Cell Biology, Molecular Biology, and Genetics - MCAT Biological and Biochemical Foundations of Living Systems
Card 1 of 2944
Which of the following criteria does not help differentiate between prokaryotes and eukaryotes?
Which of the following criteria does not help differentiate between prokaryotes and eukaryotes?
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Cell walls are present in virtually all prokaryotic cells, but are also found in certain eukayotic domains (such as plants and fungi). As such, the presence of a cell wall cannot be used to distinguish between prokaryotic and eukaryotic cells.
Cell walls are present in virtually all prokaryotic cells, but are also found in certain eukayotic domains (such as plants and fungi). As such, the presence of a cell wall cannot be used to distinguish between prokaryotic and eukaryotic cells.
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Prions are the suspected cause of a wide variety of neurodegenerative diseases in mammals. According to prevailing theory, prions are infectious particles made only of protein and found in high concentrations in the brains of infected animals. All mammals produce normal prion protein, PrPC, a transmembrane protein whose function remains unclear.
Infectious prions, PrPRes, induce conformational changes in the existing PrPC proteins according to the following reaction:
PrPC + PrPRes → PrPRes + PrPRes
The PrPRes is then suspected to accumulate in the nervous tissue of infected patients and cause disease. This model of transmission generates replicated proteins, but does so bypassing the standard model of the central dogma of molecular biology. Transcription and translation apparently do not play a role in this replication process.
This theory is a major departure from previously established biological dogma. A scientist decides to test the protein-only theory of prion propagation. He establishes his experiment as follows:
Homogenized brain matter of infected rabbits is injected into the brains of healthy rabbits, as per the following table:
Rabbit 1 and 2: injected with normal saline on days 1 and 2
The above trials serve as controls.
Rabbit 3 and 4: injected with homogenized brain matter on days 1 and 2
The above trials use unmodified brain matter.
Rabbit 5 and 6: injected with irradiated homogenized brain matter on days 1 and 2
The above trials use brain matter that has been irradiated to destroy nucleic acids in the homogenate.
Rabbit 7 and 8: injected with protein-free centrifuged homogenized brain matter on days 1 and 2
The above trials use brain matter that has been centrifuged to generate a protein-free homogenate and a protein-rich homogenate based on molecular weight.
Rabbit 9 and 10: injected with boiled homogenized brain matter on days 1 and 2
The above trials use brain matter that have been boiled to destroy any bacterial contaminants in the homogenate.
Another experiment shows that PrPC reacts with hormones that circulate among nervous tissue. As a transmembrane protein, what kinds of hormones are most likely to interact with PrPC?
I. Peptide hormones
II. Catecholamines
III. Steroid Hormones
Prions are the suspected cause of a wide variety of neurodegenerative diseases in mammals. According to prevailing theory, prions are infectious particles made only of protein and found in high concentrations in the brains of infected animals. All mammals produce normal prion protein, PrPC, a transmembrane protein whose function remains unclear.
Infectious prions, PrPRes, induce conformational changes in the existing PrPC proteins according to the following reaction:
PrPC + PrPRes → PrPRes + PrPRes
The PrPRes is then suspected to accumulate in the nervous tissue of infected patients and cause disease. This model of transmission generates replicated proteins, but does so bypassing the standard model of the central dogma of molecular biology. Transcription and translation apparently do not play a role in this replication process.
This theory is a major departure from previously established biological dogma. A scientist decides to test the protein-only theory of prion propagation. He establishes his experiment as follows:
Homogenized brain matter of infected rabbits is injected into the brains of healthy rabbits, as per the following table:
Rabbit 1 and 2: injected with normal saline on days 1 and 2
The above trials serve as controls.
Rabbit 3 and 4: injected with homogenized brain matter on days 1 and 2
The above trials use unmodified brain matter.
Rabbit 5 and 6: injected with irradiated homogenized brain matter on days 1 and 2
The above trials use brain matter that has been irradiated to destroy nucleic acids in the homogenate.
Rabbit 7 and 8: injected with protein-free centrifuged homogenized brain matter on days 1 and 2
The above trials use brain matter that has been centrifuged to generate a protein-free homogenate and a protein-rich homogenate based on molecular weight.
Rabbit 9 and 10: injected with boiled homogenized brain matter on days 1 and 2
The above trials use brain matter that have been boiled to destroy any bacterial contaminants in the homogenate.
Another experiment shows that PrPC reacts with hormones that circulate among nervous tissue. As a transmembrane protein, what kinds of hormones are most likely to interact with PrPC?
I. Peptide hormones
II. Catecholamines
III. Steroid Hormones
Tap to reveal answer
Students should know that peptide hormones (and catecholamines, but this is not required to answer the question correctly as written here) interact with surface receptors and do not freely go through a membrane. They must interact with the transmembrane surface receptors to initiate a signal transduction cascade. In contrast, steroid hormones can bypass the transmembrance protein receptors by freely diffusing across the memberane, due to their small, nonpolar nature. In this case, only peptide hormones and catecholamines will require the facilitated diffusion mechanism provided by a transmembrane protein.
