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Category Archives: Education

Biology / iOS in the classroom / microbiology / genetics / evolution

The Human Genome Project as a teenager

Human-Genome-Page-From-BookSeveral classes ago, we were talking about some modern therapies and research being done and I mentioned how the human genome was sequenced in the mid 90s as the world looked on speculating about the wealth of benefits that would ensue. We talked a while about how this sequencing effort gave us some idea of the size of the human genome as well as a number of many other organisms. The one of my students asked what real, clinical good had come from this expense of time, money and effort.

I talked about some of the benefits this information had to basic science and how we were now nearing a time that genome sequencing was becoming feasible as a clinical tool.

Several years ago, during the tenth birthday of the human genome , Nature magazine polled scientists about the importance of knowing the complete sequence of the human genome. At that time, most scientists felt that the most value rom the project was to be found in improvements of the sequencing technology itself and to basic research. Very few researchers thought that clinical medicine was receiving any benefit from the project.1

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2010 Nature Magazine Poll of Scientists

A few years ago, this sort of test was so difficult and expensive that it was generally only available to participants in research projects like those sponsored by the National Institutes of Health. But the price has plunged in just a few years from tens of thousands of dollars to around $7,000 to $9,000 for a family. Baylor College of Medicine and a handful of companies are now offering it. Insurers usually pay.2

So, what tangible benefits have been realized?

In my mind, I was thinking of a variety of changes that this had harkened in the research community and how it was a great tool to have a frame of reference for asking questions like, “Do I have any mutations in my proto-oncogenes or tumor suppressor proteins that may lead to cancer?” But I was unaware of any specific anecdote that would put a human face on the story and provide evidence of benefit.

However, I was listening to Science Times, the podcast for the New York Times Science pages on the way to class this morning and I heard just that. This article discusses several of these cases, one with a life-changing positive outcome and another with little tangible benefit as yet.

Perhaps we are starting to see spillover into clinical applications, or perhaps, as Eric Lander, a leader of the Human Genome Project, said today in an interview with WBUR’s Here and Now , it takes decades to see the benefits of breakthrough technology get to the clinic. In that case, this is just the beginning and we have much to look forward to.

In the mean time, go check out the genome data and play around. You never know what you might learn.

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Being Human

References:

1.  http://www.nature.com/news/2010/100623/full/4651000a.html

2. http://www.nytimes.com/2013/02/19/health/dna-analysis-more-accessible-than-ever-opens-new-doors.html?ref=science

 
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Posted by on February 20, 2013 in Education

 

Son of HeLa to speak at JCCC Feb 21

Last week in Microbiology, we mentioned the use of HeLa cells in the context of informed consent. This week, I found out that the son of Henrietta Lacks is appearing to speak at JCCC this month.

From the JCCC website:

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What is it like to know that cells from your mother were taken without her consent to create a global strain of cells used the world over?

David “Sonny” Lacks will answer that question and more when he visits Johnson County Community College.

In an Actor’s Studio-like conversation at 11 a.m. Thursday, Feb. 21, in Polsky Theater in the Carlsen Center, he’ll discuss his mother, Henrietta Lacks, a poor tobacco farmer and the title character of the non-fiction bookThe Immortal Life of Henrietta Lacks by Rebecca Skloot.

The event is free, and the public is invited to attend.

The Immortal Life of Henrietta Lacks is the 2012-2013 Common Read selection at JCCC. Students from Composition I classes were assigned the book, as were students from the dental hygiene and practical nursing programs.

Sonny Lacks’ appearance is a capstone to months of reading, writing, studying and discussing Henrietta Lacks, the originator of the famous HeLa cells.

HeLa cells are instrumental in medical research, gene mapping, in vitro fertilization and more, yet the woman behind these cells was all but forgotten until Skloot discovered Lacks’ name and history.

Skloot learned that in 1951, Henrietta Lacks unknowingly “donated” cells – both cancerous and cancer-free cells – that had an amazing propensity for growth. The cells were known as the “HeLa” strain, so named after the first two letters of Lacks’ first and last name.

In his appearance, Sonny Lacks will share what it meant to find out – decades after the fact – that his mother’s cells were being used in laboratories around the world, bought and sold by the billions. His visit puts a personal face to big issues such as the dark history of experimentation on African Americans, the birth of bioethics and the legal battles over “informed consent.”

