Cancerous cells, and how they divide

Today's question involves how cancerous cells divide and actually become tumors. Here's the question:

All of the following mechanisms have been shown experimentally to the contribution to the formation of cancer cells EXCEPT:
and then there were answers.

The basis of this question is the nature of cancer. Cancer is the abnormal growth (and possible spread) of cells. These cells can invade and destroy other, healthy tissues, which causes the pain and death of cancer. The question, then, is what actually causes cancer to develop?

Since its discovery, scientists have been studying the mechanism of cancer. Their experiments have been focused on both the destruction of cancerous cells, and the mechanisms needed to cause normal cells to turn cancerous. There are several ways your normal tissues can cause you problems:

1) DNA becomes damaged. All cells (with the exception of mature red blood cells) have a nucleus, and this nucleus contains the blueprint for the cells. If the portion of the blueprint that tells the cells when to stop producing gets damaged, then the cells keep dividing with no limit. That causes tumors.

2) Growth factors. Growth factors are natural proteins that stimulate reproduction and differentiation. The presence or absence of growth factors accounts for how often the cell reproduces.

3) Introduced DNA. Viruses have the annoying tendency to inject their DNA into other cells. While some viruses compeletly take over the cellular functions, some just incorporate themselves into the host DNA and for long periods of time. This foreign DNA can cause cells to react strangly, and can cause cancerous cells to develop. (Heard of the shot developed to prevent cervical cancer? That works on this basis).

These are three major factors that determine if a cell is going to turn cancerous. Now, back to our question:

All of the following mechanisms have been shown experimentally to the contribution to the formation of cancer cells EXCEPT:

A) Abnormally high energy reserves in cancer cells that cause them to divide too quickly
B) Mutations that cause excess production of growth factors by cancerous cells
C) Mutations that inactivate genes that normally inhibit cell reproduction
D) Mutations that reduce the need for growth factors in cells
E) Viruses that carry genes that transform normal cells into cancer cells

Which one of these wasn't mentioned above? A. There we go!

E. coli and the lactose operon

Well, we're back in business! I've decided to focus a bit on microorganisms, since school has started again and I need to bone up on my micro before I have to lecture about it. In light of that, here's today's question!

In E. coli, induction of the lactose operon occurs when allolactose binds to:

A)Galactosidase
B)lac mRNA
c)the operator
D)the promoter
E)the repressor

This question tests your knowledge of how gene expression works, but tries to confuse you by giving specifics about E. coli. First things first--how does gene expression work?

Genes are some of those super complex things in biology--and one of those things that has a million names attached. Fun for us! Anyhow, sections of DNA code for proteins. They do this by creating messenger RNA (or mRNA) that tells the cell what to make. However, the DNA doesn't just randomly make messenger RNA and code for proteins...specific conditions must be met for this to happen. Of course this causes things to be much more complex.

DNA has specific sequences that tell the cell when to make mRNA, when to stop making mRNA, and when to prevent mRNA from being made. All these sequences together with the actual genes are called the "operon." Often time, in addition to the operon is a regulator gene called the repressor or co-repressor that allows the operon to be turned on.

If a repressor is present, it usually stops the gene from being expressed (keeps the proteins from being made); hence the name "repressor." Certain criteria must be met for the repressor to allow gene expression.

So, lets look at E. coli specifically: this bacterium loves lactose (anyone lactose intolerant? You know that horrible feeling you get after drinking milk? That's because the E. coli in your gut loves the undigested lactose and poops out acid and gas. Thanks microbes!) and therefore has a gene dedicated to breaking down this sugar. This gene is one of those with a repressor, however. It wouldn't make much sense for E. coli to try and break apart lactose if there wasn't in the environment, now wouldn't it? When lactose is present, a metabolite of lactose called allolactose is present. Allolactose binds to the repressor, which then allows the gene to be expressed. If there is no allolactose in the environment (and therefore no lactose) the repressor stays in effect and keeps the gene dormant.

Well, back to our question:

In E. coli, induction of the lactose operon occurs when allolactose binds to:

A)Galactosidase
B)lac mRNA
c)the operator
D)the promoter
E)the repressor

Since we know that induction means "get started" and an operon is that group of DNA that includes the operator, promoter and genes, we can now answer the question. The answer is "E" the repressor. Yay!

The Effects of Colchicine

Well, vacation is over, and now it's time to get back to the great subject of biology! Let's jump right into it, shall we?

Today's question:

The addition of colchicine to a culture of actively dividing flagellated eukaryotic cells inhibits all of the following except: (And then there's a list of answers).

Well, I chose kind of a pain in the ass question, didn't I? The GRE loves throwing specific substances/structures/species at you to determine if you know what it is or not. That's fun and all, but what if you have no idea what the bloody thing is? First, I'm going to tell you all about this colchicine stuff and its effects on cells. Then I'll give you some tips to make guessing the correct answer easier.

So, what is going on with this question? First off, notice that the test writers are doing that thing where they fill the question up with lots of multi-syllable words that may or may not confuse the reader. Don't let them win! The two biggest misleading words in this question are "flagellated" and "eukaryotic," neither of which have much to do with the meat of the question, which is "what the heck is colchicine?" If you find yourself getting bogged down in the complexity of the question, just take a moment to define each of the words and decide if they actually have any affect on the question itself. In this case, "flagellated" (the state of having a flagellum, or thing, whip-like tail used to propel and organism) really just gives you more detail about the cells the colchicine is being dumped on, while "eukaryotic" (cells with membrane-bound organelles) gives you even more detail. Fun! Ignore them for now.

Now to the real question: what is colchicine? Colchicine is an organic compound (molecules that contain carbon) that also contains nitrogen as its key component. This particular nitrogen containing organic compound (or "amine" for short) is produced by the Autumn Crocus, a very pretty little plant that you really don't need to know about. What you do need to know is that colchicine is very poisonous, and is therefore used therapeutically by doctors around the globe.

Colchicine causes vomiting and defecation in humans, and is therefore prescribed to combat joint issues such as gout. (For those who don't know, gout is a very painful condition in which uric acid crystals form in the joints of the lower extremities. This condition is related to kidney stones, and flare-ups happen after intake of rich food and drink. It was known as a disease of the rich in days of yore, but is now known as a disease of the unlucky and limping).

On a cellular level, colchicine inhibits the formation of microtubules. It does this by inhibiting tubulin--the substance responsible for making microtubules.

Microtubules are exceptionally important in two areas: growth and structure. Microtubules make up the main structure of the cytoskeleton, which gives the cell its shape. No microtubules, no cytoskeleton. That's a bad thing for new cells. Microtubules are also important during mitosis.

