Why should the amoeba, Pelomyxa palustris, be of such interest to cell biologists and evolutionary biologists? There are probably several reasons for this, so don't stop with one item. Explain your answer fully.
Of what significance to cell and evolutionary biologists is the relationship between reef-building coral polyps, and the zooxanthellae which inhabit their tissues?
1. For the first two billion years of life on earth, the only thing that existed was single celled bacterium. This began to change when the eukaryotes were formed, but stuck somewhere in the middle of the two is the amoeba Pelomyxa palustris. This amoeba differs from most eukaryotes for two main reasons. The first being that it doesn’t divide by undergoing mitosis, but it uses a way that is much more similar to that of bacteria. This process is completed by pinching the nucleus into two separate parts, and cell membranes are formed around each of the divided nuclei. (Johnson and Raven 693-694)
The second major difference is because all of the eukaryotes presently, have organs like the mitochondria and the internal membrane system. In the Pelomyxa palustris, however, the mitochondria is missing, and in its place are two kinds of bacteria that carry out the same role of producing the energy for the cell’s survival. This is extremely important to biologists because it is perhaps the missing piece in the evolution of the mitochondria, from the prokaryotic cells to the eukaryotic. (Johnson and Raven 694-695)
The whole evolution process of how the mitochondria was created is called endosymbosis. Scientists have concluded that the Pelomyxa palustris eventually wrapped itself around an aerobic bacterium, and in the cell membrane, this bacterium evolved into what is today, the mitochondria. (Johnson and Raven 695)
The range of sizes that the amoeba has been found in is also very unusual and interesting. It can be found at any size, from less than 100 microns to more than 5,000 microns. Not many eukaryotes carry this characteristic of being able to differ in size by a factor of fifty without automatically creating several different species designations. (Howey)
Coral reef-building polyps and zooxanthellae both partake in a relationship that is beneficial for both parties, called mutualism. The zooxanthellae produce enough energy to continue the reef’s growth, and in turn the reef provides the photosynthetic symbionts with the protection from a shelter, and access to the light which is necessary for the algae’s photosynthesis to occur. (Knowlton and Rohwer S51)
One day of photosynthesis provides the coral with more than one day of energy, so if the zooxanthellae is later rejected by the coral, or for any reason removed, the coral has time, but only a small amount to find and house more algae before its energy is used up and it dies of coral bleaching. With situations like this increasing as of the 80s, coral reefs are becoming more and more scarce. This is a problem because coral reefs are more than just a tourist industry for costal countries. Aside from being the equivalent of the rainforest under the water and being the home for a quarter of all marine life, over thirty-five million acres of coral reefs have already been ruined. (Hopkins)
What is so unusual about the zooxanthellae is that there are several different groups of them that are all genetically diverse. It is possible for these different groups to all co-exist in the same reef, just like it’s also possible for algae living in different coral reefs far apart to genetically be the same. The reason for this to be able to happen is because of a symbiotic relationship in which the zooxanthellae and the coral both evolved separately, and not in permanently associated lineages. When both symbiots are allowed to evolve separately, it is the symbiotic relationship between the two that is driving the force. This is important because without the coral the zooxanthellae would die, and without the zooxanthellae, the coral would die, so still being able to evolve independently, it shows exactly how mutually beneficial their relationship is. (Knowlton and Rohwer S52-S55)
What is inherited maternal myopathy and cardiomyopathy?
How does this disorder differ from, say, a heart attack caused by tobacco,
alcohol, and food abuse?
From a heart damaged by viral infection?
From a hereditary cardiovascular disease?
2. Maternally inherited myopathy and cardiomyopathy are both disorders involving a dysfunction of a muscle tissue. The difference between the two is that myopathy can be the dysfunction of any muscle tissue, while cardiomyopathy is a dysfunction specifically of the heart muscle, and it can causes it to stiffen up, or to become thick and enlarged. The main purpose for the myocardium is to contract, therefore pumping the blood out of the heart. During cardiomyopathy, the heart becomes weak which makes the job of pumping blood to the heart a much more difficult task. The heart, when it is unable to have blood pumped to it, is deprived of the oxygen that is in the blood and necessary for survival. (The Cardiomyopathy Association)
There are four main variations of cardiomyopathy, including dilated cardiomyopathy, restrictive cardiomyopathy, and hypertrophic cardiomyopathy, and arrhythmogenic right ventricular cardiomyopathy. During dilated cardiomyopathy, the heart’s muscles begin to dialate and the enlarged is heart is rendered weak. When it is unable to pump blood, fluid can build up in the lungs or tissues of the body. The cause of this disease is said to be that of an intrinsic heart muscle problem.
