This Post's Title Keeps Evolving, So I'll Just Call It This

I just scrolled through my Twitter stream, and just over the most recent tweets, I saw multiple tweets devoted to just one idea:

#evolution

Although that may not sound too impressive--after all, I follow almost all science teachers--the fact that this one idea is still sparking debates and controversy after centuries of existence is actually pretty impressive when you stop to consider it. Simply clicking on the #evolution hashtag reveals a community that is updated at least once every five to ten minutes.

So what's the real idea behind evolutionary theory?

Let's go back to the beginning...although not the very beginning. Let's start in 1801, when John-Baptiste Lamarck published his Theory of Inheritance of Acquired Characteristics. Right away, if you have a background in evolutionary theory, an alarm bell will go off in your head. If you have that red flag, you've caught the big thing Lamarck got wrong. Lamarck thought that organisms could inherit acquired characteristics. For example, if a snake, throughout the course of its life, develops muscles that allow it to wriggle faster, Lamarck thought that it would pass those muscles on to its offspring.

Darwin didn't think that. He said that organisms pass on mutations, not acquired characteristics. And because organisms pass on mutations, if those mutations give an organism a certain competitive advantage, they have a better chance of producing more offspring. Those offspring may then have the same mutation, which gives them the same advantage over other organisms, giving them a better chance of producing more offspring. These offspring carry the mutation, which gives them an advantage...and the cycle continues.

Now, that's the basic mechanism of the theory of evolution--and it's known as natural selection. It's where phrases like "survival of the fittest" come from. However, that phrase isn't really accurate. Natural selection depends more upon reproduction than survival. Of course, survival helps to reproduce, but it does not guarantee offspring.

The classic, almost cliched, case of evidence for natural selection is the story of the peppered moths in Britain. There are two main phenotypes for this type of moth: light and dark. Before 1848, dark moths made up less than 2% of the total population. However, by 1898, over 95% of moths in industrialized areas were dark.

Why?

The mid-1800s was the time of the Industrial Revolution in Britain. All of those factories were emitting soot, so the landscape itself became somewhat darker. This meant that birds could see the lighter moths more frequently, and so the lighter moths were the ones that were eaten. The darker moths were able to reproduce, which produced more dark moths. Over a period of fifty years, the gene pool of the population changed, which is evolution by definition.

That is an example of microevolution--change within a species--and there are other ways in which this can occur. For example, let's spend some time talking about genetic drift. Genetic drift has to do with the change of the frequency of alleles due to random chance. Genetic drift holds more power in smaller populations, simply because even a slight change in the frequency can have an impact on the overall pool. Essentially, that means:

Genetic drift basically means that some random things will happen to a population to change its gene pool. It boils down to this: If a population is relatively small, then there is an increased chance that rare genotypes will not make it to the next generation.

There's another mechanism for microevolution--gene flow. (Don't worry--this one's much easier to understand than genetic drift!) All that gene flow says is that the migration of organisms has an effect on the gene pool. If two populations share an general boundary, there's nothing to stop them from interbreeding, introducing genes into the gene pool of both populations.



So, that's a little overview of microevolution--change within a species. Now, I realize that I've made some pretty big claims over the last few paragraphs. What evidence is there for those?

It turns out that there's a lot. First off, let's look at the fossil record. I've often been told that there simply aren't any intermediary fossils (fossils of animals that were "in between" species--they have features of both). And the more I research that claim, it's simply not true. For example, look at these fossils:

In these fossils, over a period of 50 million years, we can watch the nostrils move from the front of the skull to their current location at the top of the skull.

Another important branch of evidence for evolution is the idea of homologies. Homologous structures are structures that are shared across many species. For example, even though a cactus and a rose have very different structures that serve as leaves, they both have the same ultimate function. Another example of this is forelimbs among four-legged creatures. Even though, say, a rabbit and a lizard are clearly quite different, the bones within their forelimbs are constructed in the same manner.

Homologies can also be found at the cellular and molecular levels. For example, plant and animal cells are essentially identical--there are only two organelles in a plant cell that are not in an animal cell, and one animal organelle not in a plant. Additionally, a significant percentage of genes are shared across species. Just look at a roundworm and a human. Between those two phenotypically different species, 25% of genes are identical.

Finally, let's look at one more support column for the theory of evolution: the field of embryology. Basically, it says that, in their early stages, embryos of different vertebrates have strong similarities. This is taken to suggest that these vertebrates have a common ancestor.

So, now, I've thrown out a lot of information. I've shown the proposed mechanisms for microevolution and we've looked at evidence for macroevolution. But it doesn't mean anything if I don't accept it. Now, I do accept the theory of evolution as valid, simply because the ideas simply seem to line up. I don't see why, if there was not a common ancestor, there would be so many similarities at the molecular and cellular level of organisms that are in different kingdoms. The fossil record, to me, serves to back that belief up.

