This link provides a primer on biology topics we have covered:
1. Cell Structure
2. Genetics
3. Energy Transfers
http://www.dwm.ks.edu.tw/bio/activelearner/index.html
Tuesday, February 23, 2010
Tuesday, February 16, 2010
Study Group Link
This is an on-line study group. It will serve as resource to study for various subjects. Don't plagiarize the contents!
http://www.wepapers.com/
http://www.wepapers.com/
Howework 3: Punnet Squares of Monohybrids and Dihybrids
Go to the following and practice Punnet Squares
http://www.zerobio.com/drag_gr11/mono.htm
Copy and Paste the answers and turn in as Homework 3.
http://www.zerobio.com/drag_gr11/mono.htm
Copy and Paste the answers and turn in as Homework 3.
Monday, February 15, 2010
Genetics Lab: Rolling the Dice: Are You Susceptible?
http://science.education.nih.gov/supplements/nih1/genetic/guide/activity4-1.htm
At a Glance
Focus: Students play a game to explore the relationship between genetic variation and environmental factors in the onset of heart disease and consider the implications for disease prevention of increased knowledge about genetic variation.
Major Concepts: Studying the genetic and environmental factors involved in multifactorial diseases will lead to increased diagnosis, prevention, and treatment of disease.
Objectives: After completing this activity, students will
understand that all disease, except perhaps trauma, has both a genetic and environmental component;
recognize that certain behaviors can increase or reduce a person's risk of experiencing certain medical outcomes; and
understand that the ability to detect genes associated with common diseases increases the prospects for prevention.
Prerequisite Knowledge: Students should understand the concept of a gene.
Basic Science-Health Connection: The last few years of research have seen a gradual transition from a focus on genes associated with single-gene disorders to an increasing focus on genes associated with multifactorial diseases such as cancer, heart disease, and diabetes. In this activity, students investigate the contribution that genes associated with heart disease might make to its development in an individual's life and consider the implications of this knowledge for behavior.
Introduction
Activity 3, Molecular Medicine Comes of Age, and Activity 4, Are You Susceptible?, focus students' attention on the practical, medical applications of understanding human genetic variation at a molecular level. Activity 3 looks at treatment options that become possible with the discovery and sequencing of a disease related gene. In contrast, Activity 4 focuses on the likelihood that genetic testing for common, multifactorial diseases will increase in the future and invites students to consider the prospects for this information to help individuals make wise decisions about their personal health. Specifically, Activity 4 uses heart disease as an example of the common, multifactorial diseases that constitute the bulk of the health care burden in the United States and other developed countries. The activity builds on the treatment of variation in the prior activities and sets up the discussion of ethics that is central to Activity 5, which deals with genetics and cancer.
For the most part, the treatment of genetics in the high school curriculum focuses on single-gene traits. In addition, most of the single-gene traits discussed in the curriculum are disorders, because they provide reasonably straightforward examples of Mendelian patterns of inheritance. Research in human genetics, however, increasingly addresses multifactorial traits, that is, traits that result from the interaction of multiple genes and environmental factors. Among the multifactorial traits that come most quickly to mind are those behavioral characteristics that are controversial and that often attract media attention, for example, intelligence, sexual preference, aggression, or basic personality traits such as novelty-seeking behavior or shyness. Research into the relative genetic and environmental contributions to behavioral traits has been uneven and is confounded by the difficulty of defining and measuring the phenotypes in question with any degree of accuracy and reliability.
A more productive area of active investigation involves the multifactorial diseases that are among the leading causes of sickness and death in developed countries, for example, heart disease, cancer, diabetes, and even psychiatric disorders such as schizophrenia and bipolar disease (manic-depressive illness). Already, research has uncovered genetic markers, and in some cases specific genes, that are associated with the development of these maladies; more genetic associations are sure to emerge as research into human genetic variation expands.
The identification of more genetic associations raises the virtual certainty of genetic testing for common, multifactorial diseases. Genetic testing is not a new phenomenon; it is done routinely to determine the risk for or presence of a number of single-gene disorders, including examples of Mendelian inheritance in the high school curriculum: Tay-Sachs disease, cystic fibrosis (CF), Huntington disease, phenylketonuria (PKU), and Duchenne muscular dystrophy. The predictive power of these tests lies in their technical reliability and the direct connection between gene and phenotype. Although there is considerable variation in symptomology for many single-gene disorders, the presence of the gene (or genes) does result in the generally recognized phenotype.
Our knowledge of the biological relationship between gene and phenotype is much less certain for multifactorial diseases. It is clear, for example, that genetic factors contribute to the risk for early onset heart disease, but the exact relationship is as yet unclear, as is the case for the relationship between certain genetic markers and the risk of schizophrenia. In these cases, the distance between gene—or genes—and phenotype is greater than it is in single-gene disorders, likely because of a host of environmental variables whose influences on phenotype are difficult to discern.
Genetic testing for common, multifactorial diseases will affect more people than does testing for relatively rare, single-gene disorders. Many of the same ethical and policy questions will apply—privacy and confidentiality, for example—but the uncertainty inherent in genetic testing for multifactorial disease will introduce some new challenges for the public, chief among them the notions of susceptibility and risk. One may learn from a "positive" test that one is susceptible to developing the disease in question, but that will not mean that one is destined to develop the disease. Nor will a "negative" test mean that one definitely will not develop the disease. In addition, while one may learn that there is an increased relative risk of developing a given disease—that is, a risk that is increased above the risk for the general population—the absolute risk may still be quite low.
It is likely that a deeper understanding of both the molecular basis of common, multifactorial diseases and the advent of genetic testing for these diseases will improve the climate for the development of more focused clinical interventions and for preventive medicine. Multifactorial diseases tend to develop later in life than do single-gene disorders, which generally exact their toll in infancy, childhood, or adolescence. There is, therefore, more opportunity to ameliorate the effects of multifactorial disease through a combination of medication and environmental modification. That, of course, requires a partnership between patients and health care providers to identify and modify the environmental variables that magnify one's genetic risks. That is the ultimate message of this activity.
Materials and Preparation
You will need to prepare the following materials before conducting this activity:
Master 4.1, Rolling the Dice (make 1 copy per student)
Master 4.2, Thinking About the Game (make 1 copy per student)
dice (1 die per student)
relevant genes envelopes (make 1 envelope per student)
To make a classroom set of relevant genes envelopes, first make as many copies of Masters 4.3-4.6 as you need to provide one-fourth of your class with the genetic risk indicated on each master. To minimize copying, each master contains four of the same statements. Insert one statement into each envelope and label the envelope "Relevant Genes."
Procedure
1. Begin the activity by asking students to suggest definitions of the term "risk." You might prompt the discussion by asking the students to think about risky behaviors that are a part of adolescence. Write three or four of their definitions on the board.
Students may suggest that "risk" refers to the chance that something bad or negative will happen, as, for example, "the risk" involved with dangerous behaviors. Help students see that one way to think about risk is in terms of one's chance of experiencing a particular event. For example, if a person performs aerial acrobatics on skis, he or she has some "risk" of getting hurt.