Lorie Paldino, adjunct instructor, English, and chairperson of the Common Read program, said she thought Sonny Lacks’ visit was the perfect way to personalize those issues.

“It’s a great way of getting the family’s perspective,” she said.

The JCCC Common Read Program is in its fourth year. Common read programs have grown in popularity in communities across the nation. Colleges and universities have used such programs to infuse fresh academic and social experiences, promote critical thinking and reflection, and bolster reading beyond the classroom.

Sonny Lack’s appearance is also part of the college’s Scholar-in-Residence program, designed to bring visiting scholars to students, faculty and the public. It is co-sponsored by the English and Journalism division.

 
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Posted by on February 18, 2013 in Education

 

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RadioLab – Speed

flash-crash-dow-popupWhile listening to the latest RadioLab, “Speed” story about automating stock trading, I could immediately remember being in the kitchen, listening to NPR and hearing the updates on the crashing Dow. The flash-crash of May 6, 2010. Stock analysts were going bananas describing an unprecedented drop in the markets that was both incredibly steep and incredibly deep.

I wanted nothing more than to put any money we had into a Dow indexed fund – it was painfully obvious that this was just a computer problem and that it should correct soon (I thought perhaps over the next few weeks). Of course it was impossible to get into my ING sharebuilder account (a great saving device that everyone should have – I started mine as a poor graduate student putting just $50-100 a month into my account).

But the thing that really struck me as I listened was how like biological evolution the race for speed in stock trading is. It was mentioned that speed always wins in the market, the faster you are, the earlier you can act on key information and make easy-money trades to take advantage of

even minute swings in the price of stocks. (OK, an aside: I can’t ignore it, how is this investing? So much of this segment uncovered the truth about so much big money on Wall Street… it’s not about investing, it’s about taking advantage of the system and making money on glitches and technicalities. It’s not clear how this supports – or even has anything to do with entrepreneurial endeavors.)

The race for speed was compared to an arms race where warring parties take every opportunity to turn an advantage over their peers. But what about diminishing returns on these

investments? Can there be an end to this sort of arms race? Despite the apparent cost and distraction of focusing on details like the length of wire between your home office and the NYSE, the game is unavoidable. Why? Because it IS a game. And both game theory and evolution by natural selection can inform us about why these battles go on, and why they can’t end.

In game theory, there is the economic /  trust game referred to as the prisoner’s dilemma. Here, I lifted this description of the game from wikipedia:

“Two members of a criminal gang are arrested and imprisoned. Each prisoner is in solitary confinement with no means of speaking to or exchanging messages with the other. The police admit they don’t have enough evidence to convict the pair on the principal charge. They plan to sentence both to a year in prison on a lesser charge. Simultaneously, the police offer each prisoner a Faustian bargain. If he testifies against his partner, he will go free while the partner will get three years in prison on the main charge. Oh, yes, there is a catch … If both prisoners testify against each other, both will be sentenced to two years in jail.”

The game’s outcomes are presented in this grid, making the dilemma clear:

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Biggest payoff: convince others that you will keep your silence with them, then sing like a canary and go free while your friends rot in jail.

In this game trust is nearly impossible, but it is the only way both prisoners can benefit. But who can be trusted? Life would be so much easier if we could, but experience tells us that there will always be cheaters in games of trust and it’s best to bet on deception.

Why does this remind me of biology?

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On the left, all trees ‘agree’ to keep to a set height and no one gets shaded out. On the right, one cheater takes advantage of the others’ trust and grows tall.

Because evolution works the same way. Every organism does everything it can to get ahead. Think of trees in the forest. If only the trees could come to a deal: “None of us will grow above ten feet tall. We can all save energy that way and be better off.” After all, the whole benefit in growing tall is to monopolize the sun and shade out your neighbors. But as soon as one tree breaks the bargain, all bets are off and the arms race begins again.

Amazingly, if the arms race is allowed to go on, a situation much like that depicted on the left occurs. The only difference is that all the trees have expended much more energy and they all stand taller, evening out at the point that physics and environmental conditions become limiting.

 
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Posted by on February 11, 2013 in Education

 

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DNA Replication

DNA Replication occurs during the S (Synthesis) phase of cell cycle. The purpose of DNA replication is to create an identical copy of all the DNA in the cell so that, following cell division, both daughter cells will have complete copies of all the information required to build a cell and do all the things the cell does.