As someone with a mathematical background, I tend to accept things based primarily on the reasoning behind them. Now, I recognize that that's probably not the best idea in the other sciences, and it's something I probably need to work on. But that's another reason I think I support the theory: the reasoning behind it simply seems to, for me, line up. I don't see why it shouldn't be true.

Now...off to a #TeachIn11 post! 

Structures, But Not Architectural

WARNING: Biology post ahead!

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Recently, we've been discussing the components of DNA and how they fit together to create the genetic code. I also found this nice, although admittedly outdated piece [from the University of Arizona ;) !] that aided me in these discoveries.

First off, we have to understand that DNA is a polymer, meaning that it is comprised of several smaller pieces (the monomers) that have joined together. DNA, however, is special, so we can't just call its components monomers--they have their own names. Each monomer is called a nucleotide, and when combined, you get a polynucleotide.

Make sense so far?

Now, there are four nucleotides, and they're all mostly similar. Each one has a 5-carbon sugar (deoxyribose), a phosphate group, and a nitrogenous base. The only difference between the four is in that nitrogenous base. You're probably familiar with the notation for these bases:

A=Adenine

T=Thymine

C=Cytosine

G=Guanine

Let's take some time to examine the bases themselves in more depth.  Two, A and G, are purines, while their counterparts in the DNA sequence, T and C, are pyrimidines. (After a few minutes of Googling...I'm not even going to try to define those terms. I like going in depth, but there's a limit.). Adenine and guanine both have 5 carbon atoms and 4 nitrogen atoms, these atoms are both numbered according to their positions, and both have an NH₂ molecule attached to the rings of carbon and nitrogen. The only real difference between these two is that guanine also has an oxygen atom attached to the C₆ atom and that the NH₂ is at the C₆ atom in adenine, while it is found at the C₂ atom in guanine.

Cytosine and thymine have are also quite similar to each other, but only consist of one C/N ring, instead of two as the other two bases did. They both have 4 carbon and 2 nitrogen atoms. In fact, the only difference between the two is that thymine has an extra NH₂ molecule instead of two oxygen atoms and that guanine has an additional CH₃.

We've been focusing on the bases, so let's take some time to examine the backbone, if you will, of DNA--the deoxyribose phosphate. This structure has 5 carbon atoms, two hydroxyl groups, and one lone oxygen atom. These two hydroxyl groups bond with the phosphate groups to build the backbone. This means that there is a polarity to the chain--it goes from 5' to 3'. (Interestingly, compared to ribose, deoxyribose lacks one hydroxyl group, hence the name "DEOXYribose.")

Ok. So, now, we have one side of the DNA chain built. But DNA has a double helix shape, as Watson and Crick discovered. To explain how these sides join and why they twist, we have to examine the bonds within the DNA molecule. First off, when two of the sugar-phosphate "sides" we've been discussing combine, they do so in opposite directions--the two 5' atoms are at opposite ends of the combined chain. Now, along this backbone, the phosphate and sugar are covalently bound--pairs of electrons are shared between the two molecules. The base pairs, however, use hydrogen bonds (remember them? They're caused by charge differences between hydrogen and other atoms.) to join. This is particularly useful because when it is time for them to be separated for RNA synthesis (more on that soon!) these bonds can be easily broken. It is also interesting to note that, although adenine and thymine bond with two bonds, cytosine and guanine use three bonds.

More coming soon! 

Synthesizers: They're in Your Cells

This marks two posts in a row for Biology! Don't worry...I have a few personal ones stewing away.

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Pretty much everyone knows that DNA is in your cells. That's a well known, widely accepted fact.

Not as many people know that proteins do the dirty work of the body. When you look in the mirror, you are seeing the result of the work of proteins.

But this means that, somehow, the information encoded in your DNA has to be used to make proteins. How is this done?

The answer to this question is the RNA molecule. RNA is somewhat similar to DNA, but it has a few important differences. First off, uracil is used as a base instead of thymine. (Both uracil and thymine are pyrimidines, but uracil is missing a methyl group.) Then, the sugar used in its formation is ribose instead of deoxyribose. RNA also only has one strand instead of DNA's two.

Now, there are three classes of RNA. Let's take some time to examine each.

Messenger RNA (mRNA)

Messenger RNA is what carries the information from DNA to the ribosomes to create proteins. It's almost like the photo negative--every base in RNA is the complement of the base in DNA. For example, a DNA sequence of

ATGTGCA

would be transcribed as

UACACGU

(Remember, RNA uses uracil instead of thymine.)

Then, the strand of mRNA exits the nucleus and heads to the ribosome. Here, it meets up with...