Have we gone over the stages of mitosis yet? I don't think so--that's a long lecture so I'm avoiding it. Well, the short version is mitosis is the process by which a cell reproduces itself. There are several stages of mitosis, during which particular things happen including the copying of DNA,and the relocation of the genome to the new cell. Microtubules are responsible (in the form of spindle fibers) for pulling the DNA from the center of the mother cell into the new daughter cells. If no microtubules form, then the DNA cannot migrate to the new cell, which means no new cells. Growth is inhibited.

This inhibition of growth makes colchicine a great drug for fighting cancer cells. The hallmark of cancer is its unfettered reproduction; since colchicine stops reproduction, flooding cancerous cells with colchicine stops their growth. Good! Of course, it also stops the growth of any healthy cells it touches, so it is only used sparingly and is not a miracle cure.

Ok, now we have an idea as to what colchicine does. Lets get back to the question:

The addition of colchicine to a culture of actively dividing flagellated eukaryotic cells inhibits all of the following except:

A) Movement of flagella
B) Growth of flagella
C) Formation of mitotic apparatus
D) Formation of microtubular cytoskeleton
E) Polymerization of tubulin


The answer seems obvious, right? Hopefully? Since colchicine inhibits tubulin which therefore inhibits microtubule production, all growth is stopped (due to lack of spindle fibers), formation of mitotic apparatus is inhibited (due, once again, to lack of spindle fibers), the cytoskeleton is stunted, and polymerization of tubulin is halted. Basically, everything involving growth and reproduction is stopped. However, this substance doesn't have any effect on already formed microtubules--you see, it only stops the substance that makes up new microtubules, it doesn't break down old tubules. So movement and function of mature cells goes untouched. Movement of flagella, therefore, is unaffected by colchicine. The answer is "A." Yay!

So what happens if you're sitting at the test and have no freakin' clue what colchicine is? You may be able to figure it out with a little bit of effort. Look at the answers given here:

A) Movement of flagella
B) Growth of flagella
C) Formation of mitotic apparatus
D) Formation of microtubular cytoskeleton
E) Polymerization of tubulin

The great thing about a multiple choice exam is the answer is staring you in the face--you just have to recognize it. In this particular example, the question is asking the effects of some substance on some cells. Your first task is to break down the question to its essential parts. Don't go trying to answer a question that isn't even asked! So, what are the effect of this substance? Look at the answers--two of them (B and C) are directly related to the growth and reproduction of a cell. Formation of the cytoskeleton has to do with growth as well, and polymerization is a fancy word for "making" or "putting together" or "growth." So 4 of the 5 answers have to do somehow with growing. Whenever you see a link between most of the answers, and the question asks "which is not like the other" then you have a pretty good idea of the answer. Make sense?

Amino Acids and DNA

Let's do an easy one, shall we? Ok! Here's the question:

The cDNA fragment that includes the ricin gene is 5.7 kilobases. If the entire fragment codes for the ricen polypeptide,the approximate number of amino acids in the poly peptide would be: (enter some weird numbers with lots of zeros here).

Well, once again the GRE just loves trying to confuse people with scary names and things. In this case, it throws in that whole ricin thing to throw you off. You can really just take that out of this question, so it reads something like "The cDNA fragment is 5.7 kilobases. How many amino acids does this code for?"

Alright, this is another one of those you-have-to-know-it questions. How much DNA does it take to code for a single amino acid? First, some very basic background. Amino acids are the building blocks of protein, and really what DNA codes for. Remember when we talked about DNA? DNA strands are studded with genes. Genes are simply lengths of DNA that code for certain proteins. Since the lengths of DNA make proteins, parts of the genes must code for the building blocks of proteins, or amino acids.

The next logical question is what percentage of each length of DNA codes for each amino acid? Ok, I'll just tell you: 3 base pairs. Yep, that's it. 3. Once you know how many base pairs are in a gene, then you just divide by three and that gives you the number of amino acids the gene codes for. How many base pairs are in the gene the question is asking about? 5.7 kilobases. Once again, don't be afraid of words here. "Kilo" simply means 1000, while "bases" means, well, bases. So 5.7 kilobases is 5700 bases or base pairs. Divide that by three, and you get the nice round number of 1900. There you go!

Where do blood cells come from?

Well, conferences are over for the time being, so I'm now able to post daily once again. Here's today's question:

Exposure to high levels of radiation in humans has been demonstrated to cause anemia. The most likely explanation for this is that the radiation damages the: (and then it goes on to list some places).

Ok, this is a relatively simple question that tests your knowledge of some basic anatomy and physiology. First things first: I've noticed that these tests just love making questions seem more complex than they really are. Take this one, for example. The very first line talks about high levels of radiation. I don't know about you, but I studied very little radiation in my biology classes, so when I first read the question, I got a bit worried about what I'm supposed to know. The question is misleadingly complex. If you just take out the radiation bits, you get a question that goes something like: "Damage to what part causes anemia?" That is much, much easier to answer! So I'm just going to skip the explanation about radiation and its dangers, and jump right into the meat of the question: what is anemia?

Anemia is a deficiency of hemoglobin or red blood cells. Hemoglobin deficiency lowers the blood cell's ability to capture and transport oxygen throughout the body (bad, yes?) and a lowered red blood cell count causes basically the same thing. Either way, anemia is bad. Your tissues need oxygen, and the red blood cells are there to get it to them. Without red blood cells, you die. A lot.

Now, I'm sure some of you have been told you need to take iron to prevent or treat mild anemia. This is true, but don't let it confuse you when you go to answer the question. Iron is a precursor to hemoglobin. The most common form of anemia is lack of hemoglobin, so taking iron supplements allows your body to produce more hemoglobin and therefore transport more oxygen. Lack of oxygen can cause lethargy, hence the tired feeling associated with anemia.

This question, however, is referring to the other form of anemia: lack of red blood cells. How do I know? I looked at the answer list! Here's the question again (this time with the answer list present):

Exposure to high levels of radiation in humans has been demonstrated to cause anemia. The most likely explanation for this is that the radiation damages the:
A) Blood vessels
B) Spleen
C) Liver
D) Thymus
E) Bone marrow

I advocate answering the question before you look at the answers, but sometimes the first answer you come up with isn't listed. Here was my thought process as I read this question: "Well, anemia is caused by lack of hemoglobin or red blood cells, so radiation must attack the red blood cells themselves." As you can see, this answer isn't listed. If your top answer isn't there, go through the rest of the answers and see which one makes the most sense.

Blood vessels. While damage to the blood vessels could cause blood leakage into various body cavities and eventually cause anemia due to lack of blood cells circulating, anemia isn't the first worry. I would be much more worried about internal bleeding, which would probably present as pain or death. Tiny amounts of internal bleeding may cause anemia, but that would mean only tiny amounts of radiation damage, and that isn't likely unless the radiation was controlled in some way (as in radiation therapy). I disregard this one right off the bat.