The least common of the variations is restrictive cardiomyopathy, where the heart muscles only stiffen up, making it difficult for the muscles to complete the necessary contractions in order allow blood to enter the heart. The most common variation, Hypertrophic cardiomyopathy, occurs when the muscles in the heart thicken without any known cause, and sometimes it can lead to the stiffening muscles too. This condition is passed down every generation, usually not skipping any, and both males and females are able to pass it down, but maternally inherited myopathy and cardiomyopathy is passed on genetically through the mother since the mutations are found in mtDNA, and these point mutations are only able to be transferred by women. Arithmogenic right ventricular cardiomyopathy is the most recently discovered of the variations, and it occurs when scar tissue and fatty tissue begin to take over and replace the heart muscle. During this process, the heart’s right side will eventually dilate as the muscle is being weakened and replaced by unhealthy tissue. (The Cardiomyopathy Association)
First, maternally inherited myopathy and cardiomyopathy are the result of a genetic predisposition that is pre-decided in the miDNA. Not all variations of cardiomyopathy are only caused from their genetic pre-destination though, drinking alcohol in excess amounts can cause dilated cardiomyopathy to set in, and tobacco, alcohol, and food abuse all contribute to the risk of having a heart attack. Drinking excessively and smoking both raise blood pressure which makes the heart have to work harder to get blood circulating back to it. During cardiomyopathy, there is still pressure on the heart to work hard, but for reasons that aren’t always self-inflicted, or built up over time. When people do abuse food by overeating, or just having an unhealthy diet, they allow lots of cholesterol to enter their system, and during a heart attack, these fatty deposits are responsible for slowing or blocking blood flow. When the blood flow of the heart is flowing slowly during cardiomyopathy, it is because the heart’s muscles have all grown thicker. (The Cardiomyopathy Association)
There are also incidences of heart damage as a result of viral infections, and the damage to the heart may have been done during the initial infection. Another side effect of viral infections occurs when the virus tricks the body’s own immune system to attacking the heart, resulting in an auto immune disease. (The Cardiomyopathy Association)
Heart damage can occur from any hereditary cardiovascular disease. One positive part of hereditary cardiovascular diseases are that they can be predicted and there are different things a person with hereditary heart disease in their family can do to minimize risks by heeding the precautions that go along with it. Both of the diseases lead to slowed or stopped blood flow to at heart, but the cause of cardiomyosis is not always known or always from a gene mutation. (The Cardiomyopathy Association)
Prepare a list of 20 specific chemical compounds suspected of being
carcinogenic, mutagenic, or teratogenic. See if you can find 5 compounds from
your list whose actions can be linked to mutations of specific genes.
Briefly explain how mutagenicity of a compound is determined experimentally.
- Benzopyrene
- Nitrosamines
- Dimethylbenzoanthracen
- Polycyclic Hydrocarbons
- Carbon Monoxide
- Pyrene
- Polycholrinated Biphenyls
- Carbon Tetrachloride
- Hydrazine Sulfate
- Diethylstilbestrol
- Selenium Sulfate
- Methylene Chloride
- Antimony Trioxide
- Thalidomide
- Bromodichloromethane
- Cobalt Sulfate
- Hexachloroethane
- Thorium Dioxide
- Kepone
- Nitrosonornicotine
- Phenolphthalein
Benzopyrene, a carcinogen found in soot and cigarette smoke can cause tumors and malignant carcinomas. These lesions have mutations in either the 12th or the 61st codons.
Dimethylbenzoanthracen results in the development of mammary carcinomas containing ras codon 12 or 61 mutations. (Patnaik)
One experiment for determining the mutagenicity of a compound is the Ames test. This test founded on the principle that if a substance turns out to be mutagenic, that it is most likely going to turn out to be a carcinogen as well. It uses a strain of the bacterium called Salmonella Typhimurium which has a mutation that makes it unable to produce an enzyme that is necessary for producing the amino acid, histidine. In the experiment several strains of Salmonella Typhimurium are exposed to the suspected cells in a culture dish, in which enough histidine is contained to support cell division. Adding histidine causes a reverse mutation to occur in the Salmonella, called a back mutation. If after being introduced to the cells, these strains ever regain their ability to continue reproducing without histidines, then the substance is considered to be carcinogenic. The colonies that form after the experiment gets going are really the telling factors of whether or not the cells are mutated, because regardless if the cells turn out to be carcinogenic or not, colonies along the culture dish will still develop. Looking at the colonies and seeing whether there are dense spots is the indication that mutations are present, and this is how mutation is found. (Carr)
What are the major hypotheses to explain aging? Explain how vertebrate cancer
and aging are related. Provide some evidence to support your claims.
Ethical issues aside, explain why stems cells are of such intense research interest
to humans.