Transfer RNA (tRNA)

Transfer RNA is a single strand of RNA that curls back on itself, with a location for an amino acid. It's typically portrayed in textbooks as a cross-ish shape, like

This isn't the actual shape of tRNA, but this particular representation is useful for several reasons. First off, it shows the "intramolecular base pairing" in the arms of the cross--G and C, U and A. It also is a "charged" RNA, meaning that it is carrying an amino acid. Finally, below the molecule, we can see the "codon," and at the bottom of the molecule itself, we have the "anticodon." Codons are groups of three bases that each have their own specific meaning. (Because there are four possible bases and three bases in a codon, there are 4³=64 possible codons.)

Let's track a certain sequence of three bases through transcription (where DNA is transcribed to RNA) to translation (where mRNA is used by tRNA to create an amino acid sequence). Imagine that the sequence AGT is sitting on a DNA molecule. When transcribed to mRNA, it becomes UCA (remember, RNA becomes the complements of the bases in the DNA). This mRNA exits the nucleus and goes to the ribosomes. In the ribosome, it is paired with the tRNA carrying its anticodon, AGU. (As a matter of fact, this would result in the protein serine being added to the chain.)

Then, this general process continues for all of the codons. A series of amino acids is compiled, and finally a protein is made. Now, remember, all of this is happening in the ribosome, and an important part of the ribosome is

Ribosomal RNA (rRNA)

The ribosome is comprised of two subunits, both composed of rRNA. These two components are creatively known as the who on earth named these things large subunit (LSU) and the small subunit (SSU). When mRNA enters the ribosome for translation, it slides between the two subunits. Ribosomes have three binding sites for tRNA to enter as the mRNA is translated (known as A, P, and E). The A site binds with a charged tRNA--one that is carrying an amino acid. At the P site, another charged tRNA is waiting--and the amino acids of the P tRNA and the A tRNA bond. The tRNA that was at the P site moves to the E site, leaving its amino acid behind, and the molecule occupying the A site moves to the P site. Another tRNA molecule comes in to the A site, and the cycle continues.

That's a brief overview of the various types of RNA!

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I have a confession: Over the past month, my writing on science stuff has seemed increasingly dry. I haven't liked it, and I don't know why. Has anyone else noticed this?

Limited Resources: What Now?

I've been quiet here recently, mostly because I've been traveling and haven't wanted to take time out to type up my thoughts. But they've been in my head for a while, and here they are.

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Peter asked an interesting question in this post:

"What do you see as an alternative to a teacher who doesn't have he resources to have all the students participate in a lab, but still wants the concept to be taught?"

In my response, I suggested that if a student could successfully design an experiment--even without carrying it out--that should be evidence that the aforementioned student had sufficient comprehension of the ideas he or she was testing. I've actually done this myself--see this post (I know, I know--slideshows=bad. I was just getting tired of doing complex prezis for everything).

All that I really did, though, was design an experiment to test a certain question. (I can't claim that I knew everything, though--I did have information on the reactions between BTB, water, and carbon dioxide.)

Now, let's try this, and see if this can work to show if student has real understanding. Imagine the overall goal of a class period was to extract DNA from an organism--say our student chooses wheat germ. First off, we'd consider what needed to be done to isolate the DNA. We'd have to break down the cell membrane and the nucleus somehow so that the DNA could precipitate. At this point, the student (let's call her Jill) would have to come up with something along the lines of, "Because wheat germ has a phospholipid membrane, hot water and soap can break it down."

Ok. So, now we have a bunch of DNA floating around in water. What next? 

Well, let's ask Jill. "DNA isn't soluble in alcohol. So, if we add alcohol to the raw DNA, it should pull together into a precipitate."

Of course, I recognize that there are major flaws with my presentation here. After all, Jill would have to know that wheat germ has a phospholipid membrane which can be broken down by hot water and soap, and that DNA isn't soluble with alcohol. But that's the problem with examples. In a real classroom, these topics could either be covered ahead of time or Jill could be given this information (like I was on that experiment over photosynthesis). Then, of course, Jill would need to figure out how to apply these facts to obtain her desired result.

And isn't that skill what education should be about? 

Genetic Counseling

To learn about the field of genetic counseling, I went through the various problems here. Although I tend to prefer finding more creative ways of going about this, this time, I think I'll simply answer the questions given on the site itself.

First off: here's the pedigree described in the story:

(I apologize for the spots that are somewhat confusing. Progeny has some design problems that I eventually became tired of circumventing.)

Part II--Autosomal Dominant Traits

1. Do autosomal dominant disorders skip generations?

No. Simply because, by definition, they are dominant, then if their presence in the genotype will be reflected in the phenotype.

2.  Could Greg or his mother be carriers of the gene that causes myotonic dystrophy?

Because myotonic dystrophy is an autosomal dominant disorder, Greg or his mother could not be carriers of the gene that causes it. If they had the gene, they would suffer from the disease.