Students should know that peptide hormones (and catecholamines, but this is not required to answer the question correctly as written here) interact with surface receptors and do not freely go through a membrane. They must interact with the transmembrane surface receptors to initiate a signal transduction cascade. In contrast, steroid hormones can bypass the transmembrance protein receptors by freely diffusing across the memberane, due to their small, nonpolar nature. In this case, only peptide hormones and catecholamines will require the facilitated diffusion mechanism provided by a transmembrane protein.
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Scientists use a process called Flourescent In-Situ Hybridization, or FISH, to study genetic disorders in humans. FISH is a technique that uses spectrographic analysis to determine the presence or absence, as well as the relative abundance, of genetic material in human cells.
To use FISH, scientists apply fluorescently-labeled bits of DNA of a known color, called probes, to samples of test DNA. These probes anneal to the sample DNA, and scientists can read the colors that result using laboratory equipment. One common use of FISH is to determine the presence of extra DNA in conditions of aneuploidy, a state in which a human cell has an abnormal number of chromosomes. Chromosomes are collections of DNA, the totality of which makes up a cell’s genome. Another typical use is in the study of cancer cells, where scientists use FISH labels to ascertain if genes have moved inappropriately in a cell’s genome.
Using red fluorescent tags, scientists label probe DNA for a gene known to be expressed more heavily in cancer cells than normal cells. They then label a probe for an immediately adjacent DNA sequence with a green fluorescent tag. Both probes are then added to three dishes, shown below. In dish 1 human bladder cells are incubated with the probes, in dish 2 human epithelial cells are incubated, and in dish 3 known non-cancerous cells are used. The relative luminescence observed in regions of interest in all dishes is shown below.

The bladder cells in dish 1 begin to undergo programmed cell death, or apoptosis, when they initially become cancerous. If the cells form sodium-selective pores in their membranes to begin the process of cell death, sodium ions can begin to enter the cells without regulation. What will likely happen to a resting cell membrane potential when sodium enters?
Scientists use a process called Flourescent In-Situ Hybridization, or FISH, to study genetic disorders in humans. FISH is a technique that uses spectrographic analysis to determine the presence or absence, as well as the relative abundance, of genetic material in human cells.
To use FISH, scientists apply fluorescently-labeled bits of DNA of a known color, called probes, to samples of test DNA. These probes anneal to the sample DNA, and scientists can read the colors that result using laboratory equipment. One common use of FISH is to determine the presence of extra DNA in conditions of aneuploidy, a state in which a human cell has an abnormal number of chromosomes. Chromosomes are collections of DNA, the totality of which makes up a cell’s genome. Another typical use is in the study of cancer cells, where scientists use FISH labels to ascertain if genes have moved inappropriately in a cell’s genome.
Using red fluorescent tags, scientists label probe DNA for a gene known to be expressed more heavily in cancer cells than normal cells. They then label a probe for an immediately adjacent DNA sequence with a green fluorescent tag. Both probes are then added to three dishes, shown below. In dish 1 human bladder cells are incubated with the probes, in dish 2 human epithelial cells are incubated, and in dish 3 known non-cancerous cells are used. The relative luminescence observed in regions of interest in all dishes is shown below.

The bladder cells in dish 1 begin to undergo programmed cell death, or apoptosis, when they initially become cancerous. If the cells form sodium-selective pores in their membranes to begin the process of cell death, sodium ions can begin to enter the cells without regulation. What will likely happen to a resting cell membrane potential when sodium enters?
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The pores formed are, according to the question, sodium selective. So it is unlikely that potassium concentration changes will be a major contributor to membrane potential changes. Since sodium is postively charged, and the ions entering are sodium, the inside of the cell will become more positively charged as sodium permeability goes up. We know that sodium will enter and potassium will leave due to the established gradients determined by sodium-potassium ATPase.
The pores formed are, according to the question, sodium selective. So it is unlikely that potassium concentration changes will be a major contributor to membrane potential changes. Since sodium is postively charged, and the ions entering are sodium, the inside of the cell will become more positively charged as sodium permeability goes up. We know that sodium will enter and potassium will leave due to the established gradients determined by sodium-potassium ATPase.
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What is the average resting potential of a nerve cell membrane?
What is the average resting potential of a nerve cell membrane?
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Membrane potential is the difference between the electric potential inside the cell and the electric potential outside the cell. At rest, the membrane potential of most cells (including nerve cells) is between -70mV and -80mV due to the concentration of intracellular and extracellular potassium and sodium ions. The expulsion of sodium ions, in particular, contributes to positive charges outside the cell and lowers the charge inside.
