process. The animation showed the structure changes and exactly what the enzymes did. I finally understood the isomerization of step 5 after watching the animation. The book didn't make it clear that fructose-1,6-biphosphate was split into dehydroxyacetone phosphate and glyceraldehyde-3-phosphate AND THEN dehydroxyacetone phosphate was isomerized (restructured) by isomerase (what a perfect name!) to make another molecule of glyceraldehyde-3-phosphate. I would suggest watching the animation for review on glycolysis.


The next step concerning the breakdown of glucose is the breakdown of pyruvate to an acetyl group. The two pyruvate molecules (from glycolysis) enter the mitochondrial matrix, where each one is broken down to an acetyl group (with two carbons each) and one CO2 molecule. One NADH molecule is made by the reduction of NAD+ for each pyruvate broken down via oxidation. I found this concept generally basic.

Subsequently comes the citric acid cycle! During the citric acid cycle (or the Krebs cycle), each acetyl group is incorporated into an organic molecule, which is later oxidized to liberate two CO2 molecules. One ATP, three NADH and one FADH2 are made in this process. Because there are two acetyl groups, the total yield is four CO2, two ATP via substrate-level phosphorylation, six NADH and two FADH2. This process occurs in the mitochondrial matrix. So not to bore you all with animations, but I found this animation helpful because it uses a ferris wheel analogy and it's interactive! As you can tell from my recent posts, I love interactive animations. But in this one, it actually makes you put the molecules in the correct order in the cycle. And if you get them wrong (I did my first try) it'll make you review and retry, so it's a good learning tool. Also, you get pop-up questions as well to make sure you understand everything.


Finally comes oxidative phosphorylation! Here, the NADH and FADH2 made in the three previous steps contain high-energy electrons that can be readily transferred in a redox reaction to other molecules. Once removed from NADH or FADH2 via oxidation, these electrons release some energy, and that energy is harnessed to produce a H+ electrochemical gradient. In the process of chemiosmosis, energy stored in the H+ electrochemical gradient is used to synthesize ATP from ADP and Pi. This process is called phosphorylation because ADP has become phosphorylated. About 30 to 34 ATP molecules are made via chemiosmosis. Oxidative phosphorylation is accomplished by two components: the electron transport chain and ATP synthase. I found this article from PubMed. It describes how muscle mitochondrial oxidative phosphorylation activity is altered with abdominal obesity in sedentary men. Abdominal obesity is a great risk factor for muscle insulin resistance. In the experiment, changes in muscle mitochondrial content and function were examined according to abdominal obesity and insulin sensitivity in men. The study was conducted on the general population of Clermont-Ferrand, France. The participants were forty-two healthy sedentary men between the ages of 37 and 45 years old. They were split into four groups according to waist circumference. Group 1's measurements were 87 cm or less, group 2 was between 88 and 93 cm, group 3 measured 94 to 101 cm and group 4's circumferences were 102 cm and greater. A plasma metabolic check-up was performed and insulin sensitivity index was calculated. In addition, muscle biopsies were obtained to assess mitochondrial content, oxidative phosphorylation activity and superoxide anion (reactive oxygen species) production. The results were that abdominal obesity was negatively correlated to the insulin sensitivity index and only group 4 was insulin-resistant. There weren't any between-group differences in muscle mitochondrial content and maximal activity of key oxidative enzymes. However, the muscle mitochondrial ADP-stimulated respiration rate was 24% higher in groups 2 and 3 compared to groups 1 and 4. Mitochondrial ATP and reactive oxygen species production rates were 27 and 48% lower in group 4 than in group 1. What does all of this mean? It means abdominal obesity is associated with alteration in intrinsic muscle mitochondrial function but not content. These adaptations mainly result in the reduced mitochondrial ATP production rate in response to insulin resistance. I liked how the article related what we are learning to a real life example. Most studies from PubMed are quite intricate and confusing, but I actually fully understood this one. That's an accomplishment for me.