3. Is there a possibility that Greg’s aunt or uncle is homozygous for the myotonic dystrophy (MD) gene?

There is no possibility that Greg's family members are homozygous for the MD gene because one of their parents did not have the MD gene. Because they did not have it, they could not pass it on.

4. Symptoms of myotonic dystrophy sometimes don’t show up until after age fifty. What is the possibility that Greg’s cousin has inherited the MD gene?

There is a fifty percent chance that his cousin has the MD gene, because the cousin's mother was heterozygous (her father did not suffer) and the father does not have the gene. A Punnett square for this situation reveals a fifty percent chance of inheriting the MD gene.

5. What is the possibility that Greg and Olga’s children could inherit the MD gene?

There is no possibility of Greg and Olga's children having MD. Because their parents did not have the gene, they cannot have the gene themselves. Therefore, their children cannot get the gene from them.

Part III--Autosomal Recessive Traits

1.  What are the hallmarks of an autosomal recessive trait?

An autosomal recessive trait can skip generations, but requires two copies of the mutant gene to be apparent.

2.  What does consanguineous mean? Why is this concept especially important when discussing recessive genetic disorders?

If two people are said to be consanguineous, that means that they are descended from a common ancestor. This is important in recessive traits because if two people are consanguineous, then they often have somewhat similar genotypes--including recessive genes.

3.  What is it about the inheritance pattern of factor VIII deficiency seen in Greg and Olga’s pedigree that point toward it not being an autosomal recessive trait?

Looking at Greg and Olga's pedigree, we can see that it appears mainly in boys and only rarely is apparent. This would point towards this disorder being an X-linked gene.

Part IV--Sex-Linked Inheritance

1. What are the characteristics of X-linked recessive inheritance?

X-linked recessive inheritance is typically primarily apparent in boys because males only have one copy of the X-chromosome. This means that mutations on this chromosome are typically masked in girls by a good copy of the X-chromosome.

2.  Why does a son never inherit his father’s defective X chromosome?

A son cannot inherit his father's X chromosome because he always receives the Y chromosome from his father. This is what makes him a son and not a daughter.

3.  What is required for a woman to display a sex-linked recessive trait?

For a woman to display an X-linked recessive trait, she would need two mutant copies of the X-chromsome--one from both parents.

4.  Return to the pedigree drawn earlier for Greg and Olga; mark those persons who are carriers of the factor VIII deficiency gene.

On Greg's side of the family, his mother and maternal grandmother are carriers. On Olga's side, her maternal grandmother and her mother are carriers--and potentially, her.

5.  What is the chance that Olga carries the gene for factor VIII deficiency? Calculate the probability that she will pass it to her offspring. Will male children be affected in a different way than female children?

There is a  1/4 chance that Olga has this gene, and a 1/4 chance that she will pass this gene to her children. If she does, there is a 1/8 chance that the child will suffer from the disease (if male) and a 1/8 chance that the child will be a carrier.

6. What is the chance that Greg carries the factor VIII gene? Can he pass the gene on to his sons? His daughters? How will each be affected?

Because the factor VIII gene is on the X chromosome and he is not a sufferer, there is no chance that he has the gene. He cannot pass the gene on to his sons, because he will give a Y chromosome to them. He will give an X chromosome to his daughters, but the mutant gene will not be on it.

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I will stop here--this one's already gone on long enough, especially for one as mundane as this one. I will probably include the rest of the tutorial in a Part II, which should be up within a few days.

Dominance: Why?

As I was reflecting over the last week, I realized that, although I've heard quite a bit over my life about the dominance of alleles, I'd never heard a real explanation of why certain traits express themselves over others. So...I found out.

On this page, Stanford University scientist Ruth Tennen answers this question. Apparently, there are several different reasons this happens. The most basic one occurs when the gene's function is to make a protein. If the recessive allele does not make this protein, then because the other allele will anyway, its presence is apparent in the phenotype.

For example, consider red hair. Because the protein that the MCR1 gene makes removes red pigment, as long as a person has one working copy of the MCR1 gene, they will not have red hair. A person has to have two copies of the broken MCR1 gene in order to have red hair.

Then, believe it or not, the opposite can be true--the dominant allele can be the broken gene. This was somewhat confusing at first to me, so I'll do the best job I can to explain it, often by stealing the metaphors used on the aforementioned site.

This situation of the recessive allele being the functional gene often occurs when the broken protein made by the dominant allele gets in the way of the protein made by the recessive allele. Consider a relay team. The first runner on the relay does his job just fine--he runs his 100m. But the next runner always drops the baton on the handoff, and because of this, this relay never wins. The first runner here is like the functional protein made by the recessive allele--it does its job just fine. But then, because the broken protein can't help out along the way, it is the work of the broken protein--the dominant allele--that is expressed.