2. Ask students whether they think risks can be modified. For example, ask them if there is any way they can modify their risk of being robbed or their risk of heart attack or cancer.
Answers will vary.
3. Read the following story to the students:
Death of an Olympic Champion* Ekaterina Gordeeva and Sergei Grinkov, young Russian figure skaters, had won two Olympic gold medals in the pairs competition and were expected to continue dazzling audiences and judges for years into the future. In November 1995, however, 28-year-old Sergei suddenly collapsed and died during a practice session. He was a nonsmoker, he was physically fit, and there had been no warning signs. What happened to cause this young athlete's early death?
*Source: Courtesy of Sinauer Associates, Inc., from Mange and Mange: Basic human genetics, Second Edition, 1999.
4. Explain that Sergei Grinkov was born with a mutation [called PL(A2)] in a single gene that affects the formation of blood clots. The mutation causes clots to form in the wrong places at the wrong time. If such a clot forms in one of the arteries that supplies the heart, a heart attack can result. Ask the students to consider whether this mutant allele influenced Sergei Grinkov's risk of a premature heart attack.
The mutant allele increased Grinkov's risk of premature heart attack relative to the risk for the general population. Relative risk is the risk for any given person (or group) when considered in relation to the rest of the population. One may have an elevated relative risk, but still have a low absolute risk. For example, one may have an increased risk of 20 percent above the risk for the general population, but may still only have a 5 percent risk of suffering the disease in question by, say, age 50.
5. Ask the class to suggest ways that Sergei Grinkov could have modified his behavior had he known he was at increased risk for premature heart attack.
Given that this single-gene disorder affects the clotting process, it likely would have been difficult to reduce the risk of heart attack by modifying the environment. There is some indication that the PL(A2) mutation can interact negatively with increased cholesterol levels. If, for example, plaques formed by excess cholesterol break off from the lining of a coronary artery and create a lesion in a blood vessel, the PL(A2) mutation can cause the formation of a clot that impedes blood flow, resulting in a heart attack. Maintaining low cholesterol levels through diet and exercise, therefore, might reduce the risk of premature heart attack for a person who carries the PL(A2) mutation.
6. Explain to the students that premature heart attacks resulting from single-gene disorders are uncommon. Most heart attacks occur later in life and result from a combination of genetic and environmental factors that produce atherosclerosis, the build-up of cholesterol deposits in the arteries. In this activity, students will have an opportunity to explore the idea of medical risk and learn how genetic analysis is helping us understand and define people's risks in new ways.
7. Distribute one copy of Master 4.1, Rolling the Dice, to each student and direct the students to work in teams of three to play the game described.
Give the students about 10 minutes to finish the game.
8. Ask how many students suffered a fatal heart attack. Determine at which life stages the heart attacks occurred and record this information on the board.
9. Ask the students how the game is and is not like real life.
The game is like real life in that life expectancy depends on many risk factors. The game is not like real life because students rolled the die to determine what their risk factors would be instead of making personal choices. The game also involved only environmental risk factors, not genetic factors. If students fail to mention that the game does not address genetic risk factors, try to elicit that response by asking about Sergei Grinkov.
This part of the game is futuristic, in that at this time, we either do not have the technology available to determine each person's individual risk or, if this technology is available, conducting such genetic testing is not yet a regular part of medical care. Nevertheless, you may wish to point out to students that with the rapid pace of our progress in understanding the molecular basis for disease, such testing may well be in their future.
10. Acknowledge the importance of considering genetic risk factors in the development of heart disease and ask students what effect(s) factoring this information into the game might have.
Answers will vary. Because of the example of Sergei Grinkov and because of their own sense that sometimes heart disease tends to "run in families," students may think that including genetic factors in the game will inevitably have a negative effect. You may choose to point out that for some people, the effect might be positive, or let students discover this in Step 11.
11. Distribute one relevant genes envelope to each student and explain that this envelope contains information about his or her genetic risk for a fatal heart attack. Ask the students to open the envelopes and share their heart points until you have addressed all four values: -10, 0, +10, +40. Point out that the genetic risk falls off rapidly as genetic relatedness decreases, from 40 points for first-degree relatives to no points for third-degree relatives. Explain that this is the case generally for multifactorial diseases.
12. Distribute one copy of Master 4.2, Thinking About the Game, to each student and ask students to complete the worksheet to compare the results of the game with and without considering genetic factors.
You may wish to collect your students’ answers to these questions to evaluate how well they understand the issues involved.
13. Conclude the activity by inviting each team to offer its answer to one of the questions on Thinking About the Game. Then, invite other teams to contribute additional insights or information or to challenge ideas expressed by the team answering.
Question 3 Remember, if you exceeded 85 points in any life stage, you have had a fatal heart attack. What effect did including your points for genetic risk have on your outcome?
Answers will vary. Including the genetic data may have pushed some students over the threshold to a heart attack. Others may have escaped a heart attack because of the protective effects of their genes, while still others may have experienced no change. The important point is that the environmental risks—the choices they made—have been played out against a genetic background, which differs for each person.
Question 4 Think about the choices you made in each life stage.
a. Did everyone make the same choices?
No, each person made somewhat different choices.
b. Were all of the choices equally risky?
No, some of the choices carried greater risks than others, and some decreased the risks.
c. Were the risk factors associated with the choices reversible?
Most of the risk factors were reversible--smoking, exercise, and stress, for example.
d. Were the choices under personal control?
In the game, choices were made on the basis of a roll of a die. In life, however, most of these choices are under personal control.
Question 5 Now, think about the effects of genetic risk factors in each life stage.
a. Does everyone have the same genes?
No, each person (except identical twins) has different genes.
b. Did all of the genetic factors have the same effect?
No, some genetic factors had negative effects, some were neutral, and some provided protection.
c. Were the genetic factors reversible or under personal control?
We cannot change the genes with which we are born. We can, however, sometimes modify the effects of those genes by modifying the environment, for example, by changing some of our behaviors.
Question 6 Assume that genetic testing showed that you were at increased risk for a fatal heart attack 20 years from now. Would you want to know? Why or why not? Would that information cause you to change your behavior? If not, what kind of information or event would cause you to change your behavior?
Answers will vary, but the assumption is that knowledge of increased genetic risk would cause one to modify his or her behavior to reduce the environmental risk factors. A very important point here is that a family history of heart disease is an indication of increased genetic risk, even if we are not yet able to identify predisposing genes and attach some risk figure to them. The literature on health and behavior—and personal experience—demonstrates that people do not always change their behaviors in the face of well-documented risk. Cigarette smoking is perhaps the classic example that applies well to adolescents. Some people will not change their behavior even in the face of serious illness.
Question 7 We know about only a few genes that affect the likelihood of a heart attack, and we have the ability to test for even fewer of them. In the future, we certainly will learn about more of these genes. How will an increased knowledge of the genetic factors associated with heart disease have a positive impact on individuals and society? How will it have a negative impact?
Increased knowledge about such genes will lead to increased testing and the development of new clinical interventions. Our ability to test for genes that predispose to heart disease will mean that we can detect those genetic susceptibilities sooner and act on them more quickly, for example, with drugs targeted at the specific biochemical defects involved and with modification of risky behaviors.