So this concludes my chapter 7 post. Best of luck to everyone on the exam!

Chapter 6 Post

AKP-Vm, a Novel Alkaline Serine Protease


This article from PubMed is about an extracellular alkaline serine protease. It was secreted by Vibrio Metschnikovii (V. metschnikovii) ATCC700040 cells and was refined by 3 chromatographic steps to be characterized in terms of enzymatic kinetics and substrate specificity. 


AKP-Vm, the purified enzyme was comprised of a single polypeptide with a molecular weight of 50 kDa on 12% SDS-polyacrylamide gel in the presence of CuCl2. The optimal temperature for the enzyme was found to be 37 degrees Celsius and the optimal pH was 9.5. But the enzyme activity was inhibited by inhibitors such as aprotinin and PMSF. AKP-Vm was able to hydrolyze a peptide bond at the carboxyl end of the arginine residue, as shown by its amidolytic activity toward a chromogenic substrate, Boc-Val-Pro-Arg-pNa. The kinetic limits of the enzyme were: KM=0.91mM, kcat=0.8 sec-1 and kcat/KM=0.88 mM-1sec-1. 


AKP-Vm protease was able to cleave numerous blood coagulation-association proteins, including fibrinogen, prothrombin and thrombin. Specifically, the enzyme displayed powerful fibrinogenolytic and fibrinolytic activities, as it was able to cleave all major chains of fibrinogen and digest cross-linked fibrin. The results propose that AKP-Vm is a novel alkaline serine protease that can actively cleave fibrinogen and cross-linked fibrin.


Catalysis


I found this useful interactive animation. It shows about how reactions are driven by energy, and how enzymes act as catalysts to increase the rates at which reactions take place. It uses the ball rolling down the hill example in addition to other real-world examples. Also, it lets you add an enzyme and see the effects of it.  The animation even tests you with pop-up questions along the way to see if you're paying attention! But don't worry if you get any wrong; the animation will give you the right answers and explain why they are right.


Entropy and The 2nd Law of Thermodynamics

This video is very interesting, to say the least. It discusses entropy and the second law of thermodynamics. Everything seems to be more interesting as a song, even entropy! The lyrics go really fast, so I would suggest reading them in the info bar of the video. I like how it relates entropy and the second law of thermodynamics to real life examples. And it also does a good job of defining and explaining what entropy really is. In addition, the video mentions the scientists who contributed to our knowledge of this subject. It never hurts to learn some history. Watching this video taught me about entropy and the second law, plus it made me laugh. I think learning is most effective when it's entertaining, so hopefully everyone else can get some enjoyment while learning!

Chapter 5 Post

Glycosylation

Glycosylation is defined as "the enzyme-catalyzed covalent attachment of a carbohydrate to a polypeptide, lipid, polynucleotide, carbohydrate, or other organic compound, generally catalyzed by glycosyltransferases, utilizing specific sugar nucleotide donor substrates."

This article talks about how glycosylation relates to cancer. Specific glycan structures are common markers for tumor progression, and altered glycosylation is "a universal feature of cancer cells."

There are many forms of glycan changes in malignant cells. Examples include loss of expression, excessive expression of certain structures, persistence of incomplete structures, accumulation of precursors, and the appearance of novel structures. Of all possible glycan biosynthetic changes, only a few are commonly correlated with malignant transformation and tumor progression. Because cancer is a microevolutionary process, that only allows the fittest cells in a population to survive, the article proposes that "these specific glycan changes are selected for during tumor progression." The author later describes the most frequent changes, considering the likely biosynthetic mechanisms and the feasible biological consequences.

Proteins are generally encoded by a single gene. Unlike proteins, a glycan determinant is made by the collaborative action of several related genes. This makes it difficult to explain in detail the genetic regulatory mechanism for expression of some cell-surface glycans.