Data from several laboratories were elegantly integrated by the work of Watson and Crick to describe the structure of DNA as comprised of two anti-parallel strands bound together by polar (hydrogen) bonds between one purine and one pyrimidine.  Including:

1. Erwin Chargaff ‘s observations that

a) DNA was 50% purine (A and G) and 50% Pyrimidine (C and T) and

b) the proportion of A = the proportion of T; the proportion of C = the proportion of G .

2. Rosalind Franklin’s X ray crystallography data that indicated that DNA had a regular, repeating pattern and the molecule was of a specific width.

3. Oswald Avery’s group along with Hershey and Chase established that DNA was the genetic material (therefore making the structure of this molecule of high importance)

4. Knowledge of the distance between molecules engaged in hydrogen bonds.

5. Knowledge of the chemical properties of nucleotide molecules, comprised of hydrophilic deoxyribose sugars and phosphate groups and hydrophobic bases.

Altogether, this information provided enough background for the pair of researchers to arrive at the structure of DNA by engaging in model building.

How this all leads into the mechanism of DNA replication comes down to the following brief statement at the end of Watson and Crick’s Seminal Paper of the structure of DNA:

“It has not escaped our notice that the specific pairing we have postulated immediately suggests a possible copying mechanism for the genetic material.”1

 

What did they mean by this?

“The novel feature of this structure is the manner in which the two chains are held together by the purine and pyrimidine bases…joined together in pairs, a single base from one chain being hydrogen-bonded to a single base from the other chain… [O]nly specific pairs can bond together. These pairs are: adenine…with thymine…, and guanine… with cytosine.”1

So, if the sequence of DNA bases on one strand dictates the sequence of the other, then each of the strands can be used as a template to make another. When this is done with each of the two strands, the result is two identical DNA molecules.

It’s one thing to say that it hasn’t escaped your notice that there is a mechanism for duplicating DNA inherent in its structure, but quite another to say that you know how it works.

This was the question that Matthew Meselson and Franklin Stahl were to solve in 1958.2 They imagined three possibilities:

  1. A Conservative method of replication – the original DNA splits open and new strands are made based on that information, then the original strands comes back together and the new strands zip together. We conserve both strands of the original copy.
  2. A Semi-Conservative method of replication – The original DNA splits open and new strands are synthesized to pair with each of the originals, the new DNA then exists with one original strand and one new one.
  3. A Non-Conservative / Dispersive method of replication – Frankly, I don’t know how this would work, but the result would be two new DNA molecules where bits of each strand of each molecule may be from the original or the new DNA.

How to distinguish between these methods?

Meselson and Stahl devised an experiment that in which they grew the bacteria, E. coli in broth containing DNA made of two different isotopes of Nitrogen. In one broth, let’s call it the ‘light’ broth, they had the light form of DNA with 14N, in the other, ‘heavy’ broth, they had the heavy form of DNA with 15N.

One really is heavier than the other. When they are centrifuged, they will come to rest at different ‘heights’ in the tube.

If the bacteria is grown in broth containing only the heavy DNA, and that DNA is harvested and spun down, you would see a tube like (a) containing a single band of the heavy DNA.

If than bacteria was moved into a new medium containing light DNA, and DNA was allowed to replicate once,

Assuming  semi-conservative or dispersive models of development – you would see (b) a single band of intermediate density – because all new DNA would be partly heavy and partly light.

Assuming the conservative model – you would see (c) two distinct bands – one heavy and one light.

So this immediately tests for or against the conservative model.

The actual result was a single intermediate band was found. This eliminates the conservative model of replication, but a second round of replication in the light broth is required to discriminate between those two models.

If the Semi-Conservative model is correct, then the intermediate band would remain, but a new light band would show up (d).

If the Dispersive model is correct, then the intermediate band would inch upwards (become lighter) as more light elements are mixed in randomly within the strands. (e)

What they found was exactly like that pictured in figure d. Further, if the bacteria were allowed to grow for more generations, the ‘light’ band of DNA would become larger as more light DNA is created, while the intermediate band will remain indefinitely.

 

 

Meselson and Stahl with Chase

 

 

References

  1. Watson. J. D. and Crick F.H.C.  “A Structure for Deoxyribose Nucleic Acid”  Nature 171, 737-738 (1953).
  2. Meselson, M. and Stahl, F.W. (1958). “The Replication of DNA in Escherichia coli”. PNAS 44: 671–82.
 