The frequency of heart disease, and other common, multifactorial diseases, means that genetic testing will be applied to many more individuals, with attendant concerns about how we use the results of genetic testing. In addition, genetic testing for multifactorial diseases will require education of the public and health care providers about the meaning of susceptibility and predisposition. Activity 5 explores some of these issues in more detail.
This question is designed to draw students' attention back to the activity's major concept.
Question 8 Our ability to detect genetic variations that are related to common diseases will improve. How might that ability shift some of the responsibility for health care from physicians to individuals?
If we know that we are at increased genetic risk for a particular disease, we can try to avoid those environmental factors, such as risky behaviors, that increase the risk further. Many health care professionals think that increased understanding of genetic variation will provide an important impetus to preventive medicine. Prevention will require a close partnership between health care providers and consumers. Health care specialists may be able to provide us with tests to uncover our genetic predispositions, but it will be up to each one of us to avoid increasing those risks by engaging in high-risk behaviors. In short, each of us will have to assume more responsibility for our own health. This requires active participation by the individual and is very different from the prevailing model, which is based not on prevention but on treatment after the disease occurs. In the current model, the individual (the patient) generally is a rather passive recipient of health care.
At a Glance
Focus: Students play a game to explore the relationship between genetic variation and environmental factors in the onset of heart disease and consider the implications for disease prevention of increased knowledge about genetic variation.
Major Concepts: Studying the genetic and environmental factors involved in multifactorial diseases will lead to increased diagnosis, prevention, and treatment of disease.
Objectives: After completing this activity, students will
understand that all disease, except perhaps trauma, has both a genetic and environmental component;
recognize that certain behaviors can increase or reduce a person's risk of experiencing certain medical outcomes; and
understand that the ability to detect genes associated with common diseases increases the prospects for prevention.
Prerequisite Knowledge: Students should understand the concept of a gene.
Basic Science-Health Connection: The last few years of research have seen a gradual transition from a focus on genes associated with single-gene disorders to an increasing focus on genes associated with multifactorial diseases such as cancer, heart disease, and diabetes. In this activity, students investigate the contribution that genes associated with heart disease might make to its development in an individual's life and consider the implications of this knowledge for behavior.
Introduction
Activity 3, Molecular Medicine Comes of Age, and Activity 4, Are You Susceptible?, focus students' attention on the practical, medical applications of understanding human genetic variation at a molecular level. Activity 3 looks at treatment options that become possible with the discovery and sequencing of a disease related gene. In contrast, Activity 4 focuses on the likelihood that genetic testing for common, multifactorial diseases will increase in the future and invites students to consider the prospects for this information to help individuals make wise decisions about their personal health. Specifically, Activity 4 uses heart disease as an example of the common, multifactorial diseases that constitute the bulk of the health care burden in the United States and other developed countries. The activity builds on the treatment of variation in the prior activities and sets up the discussion of ethics that is central to Activity 5, which deals with genetics and cancer.
For the most part, the treatment of genetics in the high school curriculum focuses on single-gene traits. In addition, most of the single-gene traits discussed in the curriculum are disorders, because they provide reasonably straightforward examples of Mendelian patterns of inheritance. Research in human genetics, however, increasingly addresses multifactorial traits, that is, traits that result from the interaction of multiple genes and environmental factors. Among the multifactorial traits that come most quickly to mind are those behavioral characteristics that are controversial and that often attract media attention, for example, intelligence, sexual preference, aggression, or basic personality traits such as novelty-seeking behavior or shyness. Research into the relative genetic and environmental contributions to behavioral traits has been uneven and is confounded by the difficulty of defining and measuring the phenotypes in question with any degree of accuracy and reliability.
A more productive area of active investigation involves the multifactorial diseases that are among the leading causes of sickness and death in developed countries, for example, heart disease, cancer, diabetes, and even psychiatric disorders such as schizophrenia and bipolar disease (manic-depressive illness). Already, research has uncovered genetic markers, and in some cases specific genes, that are associated with the development of these maladies; more genetic associations are sure to emerge as research into human genetic variation expands.
The identification of more genetic associations raises the virtual certainty of genetic testing for common, multifactorial diseases. Genetic testing is not a new phenomenon; it is done routinely to determine the risk for or presence of a number of single-gene disorders, including examples of Mendelian inheritance in the high school curriculum: Tay-Sachs disease, cystic fibrosis (CF), Huntington disease, phenylketonuria (PKU), and Duchenne muscular dystrophy. The predictive power of these tests lies in their technical reliability and the direct connection between gene and phenotype. Although there is considerable variation in symptomology for many single-gene disorders, the presence of the gene (or genes) does result in the generally recognized phenotype.
Our knowledge of the biological relationship between gene and phenotype is much less certain for multifactorial diseases. It is clear, for example, that genetic factors contribute to the risk for early onset heart disease, but the exact relationship is as yet unclear, as is the case for the relationship between certain genetic markers and the risk of schizophrenia. In these cases, the distance between gene—or genes—and phenotype is greater than it is in single-gene disorders, likely because of a host of environmental variables whose influences on phenotype are difficult to discern.
Genetic testing for common, multifactorial diseases will affect more people than does testing for relatively rare, single-gene disorders. Many of the same ethical and policy questions will apply—privacy and confidentiality, for example—but the uncertainty inherent in genetic testing for multifactorial disease will introduce some new challenges for the public, chief among them the notions of susceptibility and risk. One may learn from a "positive" test that one is susceptible to developing the disease in question, but that will not mean that one is destined to develop the disease. Nor will a "negative" test mean that one definitely will not develop the disease. In addition, while one may learn that there is an increased relative risk of developing a given disease—that is, a risk that is increased above the risk for the general population—the absolute risk may still be quite low.
It is likely that a deeper understanding of both the molecular basis of common, multifactorial diseases and the advent of genetic testing for these diseases will improve the climate for the development of more focused clinical interventions and for preventive medicine. Multifactorial diseases tend to develop later in life than do single-gene disorders, which generally exact their toll in infancy, childhood, or adolescence. There is, therefore, more opportunity to ameliorate the effects of multifactorial disease through a combination of medication and environmental modification. That, of course, requires a partnership between patients and health care providers to identify and modify the environmental variables that magnify one's genetic risks. That is the ultimate message of this activity.
Materials and Preparation
You will need to prepare the following materials before conducting this activity:
Master 4.1, Rolling the Dice (make 1 copy per student)
Master 4.2, Thinking About the Game (make 1 copy per student)
dice (1 die per student)
relevant genes envelopes (make 1 envelope per student)
To make a classroom set of relevant genes envelopes, first make as many copies of Masters 4.3-4.6 as you need to provide one-fourth of your class with the genetic risk indicated on each master. To minimize copying, each master contains four of the same statements. Insert one statement into each envelope and label the envelope "Relevant Genes."
Procedure
1. Begin the activity by asking students to suggest definitions of the term "risk." You might prompt the discussion by asking the students to think about risky behaviors that are a part of adolescence. Write three or four of their definitions on the board.