Spleen. Anyone who has studied the circulatory system knows that the spleen is involved. The spleen filters worn out red blood cells and sends them to the liver for processing. It also holds a small amount of blood in reserve for times when you need that extra burst of oxygen--like exercising or hiking at high altitudes. This makes your blood system more efficient. However, you can live without this little extra burst without any ill effects. Lacking a spleen doesn't cause anemia. It just like living without a savings account--not the most comfortable way to live, but it doesn't mean your checking account has any less money than it would have otherwise.

Liver. The liver does bunches and bunches of things that you don't need to know about at the moment. One major job is the break down of red blood cells and the recycling of hemoglobin. The liver breaks down the worn out red blood cells and gets rid of the excess material via billirubin. Liver damage would cause major problems in a person, but wouldn't cause anemia.

Thymus. The thymus gland is a place where certain white blood cells go to mature. Don't worry, I'm sure there's a question about white blood cells coming up that I can use to address this issue. Just know that it doesn't cause anemia.

Bone marrow. Ah, we've found it. Bone marrow is what gives rise to all the blood cells circulating in your blood stream. Immature blood cells are formed in the bone marrow, then travel to a variety of places to mature. If the bone marrow gets damaged, it no longer can produce blood cells, which will result in a lowered red blood cell count and eventually anemia. Going back to that bank account example, while the spleen is like your savings account, the bone marrow is like your job. While you can live just fine without a stash of money somewhere, if your income gets cut off then your screwed. Bank account anemia!

So, the answer to this question is "E" bone marrow. Yay!

How DNA moves through a electrophoretic gel

Well, I'm sitting at a conference at the moment, and have decided that it has been too long since I have indulged in the joy of biological teaching. Seriously! Stop laughing. Here's the question I randomly chose for today:

The rate at which a DNA fragment moves in an electrophoretic gel is primarily a function of the fragment's....

Isn't it lucky that I totally by accident chose a question that can be answered pretty quickly? I know! Lucky! Anyhow, let me tell you a little about electrophoresis. This process is a step used in laboratories to study DNA, and is often taught in every single lab class in college simply because it's rather simple and rather impressive. (Seriously--try this the next time you're having dinner with your family "So I was studying deoxyribonucleic acid the other day, and needed to separate the fragments after I broke the bonds at known gene sites, so I simply ran an electrophoretic gel." This is good for at least an extra helping of dessert and hours of proud bragging by your mom at the next knitting circle).

Well, how exactly does this work? DNA, as you might imagine, is huge. Think about the amazinhg amount of information stored in the genetic code--all that information just sitting there waiting to be expressed. When we study DNA, we usually want to study a particular section, or a particular gene. We do this by cutting the big string of DNA into fragments using enzymes. We then copy the DNA (lots and lots and lots through PCR which I'll explain in a later post) and then somehow have to pick out the genes we want to focus upon.

This is where electrophoresis comes in. An electrophoretic gel is basically really stiff Jell-O. The gel is melted and poured into a rectangular mold, and 8 (or so) wells are formed in one end of the solidified gel. These wells give us a place to put the DNA. Now, DNA has a charge. Due to it's chemical make up and all that jazz, it has a an overall negative charge. At this point, we want to separate the DNA into its different fragments, so some smarty somewhere decided to use that overall negative charge to do just this. The gel (with its wells filled to the brim with DNA in a liquid medium) is subjected to an electrical current. The DNA fragments are pulled through the pores of the gel as it is attracted to the positively charged energy at the far end of the gel.

Now, the DNA separates depending upon its size. The bigger the DNA fragment, the harder it is to force it through those tiny, tiny pores in the solid gel. Therefore, the bigger (or longer) the DNA fragment, the more slowly it moves through the gel. After a predetermined amount of time, the electrical current is removed, and the gel is stained with some horrible substance that causes DNA to glow under a black light. You then take a picture of the gel and look at the bands (see the picture above) and the ones that are furthest away from the wells are the shortest, while the ones closest to the wells are the longest.

So, back to the question:

The rate at which a DNA fragment moves in an electrophoretic gel is primarily a function of the fragment's:
A) Length
B) double helical structure
C) Radioactivity
D) Degree of methylation
E) Adenine content

Can you pick out the correct answer now? Movement through an electrophoretic gel is strictly due to size, therefore the answer is "A."

I'm out of town for a bit....

So I'm out of town. I volunteered to be a delegate at annual conference this year, which means at the moment I'm lying in a rather musty-smelling hotel room in beautiful downtown San Bernardino, and I have to be up in a minute to go to a variety of boring meetings and vote on matters that may or may not affect me and those I care about. Oh, and it's also a thousand degrees outside. I will do what I can to get a post up, but this will be sporadic until I make it home on Sunday. Don't miss me too much!

Plant hormones

I think I'm going to be moving into the plant phase of this blog. You see, a certain percentage of the GRE involves botany (they say it's only 15-33%, but it seems like a lot more on one of the tests I am looking at). Also, in the next few week's I'll be running a week-long training for grade school teachers in botany, so I need to brush up on my skills. Here we go:

Today's question:

Which of the following plant hormones hastens apple ripening?
A) Auxin
B) Gibberellin
C) Abscisic acid
D) Cytokinin
E) Ethylene

Let's dissect the question. What exactly is a hormone? A hormone, in terms of this question, is any of a handful of plant compounds that control the growth and differentiation of plant tissues. Basically, hormones control lots of things having to do with plant growth and development.

This question entirely depends upon your knowledge of plant hormones. There's not really a good way to guess your way through this one, which makes it a bit of a pain in the ass. Get your flash cards ready! Let's go through the hormones.

Auxin: Auxin has to do with the growth of plant tissues. Anyone who has ever grown plants know they have a neat tendency to do things like grow towards the light, and the stems grow away from gravity while the roots grow down. (Oh! Try this: take a plant you have in a pot and place it on its side. After several days, the stem will bend so it is once again growing away from gravity. You can also put a plant in a dark room with one window, or in a box with a window cut in the end. After a few days, the stem will bend towards the light source, and the plant will start growing towards the light.) So what happens in these two situations? Well, plant cells have auxin in them. When light hits the tip (or growing center) of the plant from one side, then the auxin present on that side flees from the light (maybe it's a vampire?) and concentrates on the other side of the cell. This causes the illuminated side of the plant to grow more slowly than the dark side. This over zealousness makes the plant tip grow towards the light, which allows the plant to get as much light energy as possible. The same basic thing happens with gravity. The auxin in root cells drop to the lowest point of the cell, which causes that tissue to grow faster than the higher points. Make sense? Of course it does. It all breaks down to this: auxin makes tissue goes faster. Wherever there's a lot of it, that's what grows.