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Posted by on November 27, 2012 in Education

 

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Aside

The Human Microbiome Project is an NIH-sponsored initiative with the goal of identifying all of the many kinds of micro-organisms that we harbor in our bodies as healthy individuals. This is an interesting project for a number of reasons. First and foremost, because we have long assumed that micro-organisms are present only when we are sick – not healthy. Also, what we learn from this project can have a great impact on how we use antibiotics to treat many of the infections we get that do make us ill (often demanding them as patients even when they will do no good as when we have a viral infection like flu or the common cold). Lastly, we are now learning that alterations in the microbiome of our gut or elsewhere may contribute to more subtle changes in our health, like the incidence of allergy, asthma or obesity.

There have been a number of articles on this topic since the publication, in June 2012, a reference database of what constitutes a healthy microbial population. An excellent thorough examination of these data and their application was published in The New Yorker’s Annals of Science column by Michael Specter, ‘Germs are Us, Bacteria make us sick? Do they also keep us alive?’ Therein, Mr. Specter examines the impact of many modern developments that may be tweaking the population of microbiota that we harbor (especially in our gut), from the use of antibiotics, to the fiber content of the food we eat, to our obsession with cleanliness.

H. pylori

Amongst the scientists doing work that Mr. Specter refers to is Dr. Martin Blaser of New York University’s Langone Medical Center. Much of Dr. Blaser’s work has focused on the role of Helobacter pylori in health and disease. This organism is of special interest because a number of years ago this very organism was identified as causing gastric ulcers. In fact, I use this year after year in my own class as an example of how Koch’s Postulates were applied to pinpoint the cause of these ulcers. In those experiments it was shown that many ulcers have populations of H. pylori growing in them and that these organisms can be transplanted into the gut of a healthy patient and cause the same disease. Further, treatment that kills H. pylori results in amelioration of the ulcers.

Nevertheless, Dr. Blaser’s work does not focus on the role of H. pylori in disease, but rather on its role in maintaining the health of the organism. He, and others, have shown that ridding the body of H. pylori may result in an increased incidence of gastric reflux, asthma and obesity. This relationship is discussed in a short article in The New York Times from 2011. It may not be that H. pylori itself is responsible for all of these conditions, but perhaps other organisms that are eliminated by the same drugs that kill H. pylori contribute to these conditions.

Obviously, there is a lot going on within our bodies and a holistic view of how our actions impact a wide variety of systems may be required in order to successfully design treatments that target the ill-effects of some micro-organisms while preserving the health-promoting effects of others.

I’m definitely going to put some more work into researching this topic so I can incorporate a discussion of it in my microbiology class next semester, so don’t be surprised if you read more about this here in the future.

The Human Microbiome Project at Work

 
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Posted by on October 21, 2012 in Education

 

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Aside

A static view of the tree of life

Onezoom.org is an effort o display all of life and its relationship with one another in a single ‘zoomable’ phylogenetic tree. Currently one the mammalian branch of this tree is available, but it is still extraordinarily interesting and gives an idea of the grand scope of the project. Here’s an introductory video showing the intent of the project and why the organizers developed it in the way that they did.

Here’s a link to the site itself where you can try out the viewer. — By the way, +1 point on the upcoming chapter 5 quiz for any of my students who try this out and can email me a screenshot of where humans fit into this tree. I realize this requires you to go to the site, try out the viewer, find humans AND work out a way to visually document that -but there it is.

http://www.onezoom.org

I would like to thank nothinginbiology.org for pointing me toward this resource. I tried to reblog their post, but I ran into some silly technical problems and found it easier just to write up something myself.

OneZoom

 
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Posted by on October 20, 2012 in Education, Uncategorized

 

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Aside

ImageScientific method as a lens to view the world                     

Science has a problem in telling its stories to the world. The problem stems from the way that science is done and the way its discoveries are published in academic journals not known for their mass appeal. In science, seeing something happen once or hearing about an occurrence might lead one to get in the lab and ask a question, but it is never itself acceptable as an answer. Instead, multiple repetitions of an experimental question are asked until consistent results are found under controlled conditions. Compare this to watching the news or reading the paper and you’ll find a drastic difference. Mass media loves the anecdote of ‘one family’s story’ or ‘what happened to my kid.’ Stories appeal to our natural tendency to relate to people and to incorporate the underlying morals or lessons into our broader worldview. He-said-she-said arguments are presented as fair and balanced even when balance is unjustified. With this in mind, consider this story of how the birth of the scientific method changed the world we live in.