Students may suggest that "risk" refers to the chance that something bad or negative will happen, as, for example, "the risk" involved with dangerous behaviors. Help students see that one way to think about risk is in terms of one's chance of experiencing a particular event. For example, if a person performs aerial acrobatics on skis, he or she has some "risk" of getting hurt.
2. Ask students whether they think risks can be modified. For example, ask them if there is any way they can modify their risk of being robbed or their risk of heart attack or cancer.
Answers will vary.
3. Read the following story to the students:
Death of an Olympic Champion* Ekaterina Gordeeva and Sergei Grinkov, young Russian figure skaters, had won two Olympic gold medals in the pairs competition and were expected to continue dazzling audiences and judges for years into the future. In November 1995, however, 28-year-old Sergei suddenly collapsed and died during a practice session. He was a nonsmoker, he was physically fit, and there had been no warning signs. What happened to cause this young athlete's early death?
*Source: Courtesy of Sinauer Associates, Inc., from Mange and Mange: Basic human genetics, Second Edition, 1999.
4. Explain that Sergei Grinkov was born with a mutation [called PL(A2)] in a single gene that affects the formation of blood clots. The mutation causes clots to form in the wrong places at the wrong time. If such a clot forms in one of the arteries that supplies the heart, a heart attack can result. Ask the students to consider whether this mutant allele influenced Sergei Grinkov's risk of a premature heart attack.
The mutant allele increased Grinkov's risk of premature heart attack relative to the risk for the general population. Relative risk is the risk for any given person (or group) when considered in relation to the rest of the population. One may have an elevated relative risk, but still have a low absolute risk. For example, one may have an increased risk of 20 percent above the risk for the general population, but may still only have a 5 percent risk of suffering the disease in question by, say, age 50.
5. Ask the class to suggest ways that Sergei Grinkov could have modified his behavior had he known he was at increased risk for premature heart attack.
Given that this single-gene disorder affects the clotting process, it likely would have been difficult to reduce the risk of heart attack by modifying the environment. There is some indication that the PL(A2) mutation can interact negatively with increased cholesterol levels. If, for example, plaques formed by excess cholesterol break off from the lining of a coronary artery and create a lesion in a blood vessel, the PL(A2) mutation can cause the formation of a clot that impedes blood flow, resulting in a heart attack. Maintaining low cholesterol levels through diet and exercise, therefore, might reduce the risk of premature heart attack for a person who carries the PL(A2) mutation.
6. Explain to the students that premature heart attacks resulting from single-gene disorders are uncommon. Most heart attacks occur later in life and result from a combination of genetic and environmental factors that produce atherosclerosis, the build-up of cholesterol deposits in the arteries. In this activity, students will have an opportunity to explore the idea of medical risk and learn how genetic analysis is helping us understand and define people's risks in new ways.
7. Distribute one copy of Master 4.1, Rolling the Dice, to each student and direct the students to work in teams of three to play the game described.
Give the students about 10 minutes to finish the game.
8. Ask how many students suffered a fatal heart attack. Determine at which life stages the heart attacks occurred and record this information on the board.
9. Ask the students how the game is and is not like real life.
The game is like real life in that life expectancy depends on many risk factors. The game is not like real life because students rolled the die to determine what their risk factors would be instead of making personal choices. The game also involved only environmental risk factors, not genetic factors. If students fail to mention that the game does not address genetic risk factors, try to elicit that response by asking about Sergei Grinkov.
This part of the game is futuristic, in that at this time, we either do not have the technology available to determine each person's individual risk or, if this technology is available, conducting such genetic testing is not yet a regular part of medical care. Nevertheless, you may wish to point out to students that with the rapid pace of our progress in understanding the molecular basis for disease, such testing may well be in their future.
10. Acknowledge the importance of considering genetic risk factors in the development of heart disease and ask students what effect(s) factoring this information into the game might have.
Answers will vary. Because of the example of Sergei Grinkov and because of their own sense that sometimes heart disease tends to "run in families," students may think that including genetic factors in the game will inevitably have a negative effect. You may choose to point out that for some people, the effect might be positive, or let students discover this in Step 11.
11. Distribute one relevant genes envelope to each student and explain that this envelope contains information about his or her genetic risk for a fatal heart attack. Ask the students to open the envelopes and share their heart points until you have addressed all four values: -10, 0, +10, +40. Point out that the genetic risk falls off rapidly as genetic relatedness decreases, from 40 points for first-degree relatives to no points for third-degree relatives. Explain that this is the case generally for multifactorial diseases.
12. Distribute one copy of Master 4.2, Thinking About the Game, to each student and ask students to complete the worksheet to compare the results of the game with and without considering genetic factors.
You may wish to collect your students’ answers to these questions to evaluate how well they understand the issues involved.
13. Conclude the activity by inviting each team to offer its answer to one of the questions on Thinking About the Game. Then, invite other teams to contribute additional insights or information or to challenge ideas expressed by the team answering.
Question 3 Remember, if you exceeded 85 points in any life stage, you have had a fatal heart attack. What effect did including your points for genetic risk have on your outcome?
Answers will vary. Including the genetic data may have pushed some students over the threshold to a heart attack. Others may have escaped a heart attack because of the protective effects of their genes, while still others may have experienced no change. The important point is that the environmental risks—the choices they made—have been played out against a genetic background, which differs for each person.
Question 4 Think about the choices you made in each life stage.
a. Did everyone make the same choices?
No, each person made somewhat different choices.
b. Were all of the choices equally risky?
No, some of the choices carried greater risks than others, and some decreased the risks.
c. Were the risk factors associated with the choices reversible?
Most of the risk factors were reversible--smoking, exercise, and stress, for example.
d. Were the choices under personal control?
In the game, choices were made on the basis of a roll of a die. In life, however, most of these choices are under personal control.
Question 5 Now, think about the effects of genetic risk factors in each life stage.
a. Does everyone have the same genes?
No, each person (except identical twins) has different genes.
b. Did all of the genetic factors have the same effect?
No, some genetic factors had negative effects, some were neutral, and some provided protection.
c. Were the genetic factors reversible or under personal control?
We cannot change the genes with which we are born. We can, however, sometimes modify the effects of those genes by modifying the environment, for example, by changing some of our behaviors.
Question 6 Assume that genetic testing showed that you were at increased risk for a fatal heart attack 20 years from now. Would you want to know? Why or why not? Would that information cause you to change your behavior? If not, what kind of information or event would cause you to change your behavior?
Answers will vary, but the assumption is that knowledge of increased genetic risk would cause one to modify his or her behavior to reduce the environmental risk factors. A very important point here is that a family history of heart disease is an indication of increased genetic risk, even if we are not yet able to identify predisposing genes and attach some risk figure to them. The literature on health and behavior—and personal experience—demonstrates that people do not always change their behaviors in the face of well-documented risk. Cigarette smoking is perhaps the classic example that applies well to adolescents. Some people will not change their behavior even in the face of serious illness.
Question 7 We know about only a few genes that affect the likelihood of a heart attack, and we have the ability to test for even fewer of them. In the future, we certainly will learn about more of these genes. How will an increased knowledge of the genetic factors associated with heart disease have a positive impact on individuals and society? How will it have a negative impact?