There has been an increase of knowledge on the transcriptional background of cancer-associated glycan alteration from the availability of the human genome sequence, application of DNA microarray, and other molecular biological techniques to glycosyltransferases and related genes.

Various examples have demonstrated a direct association between glycan alteration and the genetic mechanism for malignant transformation of cells. One example is transcriptional induction of MGAT5 (the gene for GlcNAc transferase-V) by v-src, H-ras, and v-fps. An additional example is enhanced expression of sialyl Lewis on adult T-cell leukemia cells. They're known to have very strong tissue infiltrative activity, likely settled by selectins. The transcription activator protein, Tax, binds to the 5' regulatory region of the gene for fucosyltranserease-7, and activates its transcription. This also exemplifies the direct associated between glycan alteration and malignant transformation.

"Hold Your Wee for a Wii"

Water composes approximately 2/3 of the human body; running through blood, inhabiting cells, and enclosing the spaces between. The body constantly loses water through sweat, urination, defecation, and exhaled breath, to name a few routes. It's imperative to replace this loss but it is possible to overdo rehydration, and even have a fatal water overdose.

Jennifer Strange


In 2007, Jennifer Strange, a 28 year old woman from California died after participating in a radio contest. The contest, titled "Hold Your Wee for a Wii," forced contestants to drink increasing amounts of water every 10-15 minutes. Strange drank six liters of water in three hours, vomited, and went home complaining of a headache. It was so excruciating that she called a co-worker, crying in pain. A few hours later she was found dead of water intoxication.

Hyponatremia is defined as an insufficient amount of salt in the blood. The normal blood sodium concentration is between 135 and 145 millimoles per liter. Hyponatremia is when a blood sodium falls below 135 millimoles per liter. Severe occurrences of hyponatremia can lead to water intoxication.

The kidneys control the amount of water, salts, and other solutes that leave the human body. When someone drinks excessive water in a short amount of time, the kidneys cannot drain it quickly enough and the blood becomes saturated with water. The overabundance of water leaves the blood and eventually enters the cells, which expand to provide space for it. However, neurons do not have the room to stretch. Brain cells are packed tightly inside the skull, and there is very little space for cells to expand and swell. Brain edema, which is swelling of the brain, can be catastrophic. Rapid and severe hyponatremia can lead to seizures, brain stem herniation, and death.

If you would like to read more about Jennifer Strange's story, check out this article. If you would like to learn more about water intoxication, go to this Scientific American article.

2011 Nobel Prize Winners

The 2011 Nobel Prize winners were announced last Monday, October 3rd. This year's Nobel Prize in Physiology or Medicine was awarded to Bruce Beutler, Jules Hoffman and Ralph Steinman. Beutler and Hoffman helped to clarify innate immunity, "the non-specific array of initial responses by the body's immune system that can recognize invading microorganisms as being foreign and try to destroy them." Steinman researched dendritic cells and their importance in adaptive immunity, "the specialized response to specific invaders" that become involved when innate immunity needs assistance.

The detailed intellect of the immune system will help researchers improve vaccines and provide new attempts to excite immune reactions to cancer.

Ralph Steinman

Unfortunately, Steinman passed away on September 30, just three days before the prize announcements. He was 68 years old and had been battling pancreatic cancer for 4 years. "His life was extended using a dendritic-cell based immunotherapy of his own design," The Rockefeller University spokesman Joe Bonner stated.

This raised questions about Steinman's award, because the Nobel Committee rules state "the prize can be awarded posthumously only if the laureate dies between the October announcement and the award ceremony, held annually on December 10 in Stockholm, Sweden." The committee was apparently unaware of Steinman's death, and The Rockefeller University only learned of the news on Monday. However, the Nobel foundation announced that Steinman would remain a prize winner.

After all, I think it would be way too harsh for his family if the Nobel foundation were to revoke his prize. The man clearly deserved it, and the date of his death (which was only 3 days before the announcement) shouldn't affect his accolade. To read about the Nobel Prize winners, click on this article. To go to the Nobel Prize website, click here.