Membrane potential is the difference between the electric potential inside the cell and the electric potential outside the cell. At rest, the membrane potential of most cells (including nerve cells) is between -70mV and -80mV due to the concentration of intracellular and extracellular potassium and sodium ions. The expulsion of sodium ions, in particular, contributes to positive charges outside the cell and lowers the charge inside.
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The side of a plasma membrane receptor will bind to the ligand and the side of the plasma membrane receptor will initiate a cell response.
The side of a plasma membrane receptor will bind to the ligand and the side of the plasma membrane receptor will initiate a cell response.
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In signal transduction, a ligand binds to the extracellular side of the plasma membrane receptor. This initiates a cellular response that is facilitated by the intracellular side. The intracellular region can activate a G protein, bind to an effector, or initiate other cellular responses. These responses often result in a signal cascade that affects transcription factors and alters gene expression.
In signal transduction, a ligand binds to the extracellular side of the plasma membrane receptor. This initiates a cellular response that is facilitated by the intracellular side. The intracellular region can activate a G protein, bind to an effector, or initiate other cellular responses. These responses often result in a signal cascade that affects transcription factors and alters gene expression.
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Choose the transcript created if RNA polymerase transcribes the following template strand.
5'-ACTTGCAGGCC-3'
Choose the transcript created if RNA polymerase transcribes the following template strand.
5'-ACTTGCAGGCC-3'
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When transcribing from a template strand, here are a few things to remember:
1. RNA polymerase reads the strand in the 3' to 5' direction.
2. In the RNA transcript, thymine is replaced with uracil.
In order to double check, make sure that the two strands are complementary when antiparallel to one another.
Template: 5'-ACTTGCAGGCC-3'
Transcript: 3'-UGAACGUCCGG-5'
When transcribing from a template strand, here are a few things to remember:
1. RNA polymerase reads the strand in the 3' to 5' direction.
2. In the RNA transcript, thymine is replaced with uracil.
In order to double check, make sure that the two strands are complementary when antiparallel to one another.
Template: 5'-ACTTGCAGGCC-3'
Transcript: 3'-UGAACGUCCGG-5'
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The base sequence of one strand of tRNA is v. What is the corresponding sequence of DNA?
The base sequence of one strand of tRNA is v. What is the corresponding sequence of DNA?
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Both tRNA and DNA are complementary to mRNA, meaning that they will have the exact same sequence in the exact same direction with only one distinction: tRNA will use uracil where DNA uses thymine.
The given tRNA strand is 5'-AGUCGAUCUAGC-3'.
The corresponding DNA strand will be 5'-AGTCGATCTAGC-3'.
Both tRNA and DNA are complementary to mRNA, meaning that they will have the exact same sequence in the exact same direction with only one distinction: tRNA will use uracil where DNA uses thymine.
The given tRNA strand is 5'-AGUCGAUCUAGC-3'.
The corresponding DNA strand will be 5'-AGTCGATCTAGC-3'.
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The concept of genomic imprinting is important in human genetics. In genomic imprinting, a certain region of DNA is only expressed by one of the two chromosomes that make up a typical homologous pair. In healthy individuals, genomic imprinting results in the silencing of genes in a certain section of the maternal chromosome 15. The DNA in this part of the chromosome is "turned off" by the addition of methyl groups to the DNA molecule. Healthy people will thus only have expression of this section of chromosome 15 from paternally-derived DNA.
The two classic human diseases that illustrate defects in genomic imprinting are Prader-Willi and Angelman Syndromes. In Prader-Willi Syndrome, the section of paternal chromosome 15 that is usually expressed is disrupted, such as by a chromosomal deletion. In Angelman Syndrome, maternal genes in this section are deleted, while paternal genes are silenced. Prader-Willi Syndrome is thus closely linked to paternal inheritance, while Angelman Syndrome is linked to maternal inheritance.
Figure 1 shows the chromosome 15 homologous pair for a child with Prader-Willi Syndrome. The parental chromosomes are also shown. The genes on the mother’s chromosomes are silenced normally, as represented by the black boxes. At once, there is also a chromosomal deletion on one of the paternal chromosomes. The result is that the child does not have any genes expressed that are normally found on that region of this chromosome.

Histones are proteins that can interact with some sequences of DNA to help it coil into a more manageable arrangement within the nucleus. If the DNA-histone interaction is mediated primarily by intermolecular bonds, which of the following is likely true of histones?
The concept of genomic imprinting is important in human genetics. In genomic imprinting, a certain region of DNA is only expressed by one of the two chromosomes that make up a typical homologous pair. In healthy individuals, genomic imprinting results in the silencing of genes in a certain section of the maternal chromosome 15. The DNA in this part of the chromosome is "turned off" by the addition of methyl groups to the DNA molecule. Healthy people will thus only have expression of this section of chromosome 15 from paternally-derived DNA.