Increased knowledge about such genes will lead to increased testing and the development of new clinical interventions. Our ability to test for genes that predispose to heart disease will mean that we can detect those genetic susceptibilities sooner and act on them more quickly, for example, with drugs targeted at the specific biochemical defects involved and with modification of risky behaviors.
The frequency of heart disease, and other common, multifactorial diseases, means that genetic testing will be applied to many more individuals, with attendant concerns about how we use the results of genetic testing. In addition, genetic testing for multifactorial diseases will require education of the public and health care providers about the meaning of susceptibility and predisposition. Activity 5 explores some of these issues in more detail.
This question is designed to draw students' attention back to the activity's major concept.
Question 8 Our ability to detect genetic variations that are related to common diseases will improve. How might that ability shift some of the responsibility for health care from physicians to individuals?
If we know that we are at increased genetic risk for a particular disease, we can try to avoid those environmental factors, such as risky behaviors, that increase the risk further. Many health care professionals think that increased understanding of genetic variation will provide an important impetus to preventive medicine. Prevention will require a close partnership between health care providers and consumers. Health care specialists may be able to provide us with tests to uncover our genetic predispositions, but it will be up to each one of us to avoid increasing those risks by engaging in high-risk behaviors. In short, each of us will have to assume more responsibility for our own health. This requires active participation by the individual and is very different from the prevailing model, which is based not on prevention but on treatment after the disease occurs. In the current model, the individual (the patient) generally is a rather passive recipient of health care.
Medelian Genetics Lecture
from http://www.ndsu.edu/pubweb/~mcclean/plsc431/mendel/mendel1.htm
Mendel's First Law of Genetics (Law of Segregation)
Genetic analysis predates Gregor Mendel, but Mendel's laws form the theoretical basis of our understanding of the genetics of inheritance.
Mendel made two innovations to the science of genetics:
developed pure lines
counted his results and kept statistical notes
Pure Line - a population that breeds true for a particular trait [this was an important innovation because any non-pure (segregating) generation would and did confuse the results of genetic experiments]
Results from Mendel's Experiments
Parental Cross F1 Phenotype F2 Phenotypic Ratio F2 Ratio
Round x Wrinkled Seed Round 5474 Round:1850 Wrinkled 2.96:1
Yellow x Green Seeds Yellow 6022 Yellow:2001 Green 3.01:1
Red x White Flowers Red 705 Red:224 White 3.15:1
Tall x Dwarf Plants Tall l787 Tall:227 Dwarf 2.84:1
Terms and Results Found in the Table
Phenotype - literally means "the form that is shown"; it is the outward, physical appearance of a particular trait
Mendel's pea plants exhibited the following phenotypes:
- round or wrinkled seed phenotype
- yellow or green seed phenotype
- red or white flower phenotype
- tall or dwarf plant phenotype
Seed Color: Green and yellow seeds.
Seed Shape: Wrinkled and Round seeds.
What is seen in the F1 generation? We always see only one of the two parental phenotypes in this generation. But the F1 possesses the information needed to produce both parental phenotypes in the following generation. The F2 generation always produced a 3:1 ratio where the dominant trait is present three times as often as the recessive trait. Mendel coined two terms to describe the relationship of the two phenotypes based on the F1 and F2 phenotypes.
Dominant - the allele that expresses itself at the expense of an alternate allele; the phenotype that is expressed in the F1 generation from the cross of two pure lines
Recessive - an allele whose expression is suppressed in the presence of a dominant allele; the phenotype that disappears in the F1 generation from the cross of two pure lines and reappears in the F2 generation
Mendel's Conclusions
The hereditary determinants are of a particulate nature. These determinants are called genes.
Each parent has a gene pair in each cell for each trait studied. The F1 from a cross of two pure lines contains one allele for the dominant phenotype and one for the recessive phenotype. These two alleles comprise the gene pair.
One member of the gene pair segregates into a gamete, thus each gamete only carries one member of the gene pair.
Gametes unite at random and irrespective of the other gene pairs involved.
Mendelian Genetics Definitions
Allele - one alternative form of a given allelic pair; tall and dwarf are the alleles for the height of a pea plant; more than two alleles can exist for any specific gene, but only two of them will be found within any individual
Allelic pair - the combination of two alleles which comprise the gene pair
Homozygote - an individual which contains only one allele at the allelic pair; for example DD is homozygous dominant and dd is homozygous recessive; pure lines are homozygous for the gene of interest
Heterozygote - an individual which contains one of each member of the gene pair; for example the Dd heterozygote
Genotype - the specific allelic combination for a certain gene or set of genes
Using symbols we can depict the cross of tall and short pea plants in the following manner:
The F2 generation was created by selfing the F1 plants. This can be depicted graphically in a Punnett square. From these results Mendel coined several other terms and formulated his first law. First the Punnett Square is shown.
Union of Gametes
At Random D d Punnett
Square
D DD
(Tall) Dd
(Tall)
d Dd
(Tall) dd
(Short)
The Punnett Square allows us to determine specific genetic ratios.
Genotypic ratio of F2: 1 DD : 2 Dd : 1 dd (or 3 D_ : 1 dd)
Phenotypic ratio of F2: 3 tall : 1 dwarf
Mendel's First Law - the law of segregation; during gamete formation each member of the allelic pair separates from the other member to form the genetic constitution of the gamete
Confirmation of Mendel's First Law Hypothesis
With these observations, Mendel could form a hypothesis about segregation. To test this hypothesis, Mendel selfed the F2 plants. If his law was correct he could predict what the results would be. And indeed, the results occurred has he expected.
From these results we can now confirm the genotype of the F2 individuals. Phenotypes Genotypes Genetic Description
F2 Tall Plants 1/3 DD
2/3 Dd Pure line homozygote dominant
Heterozygotes
F2 Dwarf Plants all dd Pure line homozygote recessive
Thus the F2 is genotypically 1/4 Dd : 1/2 Dd : 1/4 dd
This data was also available from the Punnett Square using the gametes from the F1 individual. So although the phenotypic ratio is 3:1 the genotypic ratio is 1:2:1
Mendel performed one other cross to confirm the hypothesis of segregation --- the backcross. Remember, the first cross is between two pure line parents to produce an F1 heterozygote.
At this point instead of selfing the F1, Mendel crossed it to a pure line, homozygote dwarf plant.
Backcross: Dd x dd
Male
Gametes
d
Female
Gametes D DD
(Tall)
d dd
(Short)
Backcross One or (BC1) Phenotypes: 1 Tall : 1 Dwarf
BC1 Genotypes: 1 Dd : 1 dd
Backcross - the cross of an F1 hybrid to one of the homozygous parents; for pea plant height the cross would be Dd x DD or Dd x dd; most often, though a backcross is a cross to a fully recessive parent
Testcross - the cross of any individual to a homozygous recessive parent; used to determine if the individual is homozygous dominant or heterozygous
So far, all the discussion has concentrated on monohybrid crosses.