Now, of course, there are more situations than this. There's codominance and incomplete dominance and...well, you get the idea. However, the basic idea here is that it's all about the proteins and the way they get along.

See you soon! 

Are We There Yet? (The Joy of Maps)

Before I go into too much depth, I'll give credit where credit is due.

We've recently been studying the madness of chromosome mapping over the past few days, so I thought I'd give a quick overview. So...here we go!

Chromosomes can be viewed as similar to a thumb. A thumb has two separate regions, split by a knuckle, one of which is clearly longer than the middle. Similarly, a chromosome has two arms, a p arm (shorter) and a q arm (longer). These arms are split by a notch known as the centromere.

Bizarre analogies aside, let's take some time to look at a specific gene on the X chromosome: Xq28.

Let's look at what each subset of this cytogenetic locus means:

X

This simply means that this particular gene (MRX28) is located on the X chromosome (more on the significance of this later!).

q

This means that the gene is on the longer of the two arms of the chromosome--the q arm.

28

This means that this gene is on the band labeled 28. Chromosomes, when stained, show different bands. This is caused by the differing ways in which the DNA is wrapped.

Now, I chose a gene on the X chromosome for a reason. Genes on this particular chromosome are known as "x-linked." Abnormalities on the X chromosome are always apparent in males because there is not a dominant allele on the X chromosome to mask the presence of the mutant allele. For an example of this, consider color blindness. Men are color blind for red and green more often than women because the gene(s?) for detecting red and green light is on the X chromosome, and men only have one copy of the X chromosome, so defections are not masked.

The MRX28 gene I mentioned earlier is one that has been linked to mental retardation. Here are some examples of other x-linked genes and the symptoms mutations carry:

COL4A5 (Xq22)

This is the gene that causes Alport's syndrome. This syndrome damages the various blood passages within the kidneys, which leads to urine in the blood and less effective filtering by the kidneys.

ATP7A (Xq21.1)

This particular gene causes Menkes syndrome, in which the body cannot absorb enough copper. This can affect the structure of many organs within the body (including skin, hair, and nerves) and often leads to a low body temperature and bleeding in the brain.

MECP2 (Xq28)

This gene is the root of Rett syndrome. This is usually found in girls because, although a defective X chromosome can make it to a boy, the boy will not survive. A girl, however, because she has two X chromosomes, is typically strong enough to live with the syndrome. Symptoms of Retts include problems breathing, seizures, and loss of sleep.

On a slightly cheerier note, I would like to relate an accomplishment of mine that is directly related to this. While I was having my hair cut, I made a joke about already going bald. The lady cutting my hair then asked if my mother's father was bald. Although my mother was adopted, I began to realize something: the gene that causes baldness is probably on the X chromosome. (I haven't actually researched this, but it seems likely.) This would also explain why women tend not to go bald--women have two X chromosomes, so they would not suffer the symptoms of a defective X chromosome as often.

Is that right? 

Eugenics

Well, I've thrown together an extremely (for me) short prezi on the origins and impacts of eugenics.

I also really recommend the Eugenics Archive, which was also extremely influential in the development of this post.

Have fun!

Eugenics: Based on "Fact" on Prezi

Genetics: It Makes the World Go Round

Over the past week or so, I've become somewhat fascinated by genetics. Perhaps my background in mathematics is the cause, but I'm quite fascinated by the idea of simply building every idea out of another idea. 

To really understand genetics, we have to start out by going down to the molecular level. Every cell contains a nucleus, and within that nucleus, there's DNA. DNA is incredibly important to the body. It carries the information used to build an organism. But what makes it up?

DNA is composed of four different chemicals: guanine, adenine, thymine, and cytosine, which are typically abbreviated as their first letters. Within the strand itself, there are some rules these chemicals have to follow. A will always pair with T, and G will always pair with C. (Pair, by the way, means that they have been hydrogen bonded together. Picture a twisted ladder, and that's the shape of DNA. The rungs on the ladder can be thought of as hydrogen bonds between the two molecules. The sides of the ladder are actually made of sugar and phosphate bonded together.) 

Now, I read an excellent metaphor at the University of Utah website. It said that the letters of the strand can be thought of as letters of the alphabet. The letters come together to form words, and the words come together to form sentences. In the same way, different series of letters (for example, A T G T C A) can be thought of as coming together to form genes. 

Now, genes tell the cell to make certain proteins. Proteins, as we know, can give cells certain functions and abilities--for example, within a cell of the inner ear, they can allow the cell to work with other cells to hear sounds. Genes are composed of DNA, although there are many genes along a single strand of DNA. (There are approximately 25,000 genes within the human body!)