The events of the late 15th and early 16th centuries ushered in a new age. Not just in the discovery of new land to be conquered and populated by western civilizations, but also in the way westerners saw the world and their place in it. Suddenly there was half a globe of terra incognita. As Columbus revolutionized our geography, Copernicus and Galileo revolutionized astronomy. But what was good for cartographers and astronomers wasn’t so good for the royalty and the church, who had been comfortably enjoying in the status quo.

At that time, the vast majority of people were ruled by the very few who held their power by divine right. What they said was both fact and law and any who differed in opinion did so at their own peril as autocracy seldom views challenge or change as good.

But cracks were beginning to show.

Between the discovery of the west and the mounting evidence for heliocentricity, came the greatest schism the Christian church has ever seen, hammered home when Luther nailed his 95 theses to the church door in Wittenberg, Germany 1517. Within a century a new world was discovered, the earth was shifted from the center of the universe to a body orbiting the sun and even God’s own voice on earth was being challenged due to a poor financial decision granting the sale of indulgences. How unfortunate for those in power that the printing press, which Johannes Gutenburg had introduced a half century earlier, made it so easy for this news to circulate around the globe amongst a newly literate population.

By the middle 17th century, Bacon and Descartes were formalizing the rules of logic and, more specifically, of scientific inquiry. Their texts, Novum Organon and Discourse on Method display a new desire for evidence-based reasoning rather than simply accepting facts ad hominem – even in cases where the hominemis the Pope himself. Bacon wrote, “The logic now in use serves rather to fix and give stability to the errors which have their foundation in commonly received notions than to help the search after truth. So it does more harm than good.” That is, too much effort is being spent defending what we already think is true rather than just following what the data tells us. This is exemplified by Ptolemy’s

How Ptolemy saw the solar system

complex system of interlocking circles and the complex movements they require in order to explain the wanderings of the planets in the night sky. An excellent demonstration of this backwards logic can be found at http://people.highline.edu/iglozman/classes/astronotes/retrograde.htm

With the upset in worldview brought by the renaissance and its new rigor for asking scientific questions along with a few intervening centuries, one would think that we would be more discerning in our beliefs today. We should be open to new ideas that challenge accepted dogma, and be in possession of tools to discriminate between unfounded speculation and well-supported theories.

Or, perhaps not.

In many ways, we are just as easily swayed by ad hominem arguments, faulty logic and satisfaction with the status quo as we were seven hundred years ago.  But it’s not entirely our fault. We’re not built to think critically, rather, we make quick judgments based on what we see in front of us. The ability to make split second decisions were likely required to save our skin in the time of Hobbes’ “state of nature.” While labored, methodical reasoning would reason us right into the lion’s mouth. The difference today is that we are vastly more educated than our forbearers, possibly smarter -if rising IQ scores can be taken at face value- and, frankly, we do have the time to practice methodical reasoning. Rarely do we need to make life saving fight or flight decisions in modern life.

Science has taught us that the universe may not be as we see it. In fact, our senses are fooled all the time. Sticks don’t bend when we put them in water, a continuous tone may appear to change pitch as the source approaches or recedes from the observer and quantum mechanics tell us that all the matter of the world is nothing like what it appears to be. Our senses tell a variety of lies to us, but nature does reveal her laws with careful study.

Understanding scientific method is teaching oneself to remain impartial to results of experiments, to ensure that the tests applied are rigorously designed to disprove  – rather than support – your hypothesis, and to rely on the power of statistics to interpret your results rather than being swayed by anecdote or a desire to see a predetermined outcome. None of this comes easily. As I said above, we are a storytelling people, stories are the lenses through which we view the world. It’s a lot easier and exciting to believe an anecdote than it is to understand the truth. But it’s often worth the effort and sometimes there might be an interesting story behind the science too.