Gibberellin: Giberellin is also in charge of growth, but in a different way than auxin. Gibberellin takes care of stem growth upwards, as opposed to which way the plant grows. This hormone is in charge of making stems grow tall really, really quickly, especially in those plants that are usually short. (Hey, when do you think this would happen? Perhaps in plants that are trying to compete for sunlight and need to outgrow their competition. Hmm.) It is also in charge of inhibiting new root formation, and stimulating new phloem cells. We'll talk about the xylem and phloem in another post. They are rant worthy, that's for sure. Finally, giberellin break the dormancy of buds and seeds and start the flowering in some plants during their first year of life.

Abscisic acid: Abscisic acid is in charge of stopping cell growth. This primarily happens when a plant needs to go dormant to avoid damage from excessive cold. This is what causes all the trees to stop growing during the winter and whatnot.

Cytokinin: All these hormones seem to govern plant growth, don't they? Cytokinin is no different--this particular hormone causes cell division. It also has a neato interaction with auxin: in undifferentiated cells, the ratio of auxin and cytokinin becomes very important. If auxin is dominant, the cells turn into root cells. If cytokinin is dominant, then the cells turn into stem and eventually bud cells. Ah, the webs these hormones weave!

Ethylene: Ethylene seems to be the only hormone that doesn't govern growth of tissues. This hormone travels through the air--noticed that all the other hormones stick to the tissues. This stuff goes everywhere. Ethylene is in charge of ripening fruit and the loss of leaves during the change of seasons. Have you ever heard of putting unripened fruit in a bag with half an apple? When fruit gets damaged or ripe, it gives off ethylene. Ethylene causes ripening, so putting a sliced apple with some unripened fruit causes the unripened fruit to ripen quickly. This is also why you don't want bruised or over ripened fruit with fruit you don't want to ripen too quickly--the ethylene will cause everything to ripen right up.

Now that we know everything there is to know about these five hormones, back to our question:

Which of the following plant hormones hastens apple ripening?

A) Auxin
B) Gibberellin
C) Abscisic acid
D) Cytokinin
E) Ethylene

Since we know that the first four are in charge of tissue growth, that leaves ethylene as our answer. Yay!

DNA Replication (i.e. Base Pair Porn!)

Could I come up with a more boring title? I don't think so! But how in the world do you write something interesting about how DNA copies itself? Maybe "base pair porn!" That would totally work! I'm putting that now...hee for me! Anyhow, on to today's question!

When DNA replicates semi conservatively, which of the following is true of each daughter DNA molecule?

A) Both strands are newly synthesized
B) One strand is newly synthesized, whereas the other is a strand from the parent DNA molecule
C) Both strands are the original strands of the parent molecule
D) One strand has more AT-rich regions than the other strand has
E) The newly synthesized strands are more susceptible to melting and renaturation than the parental DNA strands are

Ok, the big question in this question is "What is semi conservative replication?"

Remember that blog I did about complimentary base pairing? Yeah, me too! That was a good one. Sigh. Well, this is sort of a continuation of that last post. When DNA needs to copy itself, it undergoes replication. There are three methods the books talk about when discussing DNA replication: conservative, dispersive, and semi conservative.

Conservative DNA replication is when an entirely new double helix of DNA is replicated for the new (or daughter) cell. This works just like a copy machine--it's based on the mother cell's dna, and an exact copy is made. The two new strands are what are sent on to the daughter cell, while the strands they were copied from are left in the mother cell. This method of DNA replication has not been found to be biologically significant, so most people don't really care about it. And neither do we!

Dispersive replication is when bits and pieces of the mother strands are mixed up with new sections and all put together into a new double helix. The two daughter cells end up with a strange mix-and-match version of the DNA made up of both mother and daughter sections. Just like the last one, no one thinks this is a biologically significant method of replication.

Finally, the big one: semiconservative replication. This is the main way DNA is totally replicated during cell division. During this type of replication, the entire DNA double helix unzips. A new strand is made to match up with each original strand using complimentary base pairing. The result is two double helices where only one was before. Each double helix is made up of an old strand of DNA (the mother strand) and a new strand of DNA (the daughter strand). Each new daughter cell gets a double helix of DNA--one strand from the mother cell and one brand-spankin'-new strand. This is the only replication method of the three that is considered biologically significant (meaning, this is what we care about!)

Ok, back to the question:

When DNA replicates semi conservatively, which of the following is true of each daughter DNA molecule?

A) Both strands are newly synthesized
B) One strand is newly synthesized, whereas the other is a strand from the parent DNA molecule
C) Both strands are the original strands of the parent molecule
D) One strand has more AT-rich regions than the other strand has
E) The newly synthesized strands are more susceptible to melting and renaturation than the parental DNA strands are

Let's go through the answers. "A" is obviously incorrect, since we just learned that when both strands of a double helix are newly synthesized, that is called conservative replication. "C" is also wrong, because if both strands were of the parent molecule, no replication would have happened at all....the DNA would have just moved from one cell to another. "D" just doesn't make much sense. We know from complimentary base pairing, that each strand has exactly the same number of bases, so it's impossible for a semi conservatively replicated strand to have more AT regions than the other. "E" tries to throw you off by mentioning melting and renaturation, but we don't care about that.That leaves "B." This answer is the definition of semiconservative replication--one strand is newly synthesized, whereas the other is a strand from the parent DNA molecule.

There you go! Yay us!

The lytic viral cycle

Welcome to post #2 about viruses! Remember the last one? During that post I told you about how viruses are the underdog of the living world (being that no one knows if they are actually living or not), and are composed soley of a protein coat and an inner genome. Today's question revolves around the cycle of infection the virus undergoes in order to initiate reproduction:

Successful reproduction of a lytic virus requires that all of the following processes occur EXCEPT

A) incorporation of viral DNA into host cell DNA
B) translation of viral mRNA
C) binding of the virus to the host cell's surface
D) penetration of the viral genome into the host cell
E) replication of the viral genome

First off, there are two types of cycles that viruses can undergo to take over a cell: they lytic and the lysogenic cycle. The lysogenic cycle is interesting; during this cycle, the viral DNA is integrated into the host cell's DNA for an indefinite period of time. Basically, the viral DNA just moves in and lives in a new cell until it wants a change of scene. This may be in a day, or it may be in 1000 years...there's no real way to tell from our perspective.

The question we're worried about today involves that other cycle--the lytic cycle. During the lytic cycle, the virus takes over a host cell, utilizes the host cell's ability to make ATP, then bursts the cell open. This doesn't take long at all. The lytic cycle has four major stages: Adsorption, Penetration, Biosynthesis of viral products, and Release.

The viral cell is formed kinda like a hypodermic needle. The virus comes across an appropriate host cell (due to the intimacy of viral reproduction, viral cells are closely matched with their host cells. This is why most animal viruses can't jump from species to species, and when they do it is due to a massive mutation) and attaches to proteins found on the host cell's membrane. This adsorption period takes a bit of time and usually requires a slightly elevated temperature to happen effectively.