Monohybrid cross - a cross between parents that differ at a single gene pair (usually AA x aa)
Monohybrid - the offspring of two parents that are homozygous for alternate alleles of a gene pair
Remember --- a monohybrid cross is not the cross of two monohybrids.
Monohybrids are good for describing the relationship between alleles. When an allele is homozygous it will show its phenotype. It is the phenotype of the heterozygote which permits us to determine the relationship of the alleles.
Dominance - the ability of one allele to express its phenotype at the expense of an alternate allele; the major form of interaction between alleles; generally the dominant allele will make a gene product that the recessive can not; therefore the dominant allele will express itself whenever it is present
Copyright © 2000. Phillip McClean
Mendel's First Law of Genetics (Law of Segregation)
Genetic analysis predates Gregor Mendel, but Mendel's laws form the theoretical basis of our understanding of the genetics of inheritance.
Mendel made two innovations to the science of genetics:
developed pure lines
counted his results and kept statistical notes
Pure Line - a population that breeds true for a particular trait [this was an important innovation because any non-pure (segregating) generation would and did confuse the results of genetic experiments]
Results from Mendel's Experiments
Parental Cross F1 Phenotype F2 Phenotypic Ratio F2 Ratio
Round x Wrinkled Seed Round 5474 Round:1850 Wrinkled 2.96:1
Yellow x Green Seeds Yellow 6022 Yellow:2001 Green 3.01:1
Red x White Flowers Red 705 Red:224 White 3.15:1
Tall x Dwarf Plants Tall l787 Tall:227 Dwarf 2.84:1
Terms and Results Found in the Table
Phenotype - literally means "the form that is shown"; it is the outward, physical appearance of a particular trait
Mendel's pea plants exhibited the following phenotypes:
- round or wrinkled seed phenotype
- yellow or green seed phenotype
- red or white flower phenotype
- tall or dwarf plant phenotype
Seed Color: Green and yellow seeds.
Seed Shape: Wrinkled and Round seeds.
What is seen in the F1 generation? We always see only one of the two parental phenotypes in this generation. But the F1 possesses the information needed to produce both parental phenotypes in the following generation. The F2 generation always produced a 3:1 ratio where the dominant trait is present three times as often as the recessive trait. Mendel coined two terms to describe the relationship of the two phenotypes based on the F1 and F2 phenotypes.
Dominant - the allele that expresses itself at the expense of an alternate allele; the phenotype that is expressed in the F1 generation from the cross of two pure lines
Recessive - an allele whose expression is suppressed in the presence of a dominant allele; the phenotype that disappears in the F1 generation from the cross of two pure lines and reappears in the F2 generation
Mendel's Conclusions
The hereditary determinants are of a particulate nature. These determinants are called genes.
Each parent has a gene pair in each cell for each trait studied. The F1 from a cross of two pure lines contains one allele for the dominant phenotype and one for the recessive phenotype. These two alleles comprise the gene pair.
One member of the gene pair segregates into a gamete, thus each gamete only carries one member of the gene pair.
Gametes unite at random and irrespective of the other gene pairs involved.
Mendelian Genetics Definitions
Allele - one alternative form of a given allelic pair; tall and dwarf are the alleles for the height of a pea plant; more than two alleles can exist for any specific gene, but only two of them will be found within any individual
Allelic pair - the combination of two alleles which comprise the gene pair
Homozygote - an individual which contains only one allele at the allelic pair; for example DD is homozygous dominant and dd is homozygous recessive; pure lines are homozygous for the gene of interest
Heterozygote - an individual which contains one of each member of the gene pair; for example the Dd heterozygote
Genotype - the specific allelic combination for a certain gene or set of genes
Using symbols we can depict the cross of tall and short pea plants in the following manner:
The F2 generation was created by selfing the F1 plants. This can be depicted graphically in a Punnett square. From these results Mendel coined several other terms and formulated his first law. First the Punnett Square is shown.
Union of Gametes
At Random D d Punnett
Square
D DD
(Tall) Dd
(Tall)
d Dd
(Tall) dd
(Short)
The Punnett Square allows us to determine specific genetic ratios.
Genotypic ratio of F2: 1 DD : 2 Dd : 1 dd (or 3 D_ : 1 dd)
Phenotypic ratio of F2: 3 tall : 1 dwarf
Mendel's First Law - the law of segregation; during gamete formation each member of the allelic pair separates from the other member to form the genetic constitution of the gamete
Confirmation of Mendel's First Law Hypothesis
With these observations, Mendel could form a hypothesis about segregation. To test this hypothesis, Mendel selfed the F2 plants. If his law was correct he could predict what the results would be. And indeed, the results occurred has he expected.
From these results we can now confirm the genotype of the F2 individuals. Phenotypes Genotypes Genetic Description
F2 Tall Plants 1/3 DD
2/3 Dd Pure line homozygote dominant
Heterozygotes
F2 Dwarf Plants all dd Pure line homozygote recessive
Thus the F2 is genotypically 1/4 Dd : 1/2 Dd : 1/4 dd
This data was also available from the Punnett Square using the gametes from the F1 individual. So although the phenotypic ratio is 3:1 the genotypic ratio is 1:2:1
Mendel performed one other cross to confirm the hypothesis of segregation --- the backcross. Remember, the first cross is between two pure line parents to produce an F1 heterozygote.
At this point instead of selfing the F1, Mendel crossed it to a pure line, homozygote dwarf plant.
Backcross: Dd x dd
Male
Gametes
d
Female
Gametes D DD
(Tall)
d dd
(Short)
Backcross One or (BC1) Phenotypes: 1 Tall : 1 Dwarf
BC1 Genotypes: 1 Dd : 1 dd
Backcross - the cross of an F1 hybrid to one of the homozygous parents; for pea plant height the cross would be Dd x DD or Dd x dd; most often, though a backcross is a cross to a fully recessive parent
Testcross - the cross of any individual to a homozygous recessive parent; used to determine if the individual is homozygous dominant or heterozygous
So far, all the discussion has concentrated on monohybrid crosses.
Monohybrid cross - a cross between parents that differ at a single gene pair (usually AA x aa)
Monohybrid - the offspring of two parents that are homozygous for alternate alleles of a gene pair
Remember --- a monohybrid cross is not the cross of two monohybrids.
Monohybrids are good for describing the relationship between alleles. When an allele is homozygous it will show its phenotype. It is the phenotype of the heterozygote which permits us to determine the relationship of the alleles.
Dominance - the ability of one allele to express its phenotype at the expense of an alternate allele; the major form of interaction between alleles; generally the dominant allele will make a gene product that the recessive can not; therefore the dominant allele will express itself whenever it is present
Copyright © 2000. Phillip McClean
Friday, February 12, 2010
SNOW Day Creates an Opportunity to Learn
Review the following DNA tutorial and complete the post test for extra credit.
http://dnatutorial.com/index.shtml
Answer questions here:
http://www.visionlearning.com/library/quiz_taker.php?qid=4&mid=63
Cut and paste the answers and email to myscienceclass@yahoo.com
http://dnatutorial.com/index.shtml
Answer questions here:
http://www.visionlearning.com/library/quiz_taker.php?qid=4&mid=63
Cut and paste the answers and email to myscienceclass@yahoo.com
Tuesday, February 9, 2010
Bioluminescent Bay
This unique bay contains up to 720,000 single-celled bioluminescent dinoflagellates per gallon of water. These half-plant, half-animal organisms emit a flash of bluish light when agitated at night. The high concentration of these creatures (Pyrodimium bahamense) can create enough light to read a book from.
http://www.biobay.com/
http://www.biobay.com/
DNA Extraction
Extract Your Own DNA!