The two classic human diseases that illustrate defects in genomic imprinting are Prader-Willi and Angelman Syndromes. In Prader-Willi Syndrome, the section of paternal chromosome 15 that is usually expressed is disrupted, such as by a chromosomal deletion. In Angelman Syndrome, maternal genes in this section are deleted, while paternal genes are silenced. Prader-Willi Syndrome is thus closely linked to paternal inheritance, while Angelman Syndrome is linked to maternal inheritance.
Figure 1 shows the chromosome 15 homologous pair for a child with Prader-Willi Syndrome. The parental chromosomes are also shown. The genes on the mother’s chromosomes are silenced normally, as represented by the black boxes. At once, there is also a chromosomal deletion on one of the paternal chromosomes. The result is that the child does not have any genes expressed that are normally found on that region of this chromosome.

Histones are proteins that can interact with some sequences of DNA to help it coil into a more manageable arrangement within the nucleus. If the DNA-histone interaction is mediated primarily by intermolecular bonds, which of the following is likely true of histones?
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DNA is acidic, and thus has a generally negative charge in aqueous conditions (consider what this means for the electrophoresis pattern of DNA in an agarose gel). Because the interaction has to be tight to coil DNA effectively, it must be a dipole interaction. Dipole interactions are relatively strong intermolecular forces. Covalent forces, however, are intramolecular and much more permanent than dipole interactions.
Acidic DNA has a negativecharge, which will be drawn to a basic histone with a positive charge.
DNA is acidic, and thus has a generally negative charge in aqueous conditions (consider what this means for the electrophoresis pattern of DNA in an agarose gel). Because the interaction has to be tight to coil DNA effectively, it must be a dipole interaction. Dipole interactions are relatively strong intermolecular forces. Covalent forces, however, are intramolecular and much more permanent than dipole interactions.
Acidic DNA has a negativecharge, which will be drawn to a basic histone with a positive charge.
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Which class of upstream DNA element is responsible for increasing transcription of target genes?
Which class of upstream DNA element is responsible for increasing transcription of target genes?
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An enhancer is a cis-acting element that is responsible for activating or increasing expression of a target gene. An insulator is a boundary element between inactive and active domains of DNA. Both activators and repressors are trans-acting (protein) factors that modulate gene expression.
An enhancer is a cis-acting element that is responsible for activating or increasing expression of a target gene. An insulator is a boundary element between inactive and active domains of DNA. Both activators and repressors are trans-acting (protein) factors that modulate gene expression.
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Which of the following cell organelles is responsible for making proteins?
Which of the following cell organelles is responsible for making proteins?
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Ribisomes are the protein creators within the cell. Ribisomes use a process called translation (via the use of mRNA) to form proteins.
The Golgi apparatus and rough endoplasmic reticulum are involved in protein modification and packaging. Lysosomes are involved in detoxification.
Ribisomes are the protein creators within the cell. Ribisomes use a process called translation (via the use of mRNA) to form proteins.
The Golgi apparatus and rough endoplasmic reticulum are involved in protein modification and packaging. Lysosomes are involved in detoxification.
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A mouse has a mutation in which its sister chromatids are unable to separate during cell division. What phase of mitosis should researchers target, in order to alleviate the condition using drug therapy?
A mouse has a mutation in which its sister chromatids are unable to separate during cell division. What phase of mitosis should researchers target, in order to alleviate the condition using drug therapy?
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During anaphase, sister chromatids are separated and pulled to polar ends of the cell. Drug therapy would best be able to target the mutation during this phase of mitosis.
Chromosomes condense and exit the nucleus during prophase. Alignment along the equatorial plate occurs during metaphase. Separation occurs during anaphase, and the nuclei begin to re-form during telophase in preparation for cytokinesis.
During anaphase, sister chromatids are separated and pulled to polar ends of the cell. Drug therapy would best be able to target the mutation during this phase of mitosis.
Chromosomes condense and exit the nucleus during prophase. Alignment along the equatorial plate occurs during metaphase. Separation occurs during anaphase, and the nuclei begin to re-form during telophase in preparation for cytokinesis.
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The is the site of attachment of spindle fibers to sister chromatids during mitosis.
The is the site of attachment of spindle fibers to sister chromatids during mitosis.
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Centrosomes are portions of the cell that help nucleate microtubules and form the mitotic spindle. Centrioles are composed of tubulin and are portions of the centrosome. The centromere is the portion of the chromosome where the two sister chromatids are linked. The kinetochore is a protein structure that helps associate the mitotic spindle to the sister chromatids. The outer portion of the kinetochore interacts with the microtubules, while the inner portion associates with the centromeric DNA.
Centrosomes are portions of the cell that help nucleate microtubules and form the mitotic spindle. Centrioles are composed of tubulin and are portions of the centrosome. The centromere is the portion of the chromosome where the two sister chromatids are linked. The kinetochore is a protein structure that helps associate the mitotic spindle to the sister chromatids. The outer portion of the kinetochore interacts with the microtubules, while the inner portion associates with the centromeric DNA.