Fold-It!

So, for those of you who don't know, Fold-It is an experimental video game about protein folding. It developed as a collaboration between the University of Washington's departments of Computer Science and Engineering and Biochemistry. Recently, the gamers of Fold-It solved an HIV enzyme riddle in only 3 weeks! If you would like to read about this on Scientific American, click here.

Now, to the game of Fold-It! Honestly, I expected it to be very boring. But I was pleasantly surprised to see the sharp visuals and cool features! The game even had sound effects, and we all know sound effects make everything better. I felt a great sense of accomplishment every time I finished a puzzle, and then I realized I was doing only the simple introductory ones.

So, I started off doing levels 1 and 2. These were a breeze and didn't require much thought. But in order to get to the higher level puzzles, I had to do them because you can only unlock upper levels by completing lower level ones.

Then, I completed level 3-1: Sheets Together.

This puzzle mostly involved hydrogen bonding. It started off with just one hydrogen bond, and ended with five of them. To solve the puzzle, I pressed wiggle for a few seconds, and then I pressed stop. By doing so, the protein's sidechains and backbones were wiggled into place, and hydrogen bonds were formed. Initially, the one hydrogen bond holding the two sheets was very weak. But with the addition of four more hydrogen bonds, the sheets were slightly more stable in their holding together, hence the name "Sheets Together."


Afterwards, I completed level 3-2: Lonely Sheets.

This introduced rubber bands to help solve the puzzle. I noticed there were many empty voids in the beginning. So I put two rubber bands across the greatest voids and pressed wiggle. This helped lessen the voids. However, by doing so I ended up creating some more voids! So I put another rubber band across the protein and pressed wiggle. This helped and at this point, I only needed 16 more points to complete the puzzle. I put another rubber band across the widest space of the protein, and pressed wiggle. After half of a second, I pressed stop. And thus my puzzle was complete! The usage of all of the rubber bands were to bring the sheets together and help them create bonds. The most challenging part of this puzzle was figuring out where to place the rubber bands. And I did mess up a few times. But luckily I discovered the undo feature which helped me fix any errors. In the end, the sheets were brought together and were no longer, "Lonely Sheets."

Next, I completed level 3-3: Sheets and Ladders.

This structure started out looking like a big "S". I decided to follow the same method that I used in the previous puzzle. I immediately placed a rubber band across the protein, and pressed wiggle. This caused the protein to fold up into a globular (my fave word!) shape, and a few hydrogen bonds were created. I noticed one large void towards the bottom, so I placed another rubber band across there and pressed wiggle. And just like that, I had solved the puzzle! I did it in only two moves, so I consider that an accomplishment. This puzzle didn't seem too difficult to me, because it was pretty much just building hydrogen bonds by bringing the protein together.

Next, I completed puzzles 3-4: Lock and Lower (not required) and 3-5: Rebuild (not required). Puzzle 3-4 gave me some trouble at first. I was just playing around with it, and pretty much dug myself a deep hole. At this point, I chose to reset the puzzle and not too long after I solved it. Although 3-5 looks complicated, I was able to solve it in two moves! I just used rubber bands and wiggle to do so.

Last but not least, I completed level 4-1: Hide the Hydrophobic.

For a level 4 puzzle, I was expecting it to be very complicated and difficult. But it was exactly the opposite. There was an orange hydrophobic region and a blue hydrophilic region. First I dragged the orange hydrophobic region towards the center to "hide" it from the exterior. Next, I dragged the blue hydrophilic region towards the outside, so it could be "exposed" to the exterior. The puzzle perfectly fit it's cute name, "Hide the Hydrophobic."

All in all, I actually enjoyed doing the Fold-It puzzles. I learned a little bit about proteins along the way, and I got to have fun playing with the structures. If this sounds interesting to you, I would say give it a try!