4. There are three major hypotheses to aging; the Membrane Hypothesis of Ageing, the Telomerase Theory of Ageing, and the Dysdifferentiation Hypothesis of Ageing.
The Membrane Hypothesis of Ageing
This Hypothesis is also known as the Mitochondrial Clock Theory of Ageing because the ageing is thought to be a result of free radicals entering the cells and damaging not only general DNA, but also the DNA of the mitochondria itself. These free radicals, or reactive oxygen species (ROS) increase in quantity as a person’s age increases, and the result of the damaged mitochondrion DNA is that it cannot produce the energy at the same level it had been previously, it is lowered. As the energy being produced lowers with the increase of the free radicals, death approaches, and this is where the thought that using antioxidants could help prolong the ageing process, and therefore prolonging death.
With this hypothesis, scientists hope to one day be able to commercially measure the amount of ageing with molecular tests, based on how much of the mitochondrion’s DNA has been deleted or damaged. Studies that have been done on rats have yielded that after their mitochondrion’s DNA was deleted and damaged, they had hearing loss. So hearing loss can be one factor that is attributed to ageing, probably because the inner ear is a tissue that no longer produces new cells. Tissues, like the brain, the eye, and all muscle, which don’t continue reproducing new cells, are more vulnerable to the oxidation damage that is caused by the free radicals. (Seidman)
The Telomerase Theory of Ageing
This theory focuses on the end cap of chromosomes, called the telomere. The telomere is a repeating sequence of DNA that, when we’re born, starts out at its full length and over time with cell duplication, it is shortened until eventually it is too short and then you die. This comes from the fact that each time a cell duplicates, it cannot reproduce the exact same cell; the duplicated cell loses a little more of the telomere DNA each time, eventually leading to malfunctioning cells, which leads to ageing, which leads to death. (Seidman)
The Dysdifferentiation Hypothesis
This hypothesis, like the Membrane Hypothesis, assumes that free radicals entering the cells are what help advance the ageing process. The Dysdifferentiation Hypothesis, though, assumes that there is a preprogrammed activation of the genes that deplete the cells. This activates enzymes and the reactions that cause ageing. (Seidman)
Vertebrate cancer and ageing are related because in vertebrate cells, the number of divisions that each cell can make before they reach replicative senescence, is intrinsically fixed in each cell, and this is demonstrated in the Telomerase Theory of Aging. Scientists have found that unusually short telomeres contribute to the early development of cancers, and scientists at the Johns Hopkins Kimmel Cancer Center have done studies which found shortened telomeres in an extremely high number of precancerous lesions, over 90%. (Wasta)
Throughout the embryonic stages of life, cells are continually replicating. This cell divides again and again until it becomes fully developed. As the cells begin their life dividing, they stray away from their ability to develop into any type of cell, and they are specialized. During this time, the cells are referred to as stem cells because they will eventually branch out and become a cell that is found in an adult. It takes about two weeks for a stem cell to become specialized.
Scientists began putting stem cells into cultures to monitor when exactly the cell became specialized in hopes of one day being able to manipulate this process. Scientists feel that if they could manipulate this process successfully, they could artificially direct cells into growing neurons and tissues that may need replacement later in life. One use for this would be growing neurons to help repair a spinal cord injury. Since an adult’s nerve cells do not divide, spinal cord injuries are permanent, but they could be repaired if stem cell research continues to be successful. (Hazen and Trefil 598)
Another reason that stem cells are useful is that after an organ transplant, the recipient of the organ is immediately put on anti-rejection drugs that basically shut down their immune system, so it doesn’t see the new organ as an invader. This makes the patient susceptible to contracting even a common cold that could be too severe for what’s left of the immune system to fight off, and it could turn into something fatal. This risk could be eliminated if the transplanted tissue could be created from directing the patient’s own cells into the desired specialized tissue. (Hazen and Trefil 598)
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Carr, Steven M. The Ames Test for Mutagenicity. Copyright 1999. 4 Dec. 2005.
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Howey, Richard L. “And You Thought Jabberwocks Were Weird.” July 2002.
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Johnson, George B., Raven, Peter H. Biology. 6th ed. McGraw-Hill Publishing Co. 693-696.
Knowlton, Nancy, Rohwer, Forest. “Multispecies Microbial Mutualisms on Coral Reefs: The
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Copyright 2003. S51-S62.
Patnaik, Pradyot. A Comprehensive Guide to the Hazardous Properties of Chemical
Substances. 1992. Van Nostrand Reinhold. New York, New York. 14-16.
Seidman, Michael D. Method of Determining Biological/Molecular Age. 17 Nov. 2005.
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Wasta, Vanessa. Shortened Chromosomes Linked to Early Stages of Cancer
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