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Apoptosis can be induced by mitochondria via the release of which protein from the mitochondrial inner membrane?
Apoptosis can be induced by mitochondria via the release of which protein from the mitochondrial inner membrane?
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During the intrinsic cycle of apoptosis, the mitochondrial outer membrane becomes permeable to cytochrome C. The release of cytochrome C induces multiple cellular processes that lead to apoptosis.
During the intrinsic cycle of apoptosis, the mitochondrial outer membrane becomes permeable to cytochrome C. The release of cytochrome C induces multiple cellular processes that lead to apoptosis.
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A mother is homozygous for blood type A and a father has blood type AB. Which of the following could describe their child's blood type?
A mother is homozygous for blood type A and a father has blood type AB. Which of the following could describe their child's blood type?
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We are told that the mother is homozygous for blood type A (AA) and the father has blood type AB (AB). Using a simple punnett squre we can find that 50% of the offspring would be blood type A and 50% would be blood type AB.
We are told that the mother is homozygous for blood type A (AA) and the father has blood type AB (AB). Using a simple punnett squre we can find that 50% of the offspring would be blood type A and 50% would be blood type AB.
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In fruit flies, white eyes are produced by a dominant X-linked mutation, with the wild-type being red-eyed. If a white-eyed male is mated with a red-eyed female, what will be the phenotype of the resulting offspring?
In fruit flies, white eyes are produced by a dominant X-linked mutation, with the wild-type being red-eyed. If a white-eyed male is mated with a red-eyed female, what will be the phenotype of the resulting offspring?
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We can depict the parental genotypes by using
to signify the dominant white-eye allele and
to signify the recessive red-eye allele.
The mother would have genotype
since she has red eyes. The father would have genotype
since he has white eyes.
We can see that the possible genotype for offspring will be either
for a daughter or
for a son. Any daughters must inherit the X-chromosome from both parents, and must therefore inherit a white-eye allele from the father. We can conclude that all daughters will have white eyes.
We can depict the parental genotypes by using to signify the dominant white-eye allele and
to signify the recessive red-eye allele.
The mother would have genotype since she has red eyes. The father would have genotype
since he has white eyes.
We can see that the possible genotype for offspring will be either for a daughter or
for a son. Any daughters must inherit the X-chromosome from both parents, and must therefore inherit a white-eye allele from the father. We can conclude that all daughters will have white eyes.
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Cryptosporidium is a genus of gastrointestinal parasite that infects the intestinal epithelium of mammals. Cryptosporidium is water-borne, and is an apicomplexan parasite. This phylum also includes Plasmodium, Babesia, and Toxoplasma.
Apicomplexans are unique due to their apicoplast, an apical organelle that helps penetrate mammalian epithelium. In the case of cryptosporidium, there is an interaction between the surface proteins of mammalian epithelial tissue and those of the apical portion of the cryptosporidium infective stage, or oocyst. A scientist is conducting an experiment to test the hypothesis that the oocyst secretes a peptide compound that neutralizes intestinal defense cells. These defense cells are resident in the intestinal epithelium, and defend the tissue by phagocytizing the oocysts.
She sets up the following experiment:
As the neutralizing compound was believed to be secreted by the oocyst, the scientist collected oocysts onto growth media. The oocysts were grown among intestinal epithelial cells, and then the media was collected. The media was then added to another plate where Toxoplasma gondii was growing with intestinal epithelial cells. A second plate of Toxoplasma gondii was grown with the same type of intestinal epithelium, but no oocyst-sourced media was added.
You are conducting a study of an isolated tribe in New Guinea, and you find that there is widespread resistance to cryptosporidium infection. You determine that the gene for resistance is inherited in a recessive fashion. The incidence of resistance in a normal population is 1/900. In New Guinea, it is 1/25. What are the carrier frequencies in the normal population and in New Guinea, respectively? Assume that the populations are in Hardy-Weinberg equilibrium.
Cryptosporidium is a genus of gastrointestinal parasite that infects the intestinal epithelium of mammals. Cryptosporidium is water-borne, and is an apicomplexan parasite. This phylum also includes Plasmodium, Babesia, and Toxoplasma.
Apicomplexans are unique due to their apicoplast, an apical organelle that helps penetrate mammalian epithelium. In the case of cryptosporidium, there is an interaction between the surface proteins of mammalian epithelial tissue and those of the apical portion of the cryptosporidium infective stage, or oocyst. A scientist is conducting an experiment to test the hypothesis that the oocyst secretes a peptide compound that neutralizes intestinal defense cells. These defense cells are resident in the intestinal epithelium, and defend the tissue by phagocytizing the oocysts.