This experiment allows you to extract your own DNA in your own home! You will need the help of an adult.
DNA is a complex molecule that is found inside cells. This molecule is so small that you can't normally see it with the naked eye, but if you release the DNA of thousands of cells at the same time, the molecules become visible because of their sheer number. In this experiment, you will collect some cells from the skin on the inside of your mouth, break the cells open, release the DNA and concentrate them in a liquid so you can see them.
Gather the following household materials:
500 millilitres of drinking-water
1 tablespoon of cooking salt or table salt
1 clear cup or glass, small, with a narrow mouth
125 ml of chilled rubbing alcohol (Isopropyl alcohol USP 70%) *
A few drops of blue food colouring (optional)
1 eyedropper or 1 spoon
1 drop of clear dishwashing detergent
1 stir-stick
Safety Glasses
1 pair rubber gloves
*Warning: Rubbing alcohol is a hazardous substance. It must be handled by an adult. Protective eye-wear and gloves should be worn during the experiment. Use rubbing alcohol in a well ventilated area. Keep it away from open flames or sparks. Do not drink the rubbing alcohol. If ingested, call a Poison Control Centre. We recommend using hygenic caution when handling the saliva.
Step 1:
Add the salt to the water and stir until the grains of salt have disappeared. Pour 3 tbsp of the salty water into a cup.
Step 2:
Gargle and swish all the salty water from the cup around your mouth. Do not swallow the water. Spit it back into the cup.
Step 3:
Dip the stir-stick in the drop of dishwashing detergent and gently stir it in the cup. Less froth in the cup is better so stir only two or three times.
Step 4:
Add two or three drops of food colouring to the rubbing alcohol if you want, and stir well. The blue food colouring will help you distinguish the alcohol from the water.
Step 5:
Use the eyedropper to dribble the rubbing alcohol down along the inside wall of the cup. Try to add the alcohol very gently, so that the water and the alcohol do not mix. You want the alcohol to form a separate layer on top of the water. It helps to hold the cup at about a 20-degree angle while you do this.
If you don't have an eyedropper you can use a spoon. Hold the spoon with its back facing upwards just above the surface of the water and with its tip touching the side of the cup. Dribble the alcohol onto the back of the spoon so that it slides gently off the spoon, down the side of the cup, and onto the surface of the water.
Pour enough rubbing alcohol to create a 2 cm-high layer on top of the water. Even if you added the food colouring to the alcohol, the water will remain transparent.
Step 6:
Watch the thin strands of DNA collect together in the alcohol. The strands link together and form nets or webs of DNA. Take a good look—it's a part of you that you usually don't get to see! If the alcohol is cloudy, try the experiment again and add the alcohol more slowly.
Step 7:
Discard the contents of the cup. Clean up and put everything away in its place.
What happened?
The skin cells inside your mouth were easily removed by gargling and swishing the water in your mouth. Salty water was used because it mimics the salty fluids inside our bodies. Our cells are protected by “walls” that are really a fatty layer called a membrane, but when you added the drop of detergent you broke open the cell membrane and the DNA was released into the water. When the alcohol layer was added the DNA strands gradually migrated into it and joined to other DNA strands. As more and more strands stuck together, the DNA became visible to the naked eye. Isn't it amazing that such tiny molecules hold all the information to make you so unique?
http://www.nature.ca/genome/05/051/pdfs/DNAextract_e.pdf
This experiment allows you to extract your own DNA in your own home! You will need the help of an adult.
DNA is a complex molecule that is found inside cells. This molecule is so small that you can't normally see it with the naked eye, but if you release the DNA of thousands of cells at the same time, the molecules become visible because of their sheer number. In this experiment, you will collect some cells from the skin on the inside of your mouth, break the cells open, release the DNA and concentrate them in a liquid so you can see them.
Gather the following household materials:
500 millilitres of drinking-water
1 tablespoon of cooking salt or table salt
1 clear cup or glass, small, with a narrow mouth
125 ml of chilled rubbing alcohol (Isopropyl alcohol USP 70%) *
A few drops of blue food colouring (optional)
1 eyedropper or 1 spoon
1 drop of clear dishwashing detergent
1 stir-stick
Safety Glasses
1 pair rubber gloves
*Warning: Rubbing alcohol is a hazardous substance. It must be handled by an adult. Protective eye-wear and gloves should be worn during the experiment. Use rubbing alcohol in a well ventilated area. Keep it away from open flames or sparks. Do not drink the rubbing alcohol. If ingested, call a Poison Control Centre. We recommend using hygenic caution when handling the saliva.
Step 1:
Add the salt to the water and stir until the grains of salt have disappeared. Pour 3 tbsp of the salty water into a cup.
Step 2:
Gargle and swish all the salty water from the cup around your mouth. Do not swallow the water. Spit it back into the cup.
Step 3:
Dip the stir-stick in the drop of dishwashing detergent and gently stir it in the cup. Less froth in the cup is better so stir only two or three times.
Step 4:
Add two or three drops of food colouring to the rubbing alcohol if you want, and stir well. The blue food colouring will help you distinguish the alcohol from the water.
Step 5:
Use the eyedropper to dribble the rubbing alcohol down along the inside wall of the cup. Try to add the alcohol very gently, so that the water and the alcohol do not mix. You want the alcohol to form a separate layer on top of the water. It helps to hold the cup at about a 20-degree angle while you do this.
If you don't have an eyedropper you can use a spoon. Hold the spoon with its back facing upwards just above the surface of the water and with its tip touching the side of the cup. Dribble the alcohol onto the back of the spoon so that it slides gently off the spoon, down the side of the cup, and onto the surface of the water.
Pour enough rubbing alcohol to create a 2 cm-high layer on top of the water. Even if you added the food colouring to the alcohol, the water will remain transparent.
Step 6:
Watch the thin strands of DNA collect together in the alcohol. The strands link together and form nets or webs of DNA. Take a good look—it's a part of you that you usually don't get to see! If the alcohol is cloudy, try the experiment again and add the alcohol more slowly.
Step 7:
Discard the contents of the cup. Clean up and put everything away in its place.
What happened?