Once the virus is attached to the outside of the host cell, it then injects its genome into the host cell. Can you guess what this stage of the cycle is called? Yup. Penetration. The protein coat is left on the outside of the cell while the DNA/RNA of the virus does its dirty work inside.

The viral DNA must then figure out how to take over the cell (it's like an evil mastermind!). So, it follows normal DNA replication protocol--first it unzips, and then it translates messenger RNA to send a memo to the cell saying 'Hey! Replicate me!" Which the cell does, no questions asked. Silly minions!

Once that memo gets sent, the cell stops what it was doing, and begins to synthesize the viral products during the "biosynthesis of viral products" phase. The cell reproduces new, baby viruses until all the ATP and other cell resources are gone, and the cell is just PACKED full of new viruses waiting for the chance to infect a cell of their very own.

After the host cell is tapped out--oh you viruses! It's all wham bam thank you host cell--then the host cell bursts open, releasing all the viralings into the big bad world. Release!

So, four major stages in the lytic cycle. Now, back to our question:

Successful reproduction of a lytic virus requires that all of the following processes occur EXCEPT

A) incorporation of viral DNA into host cell DNA
B) translation of viral mRNA
C) binding of the virus to the host cell's surface
D) penetration of the viral genome into the host cell
E) replication of the viral genome

This question is testing your knowledge of the lytic cycle and its differences with the lysogenic cycle. We just learned the 4 stages of the lytic cycle: Adsorption, penetration, biosynthesis, and release. Looking at the 5 answers to this question, which one isn't included in those 4 stages? Translation of viral mRNA is the first step in biosynthesis; binding of the virus to the host cell's surface is the definition of adsorption; penetration of the viral genome into the host cell actually has the word "penetration" right in the answer; and replication of the viral genome is just another way of saying biosynthesis (it's just that biosynthesis sounds more sciencey, so I teach my students to use that word. Impress your friends and family!) The only answer that is not included in the four stages is "A", incorporation of viral DNA into the host cell DNA. Remember that this is the hallmark of the lysogenic cycle--where the viral DNA is incorporated into the host cell's DNA for an indefinite amount of time. Answer: A!

Saccharmoyces cerevisiae and sex

Ah, yeast. That beautiful, single-celled organism that gives us so much good stuff--mmm...beer. Well, at them moment, the GRE doesn't seem to care about the goodness of alcohol. Instead, it cares more about the taxonomical groupings of the yeast responsible for some many drunken hookups--Saccharomyces cerevisiae.

Here's the question:

The yeast Saccharomyces cerevisiae is classified as belonging to which of the following groups?

A) Eubacteria
B) Oomycota
C) Zygomycota
D) Ascomycota
E) Basidiomycota


Scientists like grouping like things together. We don't like having all these uncategorized species just lying around all on their own. Who do they think they are?!? Anyhow, S. cerevisiae is a yeast. Yeasts are a type of fungus, and are grouped together with all those fungi you know and love--mushrooms and molds. Members of the fungal group are put together by their method of sexual reproduction.

Ok, so fungi reproduce by producing spores--hardy, thick walled thingys that can survive most any horrible thing. Most molds reproduce most of the time asexually. This takes less effort and energy than sexual reproduction, so it tends to be the go-to option for most species. When times get rough, however, almost all of the species resort to sex to make sure their offspring have a good chance of survival.

So, what "groups" do fungi fall into? There are 6 major fungal groups (specifically, they are phyla): Chytridiomycota, Oomycota, Zygomycota, Ascomycota, Deutromycota, and Basidiomycota. Notice that all the fungal groups end in -mycota (that's a big clue to this question). The Chytrids are ancient molds, mostly aquatic, and super interesting to other people. The big representative of this group is Allomyces.

The second group is Oomycota, which are filamentous, water and downy mildew molds. As all of you who know a little bit about beer and bread, S. cerevisiae is a single celled organism, so it doesn't fall into Oomycota.

The final three groups are the higher fungal groups, and our best bet for S. cerevisiae. Organisms in Zygomycota produce zygospores; those in Ascomycota produce ascospores within an ascus; Basidiomycota members produce basidiospores; and organisms in Deutromycota don't have any known sexual cycle. Granted, that last group is just a catch-all for all the organisms we've discovered that we can't make do it in the lab.

Well, what do S. cerevisiae do? They produce ascospores within an ascus. I really don't have a good way of helping you remember this--maybe just straight memorization here? Sorry!

So, back to our question:

The yeast Saccharomyces cerevisiae is classified as belonging to which of the following groups?

A) Eubacteria
B) Oomycota
C) Zygomycota
D) Ascomycota
E) Basidiomycota

As we now know, Saccharomyces cerevisiae belongs to Ascomycota. Yay!

Viruses and ATP

The past couple of posts have been about human anatomy and physiology (which is what I'm currently teaching at SJSU) so I decided to branch out just a tiny bit in today's post--today I'm going to give a brief introduction to viruses. Here's today's question:

Members of which of the following groups CANNOT produce their own ATP?

A) Lichens
B) Bacteria
C) Viruses
D) Diatoms
E) Protozoa

This question is testing two things: your knowledge of vocabulary and your knowledge of organismal groups. First off, the vocab. ATP is the big work in this question. ATP stands for Adenosine Triphospate, and is the energy source for cells (well, it's quite a bit more complex than that, but I'm not going to go into it here. If you would like a very, very in depth discussion on the chemical basis of ATP and its exact function, do a search on Wikipedia. The ATP article there is fabulous). All cells use ATP to carry out essential functions such as growth, repair, and reproduction. Most organisms produce their own ATP--they have to, or they die. So, which of the above groups doesn't? Let's look at the groups and what they are.

Lichens: Lichens are symbiotic associations of (usually) an algae and a fungus. Without getting into the varieties of lichens, or the controversy on their relationship, the particular algae and fungus cannot live alone. However, once together the lichen is able to live, grow, and reproduce all on its own, and therefore produces its own ATP.

Bacteria: Bacteria are microscopic, single celled (for the most part) organisms. These are considered one of the smallest free-living organisms we know about. Bacteria have the ability to function apart from any other organism, although many thrive when in a symbiotic or parasitic relationship with something else. Bacteria produce their own ATP.

Diatoms: Diatoms are algae with cells walls made of silica (ever heard of diatomaceous earth? Yep, that's these guys). Being algae, these singe celled organisms are able to live freely, and do so in bodies of water. A certain type of diatoms is what is responsible for red tide. Neat! Anyhow, since they are able to live freely, they produce their own ATP.