She sets up the following experiment:
As the neutralizing compound was believed to be secreted by the oocyst, the scientist collected oocysts onto growth media. The oocysts were grown among intestinal epithelial cells, and then the media was collected. The media was then added to another plate where Toxoplasma gondii was growing with intestinal epithelial cells. A second plate of Toxoplasma gondii was grown with the same type of intestinal epithelium, but no oocyst-sourced media was added.
You are conducting a study of an isolated tribe in New Guinea, and you find that there is widespread resistance to cryptosporidium infection. You determine that the gene for resistance is inherited in a recessive fashion. The incidence of resistance in a normal population is 1/900. In New Guinea, it is 1/25. What are the carrier frequencies in the normal population and in New Guinea, respectively? Assume that the populations are in Hardy-Weinberg equilibrium.
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The Hardy-Weinberg equilibrium expression says that p2+2pq+q2 = 1.
We know that the incidence of q2 (getting two recessive alleles, and thus being resistant) is 1/900 in a general population, and 1/25 in New Guinea. The recessive allele frequency, q, will be 1/30 and 1/5, respectively.
The carrier frequency is 2pq, where p = 1-q.
Using this information, we can find the respective carrier frequencies.
General population:


New Guinea:


The Hardy-Weinberg equilibrium expression says that p2+2pq+q2 = 1.
We know that the incidence of q2 (getting two recessive alleles, and thus being resistant) is 1/900 in a general population, and 1/25 in New Guinea. The recessive allele frequency, q, will be 1/30 and 1/5, respectively.
The carrier frequency is 2pq, where p = 1-q.
Using this information, we can find the respective carrier frequencies.
General population:
New Guinea:
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The concept of genomic imprinting is important in human genetics. In genomic imprinting, a certain region of DNA is only expressed by one of the two chromosomes that make up a typical homologous pair. In healthy individuals, genomic imprinting results in the silencing of genes in a certain section of the maternal chromosome 15. The DNA in this part of the chromosome is "turned off" by the addition of methyl groups to the DNA molecule. Healthy people will thus only have expression of this section of chromosome 15 from paternally-derived DNA.
The two classic human diseases that illustrate defects in genomic imprinting are Prader-Willi and Angelman Syndromes. In Prader-Willi Syndrome, the section of paternal chromosome 15 that is usually expressed is disrupted, such as by a chromosomal deletion. In Angelman Syndrome, maternal genes in this section are deleted, while paternal genes are silenced. Prader-Willi Syndrome is thus closely linked to paternal inheritance, while Angelman Syndrome is linked to maternal inheritance.
Figure 1 shows the chromosome 15 homologous pair for a child with Prader-Willi Syndrome. The parental chromosomes are also shown. The genes on the mother’s chromosomes are silenced normally, as represented by the black boxes. At once, there is also a chromosomal deletion on one of the paternal chromosomes. The result is that the child does not have any genes expressed that are normally found on that region of this chromosome.

A scientist discovers another genetic disease that has similar symptoms to Prader-Willi Syndrome. He discovers that this disease is recessive, and caused not by changes to chromosome 15, but by a point mutation on chromosome 3. He calculates the recessive allele frequency in a population to be
.
Assuming the that normal allele,
, and recessive allele,
, are the only two alleles in this population, what is the percentage of the population that has the disease?
The concept of genomic imprinting is important in human genetics. In genomic imprinting, a certain region of DNA is only expressed by one of the two chromosomes that make up a typical homologous pair. In healthy individuals, genomic imprinting results in the silencing of genes in a certain section of the maternal chromosome 15. The DNA in this part of the chromosome is "turned off" by the addition of methyl groups to the DNA molecule. Healthy people will thus only have expression of this section of chromosome 15 from paternally-derived DNA.
The two classic human diseases that illustrate defects in genomic imprinting are Prader-Willi and Angelman Syndromes. In Prader-Willi Syndrome, the section of paternal chromosome 15 that is usually expressed is disrupted, such as by a chromosomal deletion. In Angelman Syndrome, maternal genes in this section are deleted, while paternal genes are silenced. Prader-Willi Syndrome is thus closely linked to paternal inheritance, while Angelman Syndrome is linked to maternal inheritance.
Figure 1 shows the chromosome 15 homologous pair for a child with Prader-Willi Syndrome. The parental chromosomes are also shown. The genes on the mother’s chromosomes are silenced normally, as represented by the black boxes. At once, there is also a chromosomal deletion on one of the paternal chromosomes. The result is that the child does not have any genes expressed that are normally found on that region of this chromosome.

A scientist discovers another genetic disease that has similar symptoms to Prader-Willi Syndrome. He discovers that this disease is recessive, and caused not by changes to chromosome 15, but by a point mutation on chromosome 3. He calculates the recessive allele frequency in a population to be .
Assuming the that normal allele, , and recessive allele,
, are the only two alleles in this population, what is the percentage of the population that has the disease?