The skin cells inside your mouth were easily removed by gargling and swishing the water in your mouth. Salty water was used because it mimics the salty fluids inside our bodies. Our cells are protected by “walls” that are really a fatty layer called a membrane, but when you added the drop of detergent you broke open the cell membrane and the DNA was released into the water. When the alcohol layer was added the DNA strands gradually migrated into it and joined to other DNA strands. As more and more strands stuck together, the DNA became visible to the naked eye. Isn't it amazing that such tiny molecules hold all the information to make you so unique?
http://www.nature.ca/genome/05/051/pdfs/DNAextract_e.pdf
Monday, February 8, 2010
DNA Videos
DNA Replication Song
http://www.youtube.com/watch?v=dIZpb93NYlw
It's Too Late to Apotosize
http://www.youtube.com/watch?v=mHOX43-4PvE
http://www.youtube.com/watch?v=dIZpb93NYlw
It's Too Late to Apotosize
http://www.youtube.com/watch?v=mHOX43-4PvE
Cells and Taxonomy: Extra Credit
http://www.roomd113.com/Taks%20Assignments/Cells.pdf
http://www.roomd113.com/Taks%20Assignments/Taxonomy.pdf
For a 3D model of plant and animal cells:
http://www.forgefx.com/casestudies/prenticehall/ph/cells/cells.htm
http://www.roomd113.com/Taks%20Assignments/Taxonomy.pdf
For a 3D model of plant and animal cells:
http://www.forgefx.com/casestudies/prenticehall/ph/cells/cells.htm
DNA Homework 2
Nucleic Acids & Mechanism of Genetics
1. Describe components of deoxyribonucleic acid (DNA), and illustrate how
information for specifying the traits of an organism is carried in the DNA
2. Explain replication, transcription, and translation using models of DNA and
ribonucleic acid (RNA)
DNA and RNA
1. Deoxyribonucleic acid (DNA) is along molecule comprised of four bases: ______,
______, ______, and ______.
2. Of the four DNA bases, ______ bonds to thymine and ______ bonds to guanine.
3. Cells use strands of nucleic acids called ______ to synthesize proteins based on DNA
sequences.
4. In RNA, ______ replaces thymine as the base that bonds to adenine.
5. ______ is a six-protein enzyme that unzips the double-stranded DNA during
transcription.
6. Portions of the RNA strand that are integral to its purpose are called ______, while the
unnecessary segments hat are removed are called ______.
7. The straight chain of amino acids is called the ______ structure of the protein.
8. A ______ is a three-nucleotide sequence in mRNA that specifies a particular amino
acid or termination signal and functions as the basic unit of the genetic code.
______.
9. All living things have either ______ or ______ as their genetic material.
10. The shape of DNA is called a ______ , and is comprised of two strands that coil
around each other.
11. The bonds responsible for base-base pairing in DNA are ______ bonds.
12. While DNA takes the form of a double helix, RNA is a ______ strand of bases.
13. ______ refers to the process by which mRNA is made from a DNA template.
14. The ______ is a small segment of DNA that tells the RNA polymerase where to begin
transcription.
15. ______ is the process by which proteins are synthesized.
16. ______ and ______ are two kinds of organelles that have their own DNA.
17. An ______ is a kind of protein that acts like a catalyst; it drives a reaction toward its
equilibrium state
as quickly as possible.
18. During ______, all of the unnecessary parts of the RNA sequence are removed.
Answers
1. adenine, thymine, cytosine, and guanine
2. adenine, cytosine
3. RNA
4. uracil
5. RNA polymerase
6. exons, introns
7. primary
8. codon
9. DNA or RNA
10. double helix
12. hydrogen
12. single
13. transcription
14. promoter region
15. translation
16. mitochondria and chloroplasts
17. enzyme
18. RNA processing
http://www.roomd113.com/Taks%20Assignments/Nucleic%20Acids.pdf
DNA/RNA Tutorial
http://www.visionlearning.com/library/module_viewer.php?mid=63&mcid=&l=
1. Describe components of deoxyribonucleic acid (DNA), and illustrate how
information for specifying the traits of an organism is carried in the DNA
2. Explain replication, transcription, and translation using models of DNA and
ribonucleic acid (RNA)
DNA and RNA
1. Deoxyribonucleic acid (DNA) is along molecule comprised of four bases: ______,
______, ______, and ______.
2. Of the four DNA bases, ______ bonds to thymine and ______ bonds to guanine.
3. Cells use strands of nucleic acids called ______ to synthesize proteins based on DNA
sequences.
4. In RNA, ______ replaces thymine as the base that bonds to adenine.
5. ______ is a six-protein enzyme that unzips the double-stranded DNA during
transcription.
6. Portions of the RNA strand that are integral to its purpose are called ______, while the
unnecessary segments hat are removed are called ______.
7. The straight chain of amino acids is called the ______ structure of the protein.
8. A ______ is a three-nucleotide sequence in mRNA that specifies a particular amino
acid or termination signal and functions as the basic unit of the genetic code.
______.
9. All living things have either ______ or ______ as their genetic material.
10. The shape of DNA is called a ______ , and is comprised of two strands that coil
around each other.
11. The bonds responsible for base-base pairing in DNA are ______ bonds.
12. While DNA takes the form of a double helix, RNA is a ______ strand of bases.
13. ______ refers to the process by which mRNA is made from a DNA template.
14. The ______ is a small segment of DNA that tells the RNA polymerase where to begin
transcription.
15. ______ is the process by which proteins are synthesized.
16. ______ and ______ are two kinds of organelles that have their own DNA.
17. An ______ is a kind of protein that acts like a catalyst; it drives a reaction toward its
equilibrium state
as quickly as possible.
18. During ______, all of the unnecessary parts of the RNA sequence are removed.
Answers
1. adenine, thymine, cytosine, and guanine
2. adenine, cytosine
3. RNA
4. uracil
5. RNA polymerase
6. exons, introns
7. primary
8. codon
9. DNA or RNA
10. double helix
12. hydrogen
12. single
13. transcription
14. promoter region
15. translation
16. mitochondria and chloroplasts
17. enzyme
18. RNA processing
http://www.roomd113.com/Taks%20Assignments/Nucleic%20Acids.pdf
DNA/RNA Tutorial
http://www.visionlearning.com/library/module_viewer.php?mid=63&mcid=&l=
Saturday, February 6, 2010
Micropolitan Museum
Resource to find and see all things microscopic.
http://www.microscopy-uk.org.uk/micropolitan/index.html
http://www.microscopy-uk.org.uk/micropolitan/index.html
Tuesday, February 2, 2010
Cell Division and Organization of Systems
Asexual Reproduction
spontaneous generation
budding
fragmentation
binary fission
parthenogenesis
Sexual Reproduction
Allogeny and Autogamy
Mitosis and Meiosis (Phases)
Prophase
Metaphase
Anaphase
Telophase
Cytokinesis
Interphase
PMAT I and PMAT II
Heirarchy of Order
Kingdom
Phylum
Class
Order
Family
Genus
Species
spontaneous generation
budding
fragmentation
binary fission
parthenogenesis
Sexual Reproduction
Allogeny and Autogamy
Mitosis and Meiosis (Phases)
Prophase
Metaphase
Anaphase
Telophase
Cytokinesis
Interphase
PMAT I and PMAT II
Heirarchy of Order
Kingdom
Phylum
Class
Order
Family
Genus
Species
Bellringer 3
Prokaryotes differ from eukaryotes in the following ways except for:
1. have a nucleus
2. have a cell wall
3. unicellular
4. all of the above
1. have a nucleus
2. have a cell wall
3. unicellular
4. all of the above
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