Protozoa: Protozoa are single celled, eukaryotic (have a membrane bound nucleus) organisms that are, for the most part, motile. They are much larger than bacteria, and differ in many other ways that I won't get into here. Once again, however, single celled organisms capable of moving/growing/reproducing without other organisms, so they must produce their own ATP.

Viruses: Ah, viruses. Viruses are the bane of many a biologist. There have been whole summits on if a virus is alive or not, and the latest answer to come from the top minds in the field is "um...dunno." Viruses simple beasts--they consists solely of a protein coat and an inner genome (either DNA or RNA, but not both) and are unable to carry out basic processes such as growth or reproduction without the assistance of another cell. This is where the controversy comes in--if they are unable to grow and reproduce on their own, are they really alive? Well, that's neither here nor there for the moment. What we're worried about is how viruses work. Viruses must hijack another cell and take over its ATP producing capabilities in order to do anything. It does this by injecting its genome into the host cell's genome, and telling the host cell what to do from there. The host cell is sometimes destroyed during this process, and the virus goes on to infect another host.

So, the answer we're looking for is "C" virus. Viruses must hijack another cell for basic functions, and therfore don't produce their own ATP.

Quick morning note! Awesome story!

A Canadian newspaper is reporting a case of dark green blood in a surgery patient. I know! How neat is that?!?

Alight, this is a perfect opportunity to give a quick lesson on analyzing the things you read. This is basically an assignment I give in my Human Biology classes--especially if a really interesting story (like one about a guy with green blood!!) comes out in the news. How can you tell if a story you read or hear about is actually credible?

Step 1: Consider the source. I first heard about this story during my morning perusal of Boing Boing , one of my favorite sites for interesting and strange bits of non-news. Now, as much as I love these guys, I don't consider them a totally credible source. They are, after all, a blog that reads internet sources and passes on the most interesting bits to me. Don't get me wrong--when I say I don't consider them credible I don't mean I don't read their work with a stalker-like fervor then instantly look up more information on the best parts. Nope, that's exactly what I do. What I mean about "not credible" is I wouldn't source boingboing.net in my next publication, or quote their words as fact without doing some extra research.

Source of information is very, very important when determining if a bit of information is credible. What is the author's credentials? Where is the work published? Most scientists are very proud of their background and work, so they will announce it to the world. It shouldn't be too hard to figure out if the person knows what they are talking about. (Quick hint: most general journalists, yes, even those who work for NPR, have a very basic knowledge of science and biology, and routinely make glaring errors in articles. Make sure you double check the facts!) Make sure the information is published somewhere where the author knows what he is talking about. This can be pretty much assured if the information is published in a journal that is peer reviewed, meaning other scientists with the same basic knowledge as the author have read the author's work and have agreed with the facts and conclusions.

Most scientific journals are peer reviewed, and are therefore considered credible sources. If you read an article that mentions the information was published in some big peer reviewed journal (like the Lancet), go and read the original article to make sure the site your reading just didn't make stuff up (which they do, sometimes). Which brings us to:

Step 2: Make sure the information is real. Because many journalists and bloggers are not scientists, they can easily misread information in a credible source, or misunderstand conclusions. If you read a part of an article that just doesn't make sense to you, look up the facts. You'd be surprised how many basic journalists seem to forget they can just pick up a high school bio book. Now, just because a writer gets some information wrong doesn't mean the entire article should be discarded. Most of the time the premise is correct; it's just the details that don't work. Look up the information and see what's what. Enjoy the green blood article and tell your friends!

DNA and RNA Base Pairing

Today's subject involves the basics of DNA and RNA. Here's the question from the GRE practice test I'll be answering:

"The complementary RNA sequence for GATCAA is...." (and then there is a list of answers).

This is actually a simple question, provided you know a two key bits of information--1) What is RNA? 2) What the hell are all those letters? I'll tell you!

I'm sure by this time in your life, no matter what level of education you currently have stuffed into your pretty little brain, you have heard of DNA. DNA is the handy short-hand for deoxyribose nucleic acid, and is a double stranded helical structure found in the nucleus of eukaryotic cells. The
double helix resembles a ladder, with two parallel sides and pairs of bases that match up and form the rungs.

These "rungs" are called nucleotides, and are made up of a sugar (in the case of DNA, that sugar is dexoyribose), one phosphate group, and a nitrogenous base. That nitrogenous base is what we are interested in today. Don't let the phrase "nitrogenous base" scare you--this is just a way for biologists to sound smart when talking about something relatively simple. In this case, a nitrogenous base is simply a compound that contains nitrogen and happens to be basic. Easy, yes? Ok, so the rungs of the double helix are made of a pair of nitrogenous bases--two of these nitrogen containing bases that pair up.

There are four of these bases involved with DNA: Adenine (A), Thymine (T), Guanine (G), and Cytosine (C), and these bases follow a concept called complimentary base pairing. This fancy sounding process simply means that each base only pairs up with the one that is likes the best, or the one that compliments it: adenine pairs with thymine, and guanine pairs with cytosine. Biologists hate writing out the full name of things, so each of these bases is abbreviated down to the first letter of its name: A pairs with T, and G pairs with C--AT, GC.

When DNA replicates, the double helix unzips, and free-floating bases pair up with their partners to form new strands. If we know the sequence of bases on one strand, we can predict what the complimentary strand will look like using complimentary base pairing:

ATTTCGGA will pair up with the strand TAAAGCCT. See how that works? The bases pair up with their favorite, and form a new strand in the process. There's the basics!

Now, DNA doesn't just make copies of itself. On the contrary, it most of the time codes for proteins that build things or activate things or deactivate things, or do any number of jobs in the cell. In order to code for these proteins, the DNA needs to get its message to the rest of the cell. It does this via RNA

RNA stands for ribonucleic acid--it looks a heck of a lot like DNA, except it is made up of the sugar ribose instead of deoxyribose. RNA is the messenger unit of the cell. It's job is to take memos from DNA, and give that information to the rest of the cell. RNA gets its memos from DNA via complimentary base pairing. Who knew?! When DNA wants the cell to make a protein, it unzips that little portion of the double helix that codes for that protein, RNA zips in and makes a copy of the information using complimentary base pairing, and zips out again to take the information to the rest of the cell.

So how can we tell the difference between RNA and DNA? Well, other than the fact that RNA is made of ribose while DNA is made of deoxyribose, they also use slightly different nitrogenous bases. While DNA uses the bases adenine, thymine, guanine, and cytosine, RNA uses adenine, URACIL, guanine, and cytosine. In DNA, adenine pairs up with thymine (AT). In RNA, adenine pairs up with uracil (AU). Just think of it as if RNA can't seem to produce a T, so it has to produce something else to match up with A. So, if I were to ask you, say, what is complimentary RNA sequence for GATCAA, you would say CUAGUU. See how that works? Every time you see a "G" you match it up with "C." When you see a "T" you match it up with "A," and when you see an "A" you match it up with "U."