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Based on Hardy-Weinberg principles, we can predict the phenotype and genotype frequencies of a given population based on the equation
. In this equation,
is the recessive allele frequency and
is the recessive phenotype frequency, or frequency of homozygous recessive genotypes.
The genotype frequency of
, necessary for the development of a recessive disease, is going to be the square of the recessive allele frequency,
.


Based on Hardy-Weinberg principles, we can predict the phenotype and genotype frequencies of a given population based on the equation . In this equation,
is the recessive allele frequency and
is the recessive phenotype frequency, or frequency of homozygous recessive genotypes.
The genotype frequency of , necessary for the development of a recessive disease, is going to be the square of the recessive allele frequency,
.
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Which of the following criteria does not help differentiate between prokaryotes and eukaryotes?
Which of the following criteria does not help differentiate between prokaryotes and eukaryotes?
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Cell walls are present in virtually all prokaryotic cells, but are also found in certain eukayotic domains (such as plants and fungi). As such, the presence of a cell wall cannot be used to distinguish between prokaryotic and eukaryotic cells.
Cell walls are present in virtually all prokaryotic cells, but are also found in certain eukayotic domains (such as plants and fungi). As such, the presence of a cell wall cannot be used to distinguish between prokaryotic and eukaryotic cells.
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Prions are the suspected cause of a wide variety of neurodegenerative diseases in mammals. According to prevailing theory, prions are infectious particles made only of protein and found in high concentrations in the brains of infected animals. All mammals produce normal prion protein, PrPC, a transmembrane protein whose function remains unclear.
Infectious prions, PrPRes, induce conformational changes in the existing PrPC proteins according to the following reaction:
PrPC + PrPRes → PrPRes + PrPRes
The PrPRes is then suspected to accumulate in the nervous tissue of infected patients and cause disease. This model of transmission generates replicated proteins, but does so bypassing the standard model of the central dogma of molecular biology. Transcription and translation apparently do not play a role in this replication process.
This theory is a major departure from previously established biological dogma. A scientist decides to test the protein-only theory of prion propagation. He establishes his experiment as follows:
Homogenized brain matter of infected rabbits is injected into the brains of healthy rabbits, as per the following table:
Rabbit 1 and 2: injected with normal saline on days 1 and 2
The above trials serve as controls.
Rabbit 3 and 4: injected with homogenized brain matter on days 1 and 2
The above trials use unmodified brain matter.
Rabbit 5 and 6: injected with irradiated homogenized brain matter on days 1 and 2
The above trials use brain matter that has been irradiated to destroy nucleic acids in the homogenate.
Rabbit 7 and 8: injected with protein-free centrifuged homogenized brain matter on days 1 and 2
The above trials use brain matter that has been centrifuged to generate a protein-free homogenate and a protein-rich homogenate based on molecular weight.
Rabbit 9 and 10: injected with boiled homogenized brain matter on days 1 and 2
The above trials use brain matter that have been boiled to destroy any bacterial contaminants in the homogenate.
Another experiment shows that PrPC reacts with hormones that circulate among nervous tissue. As a transmembrane protein, what kinds of hormones are most likely to interact with PrPC?
I. Peptide hormones
II. Catecholamines
III. Steroid Hormones
Prions are the suspected cause of a wide variety of neurodegenerative diseases in mammals. According to prevailing theory, prions are infectious particles made only of protein and found in high concentrations in the brains of infected animals. All mammals produce normal prion protein, PrPC, a transmembrane protein whose function remains unclear.
Infectious prions, PrPRes, induce conformational changes in the existing PrPC proteins according to the following reaction:
PrPC + PrPRes → PrPRes + PrPRes
The PrPRes is then suspected to accumulate in the nervous tissue of infected patients and cause disease. This model of transmission generates replicated proteins, but does so bypassing the standard model of the central dogma of molecular biology. Transcription and translation apparently do not play a role in this replication process.
This theory is a major departure from previously established biological dogma. A scientist decides to test the protein-only theory of prion propagation. He establishes his experiment as follows:
Homogenized brain matter of infected rabbits is injected into the brains of healthy rabbits, as per the following table:
Rabbit 1 and 2: injected with normal saline on days 1 and 2
The above trials serve as controls.
Rabbit 3 and 4: injected with homogenized brain matter on days 1 and 2
The above trials use unmodified brain matter.
Rabbit 5 and 6: injected with irradiated homogenized brain matter on days 1 and 2
The above trials use brain matter that has been irradiated to destroy nucleic acids in the homogenate.
Rabbit 7 and 8: injected with protein-free centrifuged homogenized brain matter on days 1 and 2
The above trials use brain matter that has been centrifuged to generate a protein-free homogenate and a protein-rich homogenate based on molecular weight.
Rabbit 9 and 10: injected with boiled homogenized brain matter on days 1 and 2
The above trials use brain matter that have been boiled to destroy any bacterial contaminants in the homogenate.