Of course, DNA isn't simply laying around the nucleus of the cell. It's packaged into units known as chromosomes. Chromosomes are simply big chunks of DNA with protein wrapped around it. Every human cell contains 23 pairs of chromosomes--46 in all. Each chromosome carries different DNA with different genes, which means that each one controls different traits. For example, the 23rd chromosome contains either an X and a Y chromosome or two X chromosomes. Whichever one of the pairs actually occurs defines the sex of the person.

This brings us into our next big topic, which is heredity. If you need a refresher, see my post on mitosis and meiosis before reading on. 

Because genes carry certain traits, and because each parent gives one set of 23 chromosomes to the child, a child will inherit certain traits from each parent. (Fans of the Harry Potter series will recognize that Harry inherited his father's hair and general appearance but his mother's eyes.) Because of this, each child has a different genotype (genetic makeup) and phenotype (physical appearance). When these children have children, they will pass on some genes from their mother and some genes from their father. This is how traits can pass through multiple generations.

Now, let's mix heredity and genes together. Genes are made up of what are called alleles. An allele can be either recessive or dominant. If it is dominant, its presence will be apparent in the child's phenotype regardless of whether another gene is present. If it is recessive, however, it will only be visible if it is paired with another recessive gene. Basically, dominant alleles are just that--dominant. They mask recessive alleles. 

Of course, it's possible for some interesting combinations to occur. If a person has two dominant alleles or two recessive alleles, they are known as homozygous. If they have a combination of  dominant and recessive alleles, they are heterozygous. Now, here is where inheritance becomes interesting. If two people, one who is homozygous dominant for a trait and another who is heterozygous for the same trait have a child, their child's phenotype will display the dominant allele. However, if they receive the recessive allele from their heterozygous parent, and they have a child with someone who also has a recessive allele for the same trait, then it is possible for their child to show the recessive trait! This is how traits can skip generations.

Well, I think that's all for now! Let me know if I mangled anything! 

Cells: They Reproduce

Well...I'm back. It's been a while.

DISCLAIMER: This material is confusing. I've done my best to explain it in a clear fashion, but there might be a few places where readers may get lost. My apologies! 

Recently, I've been studying the various ways in which cells divide and reproduce. There are two primary methods through which this is accomplished: mitosis and meiosis. On the surface, the differences are somewhat slight: one produces two cells with two pair of chromosomes; the other, four cells with only twenty-three chromosomes each. 

Now, I decided that I was going to stop starting paragraphs with, "Let's take a deeper look at each." With that said, I will instead finish this paragraph with: Let's take a deeper look at each.

To understand mitosis, one must comprehend the cell cycle. After one series of mitosis has ended, the daughter cells enter what is known as "G1," in which all that happens is growth of the cell. Then, during the next period of time, the chromosomes duplicate, causing this phase to be known as "synthesis." Another phase of growth, this time, "G2," occurs. The previous three phases are collectively known as "interphase."

Now, the mitotic cycle starts. This is where it gets really interesting. The chromosomes become visible under a microscope and the nucleolus dissolves. This period of time is known as "prophase." Now, the chromosomes appear in an X shape because their duplicates formed during the synthesis phase are joined in the middle, along what is known as the centromere. Next, the sister chromatids line up along the middle of a cell, known as the metaphase plate, as this time is called "metaphase." Then, the sister chromatids are pulled apart along the centromeres by fibers emitted from the centrioles (poles at both ends of the cell), and the chromosomes head to opposite ends of the cell in "anaphase." Finally, the cell's membrane splits the cell into two distinct cells. This is known as "telophase."

Meiosis has a few differences. First off, the goal of meiosis is to produce a cell with only twenty-three chromosomes so that it can share its chromosomes with another cell in order to produce a cell with unique genes that is then capable of developing into a baby of the species. Therefore, the cells undergo one more division than they do in mitosis.

Now, meiosis starts out just like mitosis does, with the chromosomes replicating and then condensing. However, the first difference comes in what is known as "Prophase I." Here, the condensed chromosomes pair up with their corresponding chromosomes (remember, each cell has a two sets of chromosomes). While they are paired up, enzymes cut sections of DNA from each chromosome and exchanges it with the other. This allows genes (more on those later!) to be transferred between the strands.

Then, the centrioles attach to the pairs of chromosomes--fibers from both centrioles to 23 chromosomes. The centrioles pull the chromosomes (as in metaphase), but instead of lining up along the metaphase plate, the chromosomes line up so that the pairs of chromosomes are divided by the plate. The pairs of chromosomes are now separated as one member of each pair is pulled to both sides of the cell. The sister chromatids, however, are still attached. The sister chromatids arrive at opposite ends of the cell, and nuclei form around them. Telophase I occurs and the cell divides into two cells, each with one set of 23 chromosomes that were duplicated during the synthesis phase.

So, quick recap: Originally, there were two pairs of 23 chromosomes. Each pair duplicated, creating four pairs. Then, the cell divided, creating two cells, each with two pairs of 23 chromosomes.