Back to the question:

The complementary RNA sequence for GATCAA is:

A) CTAGTT
B) CUAGUU
C) AGCTGG
D) AGCUGG
E) TCGACC

In this case, you can immediately knock out three of the answers. Since we know that RNA doesn't produce any T's, then we can get rid of A, C, and E. That leaves B and D to choose from. We are also familiar with the concept of complimentary base pairing, so we know that G always pairs with C, and A with T/U. This is one of those questions that I suggest answering before you look at the answers, then just scanning the answers for the one that matches what you came up with. In this case, the answer is "B."

Incidentally, as I was scanning through the GRE, I noticed another question along these same lines:

When DNA is extracted from cells of E. coli and analyzed for base composition, it is found that 38 percent of the bases are cytosine. What percentage of the bases are adenine?

Because we know about complimentary base pairing now, we can figure out this question pretty easily. I've noticed that the GRE likes trying to scare test-takers by saying things like "DNA is extracted from E. coli." Don't let them! DNA is DNA, and it doesn't matter what species it's extracted from, it is still made up of those same 4 bases. (Isn't that amazing, by the way? This is why I love biology!).

The question tells us that 38% of the bases were cytosine. We know cytosine pairs up with guanine, so another 38% must be guanine. (Think about this for a second--remember that both strands of the double helix were being analyzed here, so every instance of cytosine was counted. You don't find cytosine in DNA with it's best friend guanine, so if 38% were cytosine, then 38% had to be guanine). Ok, 38 + 38 = 76% of the DNA accounted for. What does that leave? 24% of the bases must be adenine and thymine. Since these guys are paired up equally, then half of that 24% must be adenine, and the other half thymine, therefore 12% of the bases are adenine and 12% thymine. Here's the question again:


When DNA is extracted from cells of E. coli and analyzed for base composition, it is found that 38 percent of the bases are cytosine. What percentage of the bases are adenine?

A) 12%
B) 24%
C) 38%
D) 62%
E) 76%

Do you see how annoying the answer writers of this test can be? They put in all the possible numbers you could come up with when figuring out this answer: 12% (the percentage of adenine in the DNA), 24% (the percentage of adenine and thymine together in the DNA), 38% (the percentage of cytosine or guanine) and 76% (the percentage of guanine and cytosine together). However, because you know the basics of complimentary base pairing you are able to figure out that the correct answer is "A." Good for you!

Linktastic (Or: I'm feeling crappy so I can't really write....)

Ok, so today was a cruddy day. Ever heard of endometriosis? Well, I have it all bad like, and I therefore spent most of today unconscious. Fun for me! Today's post, therefore, is admittedly a bit phoned-in (I'm pretty sure the spelling is going to be bad, too). Here are some interesting links about things you should know about. Enjoy! I'll be back when I'm feeling better.

How to take multiple choice tests
The GRE is multiple choice, after all, so knowing how to effectively manage a multiple choice test is critical.


What is endometriosis?
The stupidest, worstest, most horrible thing afflicting my lower abdomen at the moment. That's what it is.

XKCD
Oh, man, is this a funny comic. Start at the beginning (his first ones are a bit strange--I think he was just doodling at first). They get really, really funny after awhile. Awesome!

The Rh factor and hemolytic disease of the newborn

This is how I'm going to structure things (at least until I figure out a better way or someone asks a question): I have gotten my hands on a variety of old GRE subject tests, and I have gone through them and read the questions. During my study groups, I have the students take practice tests and we go over the answers. I'm going to post one (or two or three) question(s) that are about a particular subject, then explain the concepts that are involved. How's that? Good! Let's get started.

Question: A homozygous, Rh-positive man (RR) marries an Rh-negative (rr) woman. Their first child is normal, but their second child has hemolytic disease (Rh disease). The first child did not have hemolytic disease because....

Alright--this questions is mostly about the Rh factor and its effect on the unborn child. First: the vocab of this question.

Homozygous--the condition of having two identical alleles for a particular gene
Rh-factor--a specific antigen present on the surface of the red blood cell
Hemolytic disease--a condition in which the red blood cells of an Rh-positive fetus or newborn are destroyed by anti-Rh antibodies previously produced in the bloodstream of an Rh-negative mother.

The first thing you need to do when reading a question about biology is to dissect the question itself. This questions has a lot of vocab and parenthesis that may cause confusion. Read the question at least twice to get at the real meat. The question introduces you to a couple with, now, two children. We learn the genotype (genetic makeup) of the parents: both are homozygous for the Rh-factor; dad is homozygous dominant for the Rh-factor, while mom is homozygous recessive.

The question is really testing your knowledge of red blood cells and the antigens present on the cells. An antigen is anything that causes an immune response. Every person has a blood type depending up on the glycoproteins (carbohydrates attached to proteins) attached to the red blood cell membrane. The lucky person who discovered these glycoproteins decided to give each type a letter: A or B. A person who has glycoprotein "A" on his blood cells has type A blood. A person who has glycoprotein "B" has type B blood. A person who has both glycoproteins on his blood cells has type AB blood, and a person with neither of these glycoproteins has type O blood.

What these blood types are missing is that "+" or "-" that you all see on your birth certificate. The positive or negative is called the Rh-factor, and either you have it or you don't. "Rh" stands for rhesus, and was named for the rhesus monkey, which is where the protein was first noticed. This protein reacts just like the other glycoproteins on your blood cells--if your body recognizes the antigen (glycoprotein) then it will not attack it. If your body doesn't recognize the antigen, then it will initiate the non specific and specific defenses to attack the perceived threat. If this was the first time your body saw the antigen, the non specific defenses would take care of the problem, while the specific defenses created antibodies to protect the body from future invasions. (Well, actually it's a bit more complicated than that, but I'll go into the intricacies of immuno-defense in a later post).

Your blood type becomes important when you need blood from a donor, or you are donating blood to someone who needs it. In the case of an emergency, hospitals use type 0- blood, since these red blood cells have no antigens on them at all, any person will accept this blood into his veins without triggering the immune system. This same idea applies to the transfer of blood from mother to child.

During most of pregnancy, the fetal circulatory system is closed off from the mother's circulatory system. The fetus produces its own red blood cells, which accept oxygen and nutrients from the mother's blood stream via capillaries in the placenta. The mother's red blood cells do not cross over to the fetus, and the fetus's red blood cells do not cross into the mother's blood stream. During the trauma of birth, however, blood exchange happens. This usually isn't that big of a deal, however. Even if the baby's blood type is different from the mom's, mom's immune system will take care of any foreign blood cells quickly (and produce antibodies against future invasion from these blood cells). A problem arises only during the second pregnancy and in relation to the Rh-factor.