Another experiment shows that PrPC reacts with hormones that circulate among nervous tissue. As a transmembrane protein, what kinds of hormones are most likely to interact with PrPC?
I. Peptide hormones
II. Catecholamines
III. Steroid Hormones
Tap to reveal answer
Students should know that peptide hormones (and catecholamines, but this is not required to answer the question correctly as written here) interact with surface receptors and do not freely go through a membrane. They must interact with the transmembrane surface receptors to initiate a signal transduction cascade. In contrast, steroid hormones can bypass the transmembrance protein receptors by freely diffusing across the memberane, due to their small, nonpolar nature. In this case, only peptide hormones and catecholamines will require the facilitated diffusion mechanism provided by a transmembrane protein.
Students should know that peptide hormones (and catecholamines, but this is not required to answer the question correctly as written here) interact with surface receptors and do not freely go through a membrane. They must interact with the transmembrane surface receptors to initiate a signal transduction cascade. In contrast, steroid hormones can bypass the transmembrance protein receptors by freely diffusing across the memberane, due to their small, nonpolar nature. In this case, only peptide hormones and catecholamines will require the facilitated diffusion mechanism provided by a transmembrane protein.
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Scientists use a process called Flourescent In-Situ Hybridization, or FISH, to study genetic disorders in humans. FISH is a technique that uses spectrographic analysis to determine the presence or absence, as well as the relative abundance, of genetic material in human cells.
To use FISH, scientists apply fluorescently-labeled bits of DNA of a known color, called probes, to samples of test DNA. These probes anneal to the sample DNA, and scientists can read the colors that result using laboratory equipment. One common use of FISH is to determine the presence of extra DNA in conditions of aneuploidy, a state in which a human cell has an abnormal number of chromosomes. Chromosomes are collections of DNA, the totality of which makes up a cell’s genome. Another typical use is in the study of cancer cells, where scientists use FISH labels to ascertain if genes have moved inappropriately in a cell’s genome.
Using red fluorescent tags, scientists label probe DNA for a gene known to be expressed more heavily in cancer cells than normal cells. They then label a probe for an immediately adjacent DNA sequence with a green fluorescent tag. Both probes are then added to three dishes, shown below. In dish 1 human bladder cells are incubated with the probes, in dish 2 human epithelial cells are incubated, and in dish 3 known non-cancerous cells are used. The relative luminescence observed in regions of interest in all dishes is shown below.

The bladder cells in dish 1 begin to undergo programmed cell death, or apoptosis, when they initially become cancerous. If the cells form sodium-selective pores in their membranes to begin the process of cell death, sodium ions can begin to enter the cells without regulation. What will likely happen to a resting cell membrane potential when sodium enters?
Scientists use a process called Flourescent In-Situ Hybridization, or FISH, to study genetic disorders in humans. FISH is a technique that uses spectrographic analysis to determine the presence or absence, as well as the relative abundance, of genetic material in human cells.
To use FISH, scientists apply fluorescently-labeled bits of DNA of a known color, called probes, to samples of test DNA. These probes anneal to the sample DNA, and scientists can read the colors that result using laboratory equipment. One common use of FISH is to determine the presence of extra DNA in conditions of aneuploidy, a state in which a human cell has an abnormal number of chromosomes. Chromosomes are collections of DNA, the totality of which makes up a cell’s genome. Another typical use is in the study of cancer cells, where scientists use FISH labels to ascertain if genes have moved inappropriately in a cell’s genome.
Using red fluorescent tags, scientists label probe DNA for a gene known to be expressed more heavily in cancer cells than normal cells. They then label a probe for an immediately adjacent DNA sequence with a green fluorescent tag. Both probes are then added to three dishes, shown below. In dish 1 human bladder cells are incubated with the probes, in dish 2 human epithelial cells are incubated, and in dish 3 known non-cancerous cells are used. The relative luminescence observed in regions of interest in all dishes is shown below.

The bladder cells in dish 1 begin to undergo programmed cell death, or apoptosis, when they initially become cancerous. If the cells form sodium-selective pores in their membranes to begin the process of cell death, sodium ions can begin to enter the cells without regulation. What will likely happen to a resting cell membrane potential when sodium enters?
Tap to reveal answer
The pores formed are, according to the question, sodium selective. So it is unlikely that potassium concentration changes will be a major contributor to membrane potential changes. Since sodium is postively charged, and the ions entering are sodium, the inside of the cell will become more positively charged as sodium permeability goes up. We know that sodium will enter and potassium will leave due to the established gradients determined by sodium-potassium ATPase.
The pores formed are, according to the question, sodium selective. So it is unlikely that potassium concentration changes will be a major contributor to membrane potential changes. Since sodium is postively charged, and the ions entering are sodium, the inside of the cell will become more positively charged as sodium permeability goes up. We know that sodium will enter and potassium will leave due to the established gradients determined by sodium-potassium ATPase.
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