Now, the two cells basically perform mitosis again. The chromosomes condense into chromatids, line up along the metaphase pate, divide along the centromere, and a new membrane forms. Because each cell (which had two set of 23 chromosomes) has now divided into two, there are now four cells with one set of 23 chromosomes--the original goal of meiosis.

Well, that's that! See you again soon! 

The Longest Prezi You Will See in Your Life

Well...this one's a biggie.

It's pretty self-explanatory, so I won't say much more.

However, I will point out that my energy and focus was gone by the time I got around to the Calvin Cycle, so if typos and mistakes abound...you know why.

Have fun!

Green Humans? Why Not? on Prezi

The Joy of Making Bubbles with Enzymes

Well, we did a little experiment with enzymes to see just how they worked. Our setup was relatively simple: 3 mL of water and 3 mL of hydrogen peroxide. Our enzyme was simply yeast, and the object was to manipulate various variables with the reaction to see what the change would be. My attempt at explaining what was going on is that the yeast breaks off the oxygen from the hydrogen peroxide and releases the oxygen into the atmosphere. This created the pressure we measured with a pressure probe.

Here are the various graphs we managed to draw from the experiment. I'll explain the meaning of each as we go along. 

This graph shows the change in the rate of reaction as we changed the concentration of the enzyme. The slope of this graph is relatively constant, suggesting that the rate of reaction is directly related to the concentration of the enzyme.

This graph (although admittedly bizarre) shows the change of the rate of reaction as the pH level of the solution the reaction was occurring in changed. We used buffers to hold the pH at constant levels of 4, 7, and 10, and found that the highest rate of reaction was when the pH was the pH of water--7.

This graph shows the change of the rate of reaction as we changed the temperature of the solutions that the reaction was occurring in. We used four different temperatures, namely, 0, 25, 38, and 80 (all of which were measured in degrees Celsius). By looking at this graph, we can see that the greatest rate of reaction occurred at slightly warmer than room temperature, but that the enzymes' productivity fell dramatically as the heat increased too much. This was explained when we realized that the heat could cause the enzymes to become denatured (meaning that the shape changed).

Unpronouncable Words...And Lots of Them

As we've spent a large proportion of time recently discussing enzymes, I thought I'd put together a little post on a disorder of an enzyme: PKU. (I found most of this information in the Mayo Clinic article.)

Phenylketonuria (fen-ul-ke-toe-NU-re-uh) is a genetic defect that results in too much of the acid phenylalanine. It's caused by mutation within a gene that contains the instructions to make the enzyme that breaks it down. Amino acids are the fundamental building blocks of proteins, but too much of phenylalanine results in various health problems. People who have this excess of the phenylalanine, referred to as PKU, must carefully limit their diets so that they do not consume too much phenylalanine (which is found primarily in protein-rich foods).

At birth, babies within the U.S. and several other countries are screened for PKU. When it is caught soon after birth, serious complications can be prevented.

  

When a baby is born with PKU, he or she has no symptoms. Soon after, however, the various complications arise. These include:

• Mental retardation
• Behavioral or social problems
• Seizures, tremors or jerking movements in the arms and legs)
• Hyperactivity
• Stunted growth
• Skin rashes (eczema)
• Small head size (microcephaly)
• A musty odor in the child's breath, skin or urine, caused by too much phenylalanine in the body
• Fair skin and blue eyes, because phenylalanine cannot transform into melanin — the pigment responsible for hair and skin tone

Let's go a little deeper with the causes of PKU:

PKU is caused by a genetic mutation. The gene that is defective is the one that carries the information used to make an enzyme that breaks down phenylalanine. Because this particular amino acid is allowed to flourish, a hazardous buildup of the acid can occur when a patient eats foods such as milk, cheese, nuts, or meats (foods that are rich in protein). This buildup leads to potentially serious health problems.

Because PKU is a genetic disease, the defective gene must be passed on to a child from both the mother and the father. This typically happens when the parents do not know that they have the defective gene. (Think of Typhoid Mary. People who have the defective gene but not PKU are known as carriers.)

Well, I think that's all for now! Who knows? I might actually stay on top of blog posts this time!

(Ha ha! How funny that is!) 

Poisonous Thoughts

Mustard gas. What is it really?

An article I found gave me a few answers. It's a poison that is particularly bad for the skin and the eyes, but can also affect the lungs and other organs if it is inhaled. Although it is typically not fatal, it does have severe effects. However, these effects do not occur immediately after exposure; rather, symptoms take up to six hours to develop. This can be a problem because permanent damage can occur before the victim even knows that they need medical treatment!