An old essay I wrote about the scientific method

 
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Posted by on October 20, 2012 in Education

 

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Aside

Who’s doing what here and why in this famous painting depicting one of the preludes to a major battle that turned the tide of the war in favor of the Continental Army?Image

Insight into an Extra Credit Question

 
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Posted by on October 19, 2012 in Education

 

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Crossover events in Prophase I of Meiosis

There are two mechanisms for establishing diversity amongst progeny that are employed in meiosis. The first is independent assortment, which is the random distribution of chromosomes into sex cells, the second is crossover events that randomize DNA between paired homologous chromosomes.

Recall that in Prophase I pairs of chromosomes come together. This will ensure that when the chromosomes are distributed between the two daughter cells produced in Meiosis I each cell gets one of each pair. The pairing forms a structure known as a tetrad (referring to the four chromatids of the paired chromosomes). When the chromosomes are joined in this way it is possible (indeed likely) that there will be breaks that occur and swapping of genetic material from one chromatid to another.

Here’s a good (but dry) animation of this process presented by McGraw Hill:

Thomas Hunt Morgan ran one of the first labs studying crossover events (he was looking at fruit flies). We’ll be looking at his work in my class later in the semester, but here’s a preview that might help visualize what is happening using Morgan’s own sketches. This is the same process as described above, however Morgan only drew one chromatid for each chromosome – this does make the illustration simpler, but keep in mind that there are two chromatids present in the chromosomes of organisms during this stage (Prophase I)

Top – paired chromosomes prior to crossover; Middle – crossover occurring; Bottom – Chromosomes following crossover

 
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Posted by on October 16, 2012 in Education

 

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Cell Cycle and Cancer

Cell Cycle in intimately connected to cancer because, in essence, cancer is a disease of cell cycle dysregulation. The purpose of regulating the cell cycle is to maintain genomic integrity, therefore the checkpoints of cell cycle progression specifically interrogate the DNA’s suitability to replicate, to divide and to be assorted into new, ‘daughter’ cells.

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If a cell replicates DNA when there is damage to the DNA, then poor copies are perpetuated. If a cell commits to division when there is DNA damage, the same result might ensue – i.e. daughter cells may receive poor copies of the DNA. If a cell divides when chromosomes are not properly assorted then neither cell is healthy.

All three mechanisms have the same goal: ensure high fidelity copying.

With cell cycle checkpoints intact, cells can only pass when their DNA is in good condition or when chromosomes are being handled properly. The result is one healthy cell gives rise to two healthy cells. If a cell reaches a checkpoint and damage is detected, then the cell ‘arrests’ cycle progression for a short period of time. During this arrest, the cell has the opportunity to rescue the DNA and resume cycling. If this does not happen, then the cell is triggered to commit apoptosis –  cellular suicide. In this was, the cell gives its life for the good of the organism.

In this way, the cell is very analogous to a bee stinging an intruder. Although the bee will die now, it has contributed to the good of the colony in its sacrifice. After all, the worker bee cannot reproduce herself, her genetic heritage is intimately tied to the fate of the colony and its queen. Similarly, the cell dies to preserve the organism against what might be a harmful alteration / mutation. And, like the bee, this cell likely could not reproduce by itself anyway, it’s genetic heritage is tied to that of a larger body where only the gonads produce reproductive cells.

When cell cycle checkpoints are not functional, poor copies of DNA / cells get through. Furthermore, these cells are now inherently unstable because they have a compromised checkpoint, and additional errors may accumulate. Sometimes these errors disrupt other regulators of cell cycle, leading to a compounded problem. Over time, these cells may develop into cancerous cells.

The other point of cell cycle regulation is in the midst of mitosis, during metaphase. At this time, the cell has bound the chromosomes with spindle fibers that attempt to shorten and pull the chromosomes to a flat plane in the middle of the cell called the metaphase plate. The checkpoint here is to find out whether every single chromosome has attached to each side and each daughter cell will get the correct number. If this fails, cells will have incorrect distributions of the chromosomes and are unlikely to survive. Further, if these cells did survive, they would never be able to correct the error.

Here, the bee analogy would be too strained to continue, but it is not too difficult to see that when a cell disentangles itself from preserving the health of the body and instead looks only after its own short-sighted interests that these cells will grow and compete directly against the rest of the body for space and resources. Initially, when a tumor is small, this may have little consequence, but as a tumor becomes larger or more dispersed in the body, this selfishness can severely impact the larger organism, ironically (for the cancer cell) undermining even the tumor’s self interest.

 
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Posted by on October 14, 2012 in Education, Uncategorized

 

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