If mom is Rh-positive, it doesn't matter what her child is (Rh-negative or Rh-positive) her body will not react to the child's blood during birth. Her immune system will recognize the Rh protein, and therefore not attack a cell that is Rh positive. If it encounters a cell without the Rh-factor, it won't recognize the cell as foreign because it is the protein present on the cell's membrane that identifies it as foreign. If there's no protein, there's no problem. However, if mom is Rh-negative, her body will recognize any Rh-positive blood cell as foreign, and activate her immune system accordingly. The Rh-factor is passed on via normal Mendelian genetics, with Rh-positive being dominant and Rh-negative being recessive. Therefore, it is possible to determine the possible genotypes of the child in regards to the Rh-factor using a simple Punnett square.


R R
__________________


r Rr Rr

__________________


r Rr Rr

__________________


If mom is Rh-negative, as she is in this GRE question, then her first pregnancy will proceed normally. No matter what the blood type of her baby, her blood won't come in contact with the baby's blood cells (and therefore any possible antigens) until birth. After birth, the baby is pretty much safe from any antibodies mom's immune system produces. The problem arises when mom and dad want to give junior a little brother or sister. If mom is Rh-negative and bundle-of-joy #1 is Rh-positive, mom's immune system gets exposed to the Rh antigen. Her immune system reacts accordingly, destroying the perceived threat, and producing antibodies to protect her against future invasions. If bundle-of-joy #2 is also Rh-positive, mom is already primed and ready to kill off any Rh proteins she sees. Red blood cells don't cross over the placental barrier, but antibodies do. Can you see the problem? Mom's antibodies attack the fetus's red blood cells, causing the fetus to die from lack of oxygen and nutrients, or causing the baby to be born severely anemic. This condition is called "hemolytic disease of the newborn." Look familiar? Yep! This is the disease to which the question is referring.

So, now that we know the basics, let's get back to the question:

A homozygous Rh-positive man marries an Rh-negative woman. Their first child is normal, but their second child has hemolytic disease.

This part makes sense, doesn't it? We know the genotype of both mom and dad, so we can use a Punnett square to predict all the possible genotypes of the children: Rr, Rr, Rr, and Rr.

It appears that all the children will be heterozygous for Rh-positive. Now, we know that there may be a problem between an Rh-negative mother and an Rh-positive fetus due to mom's immune system. However, mom's immune system is not exposed to the Rh antigen until the moment of the first baby's birth, so baby #1 is protected. When mom gets pregnant again, though, the child is afflicted by hemolytic disease. "Hemo" refers to blood, while "lytic" refers to bursting; "hemolytic" is the bursting of red blood cells. Bad! This occurs because mom's immune system is primed and ready to kill off the Rh-antigen the moment it sees it, so baby #2 is attacked as soon as he begins to make red blood cells.

Good! So there is the main concept behind the question. Let's get to the actual question part, though:

The first child did not have hemolytic disease because....

Well, can you answer the question? Yep, the first child didn't have hemolytic disease because mom's immune system had not yet been exposed to the Rh-antigen and therefore did not have any antibodies capable of crossing the placental barrier and attacking the fetus's red blood cells.

Here are the multiple choice answers given to this question:

A) the child was heterozygous (Rr)
B) the child lacked the Rh antigens
C) the mother had a previous blood transfusion that protected the child against antibodies
D) anti-Rh antibodies present in the mother were destroyed by the child's immune system
E) anti-Rh antibodies were not induced in the mother until the delivery of the child

So, given what we know, the answer to this question is E. Yes, the child was heterozygous (Rr), but this does not answer the question, and is not the reason the child did not have hemolytic disease. Because the child was Rr, we know he had the Rh antigens (remember Rh-positive is the dominant trait), so answer B doesn't even make sense. Answer "C" just seems ridiculous to me, and hopefully to you, too. Blood transfusions don't change the mom's immune system, nor what diseases she is protected against. A blood transfusion is primarily used to ensure the presence of adequate red blood cells and blood volume in the circulatory system. It has nothing to do with protecting a fetus against antibodies. The growing fetus is still building its immune system, so he must rely on mom for protection and immunity. He doesn't yet have the capacity to fight off foreign cells, so he has no defense against mom's antibodies. Therefore, option "E" is the correct answer!

How is it, then, that Rh-negative moms have more than one child? Why aren't they all still born? Scientists attacked the problem of hemolytic disease some time ago. One of the first questions a doctor asks a pregnant couple is their blood types. If mom is Rh-negative and dad is Rh-positive, then during the birth (or soon thereafter) mom will be injected with a serum named RhoGAM, which contains antibodies against the Rh antigen. This serum takes care of any Rh-positive red blood cells circulating in mom's blood, so her immune system doesn't have the chance to get all annoyed. She doesn't make any of her own antibodies against the Rh antigen, and her future children are protected.

Questions? Comments? I hope this helped!

Ah, the GRE!

Well, kiddies, it's that time of year again. Now that the seniors have walked off our intrepid campus and into the sunset, the juniors begin to plan their (hopefully) final year at school. Whether you are finishing up four years of high school or 7 years of graduate school, if you want to go on for an even higher degree then you have the unsurpassed pleasure of sitting for a variety of standardized tests. Lucky you! The problem is this: many great schools use your GRE scores as a way to weed out the slackers from the future Einsteins (well, Einstein was really bad at standardized tests--so maybe not future Einsteins...maybe Bill Gates? Nope, bad at tests, too...Ok, future moderate-highly paid managers of large already established businesses). There is a plethora of study classes out there--well, a plethora if you have nearly a thousand dollars just lying around doing nothing. Huh? Do ya? Yep. Me neither. Does it seem fair to you that you are expected to sit for a test for which a good portion of the other test takers had professional help in preparation? I certainly don't.

Let me introduce myself. I'm a lecturer in biology at San Jose State University. I've been teaching general biology, human biology, anatomy, physiology, cell biology, botany, zoology entomology, microbiology, and bacteriology for the better part of a decade. As I teach these classes and watch my students graduate and go on for advanced degrees, I have fielded many questions about how to study for the GRE subject tests, what subjects are covered, and how to best prepare if money is an issue. I began organizing GRE study sessions several years ago, and have drawn upon my research and experience to help out students facing the mountain of study needed to get ready for this subject test. So far, so good!

So what am I doing now? I thought that since there was so much interest in my on-campus groups that I'd start a blog where I'd post my lectures each day in an effort to archive and share them with a larger audience. I have so far focused only on the biology subject test, but I am thinking of expanding this to other subject areas and the general test as well. I'll let you know! Until that time, I will be posting new lectures on various biological subjects found on the GRE, along with study tips, anecdotes, and success stories as they come to me. I do hope this helps. If you have any questions, just ask and I'll do my best to answer as soon as possible!

Adrienne