Mustard gas is a so-called "blister agent," meaning that it is a chemical that can damage the skin, eyes, and lungs. In comparison with "nerve agents," (chemicals that prevent the nervous system from properly functioning) it is not as likely to become fatal. However, the amount to which a victim is exposed plays a role in the long-term effects. Long-lasting complications (such as cancer) can be traced back to mustard gas.

Another article gave me some more in-depth information on the processes of mustard gas. As an alkylating agents, it binds to nucleophilic molecules (molecules that share electrons with another molecule to bind with them) such as both types of nucleic acids as well as proteins and various parts of cell membranes. Obviously, this can be bad. For example, when it bonds with DNA, it can cause the strands of DNA to break or develop various other problems. When mustard gas bonds with RNA, it can alter the creation of proteins that are dependent upon the RNA, which results in the death of the cell.  Because mustard gas also binds to some proteins, it can change the shape of those proteins, which can alter the enzyme activity. Finally, mustard gas can also alter the structural proteins of the membrane of the cell or cause the lipids within the cell to be damaged, both of which can cause the death of the cell.

Can anything be done for people who have been exposed to mustard gas? Unfortunately, the answer is "not too much." It seems that decontamination is the primary method of treatment for exposure to mustard gas. There is no antidote (at least at the time of publication of the latter article) and, although thiols have been suggested as possible treatment, there is not a wide acceptance of this method.

Photosynthetic Imagination

Well, after complaints from my audience (meaning: me) about the high concentration of prezis, I've reverted to Power Points. Here's a little thing I threw together about an imaginary experiment (literally, a thought experiment).

Embedding is not working well (read: not working at all) so, for now, I'll give you a link to the presentation. Hopefully, I can get it embedded sometime!

I'm Not Sure This One's Long Enough

Well, I've been traveling. I haven't been thinking about biology at all.

Because of this, you're about to see what should be approximately eighteen posts all merged into one prezi.

(Getting tired of prezis yet?)

Well, make sure you've got about an hour of free time ahead of you, and then click play!

All Locked Up in a Cell on Prezi

The Amazing, Conceptual, Concept Map of Science!

Well, after an entire period of wrangling with different web hosts, this image file is finally ready!

I thought I'd just throw together this little concept map to show just how my mind works. Hope you enjoy it!

The Prestigious College of Collagen

First off, an apology: This blog has, over the last week, fallen into complete, utter, total neglect. We here at the Department of Michael 'R' Us will try and prevent this from happening again, and we apologize for the inconvenience. We will be willing to provide free tickets to two future blogs in the future.

(Sorry!) 

Now, some musings on the protein of the month: collagen.

Collagen: What It Doesn't Do, You Don't Need on Prezi

To be honest, I don't like this one as much as my prezi on the properties of water. Oh, well!

Various Popes...Or Possibly Other Kinds of Benedicts

In the past couple of days, we've been mixing various foods with Benedict's solution and iodine to observe what kind of sugars (saccharide units) were in each.

Now, I'm not the kind of guy who likes "Well, it works that way because it does!" I prefer to know everything possible going on in a reaction such as this one.

So, I tried to go a little deeper. Although I'm not quite perfect on the details yet, I'm pretty sure I have the general idea.

Benedict's solution is nothing but a copper sulphate (Cu⁺²) mixed with alkaline solution. When a simple sugar is heated, it loses an electron, which goes into the copper. This reduction makes the copper Cu⁺¹. Now, it can react with oxygen to create copper oxide, creating the orange-ish color that indicates the presence of a mono-or-di-saccharide.

Ok...so I guess that might not have been very in depth, but hey...close enough?

Notes on Molelecular Structure

I thought I'd just go ahead and post my notes from today. Since these are notes, taken during class, these are disjointed and not exactly a masterpiece of the English language.

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Shape matters in biochemistry! Simple structure changes have profound effects on the chemical properties of a molecule.

Monosaccharides often do not stay "mono." They bond together and become disaccharides--for example, glucose and fructose become sucrose. Double glucose is maltose, and glucose and galactose become lactose. (Lactose-intolerance is caused by lack of an enzyme that breaks the glucose and galactose bonds.)

Then, there are polysaccharides. "Simple" sugars (monosaccharides) are combined many times (a condensation reaction--water is released). For example, many glucose molecules are combined to create amylose. Amlopeclin is very similar to amylose, but has extra branches. These are considered starches.

Glucose can be combined (through condensation reactions) to create glycogen. This chemical is found in human cells, particularly muscle and liver tissue. Cellulose is when the glucose chains are "flipped." Between these chains, hydrogen bonds can be found. Because of this, these can be used to create structural support (such as a cell wall in plant cells).

Cellulose cannot be broken down (for the same reason that causes lactose-intolerance--the lack of an enzyme that can do so.)

Bugs are crunchy for the same reason--their exoskeleton is formed from chitin, which provides support because of the hydrogen bonds.