Compare and contrast a human somatic cell to a human gamete.
Somatic cells have 46 chromosomes and are diploid, whereas gametes have half as many chromosomes as found in somatic cells.
Somatic cells have 23 chromosomes and are diploid, whereas gametes have half as many chromosomes are are present in somatic cells.
Somatic cells have 46 chromosomes and are haploid, whereas gametes have 23 chromosomes and are diploid.
Somatic cells have 46 chromosomes with one sex chromosome. In gametes, 23 chromosomes are present with two sex chromosomes.
23.
Eukaryotic chromosomes are thousands of times longer than a typical cell. Explain how chromosomes can fit inside a eukaryotic nucleus.
The genetic material remains distributed in the nucleus, mitochondria, and chloroplast.
The genome is present in a looped structure, thus it fits the size of the nucleus.
The DNA remains coiled around proteins to form nucleosomes.
The genetic material remains bound to the nuclear envelope, forming invaginations.
24.
Briefly describe the events that occur in each phase of interphase.
- cell grows and prepares materials for the synthesis phase , S - duplication of genetic material, - duplication of organelles and dismantling of cytoskeleton
- duplication of organelles, S - duplication of DNA, - assessment of DNA damage
- synthesis of DNA, S - synthesis of organelle genetic material, - assessment of DNA damage
- preparation for DNA synthesis, S - assessment of DNA damage, M - Division of cell
25.
Chemotherapy drugs such as vincristine and colchicines disrupt mitosis by binding to tubulin (the subunit of microtubules) and interfering with microtubule assembly and disassembly. Exactly what mitotic structure do these drugs target, and what effect would that have on cell division?
The drugs bind tubulin and inhibit the formation of the metaphase plate. This can arrest the cell cycle.
The drugs bind the tubulin, which leads to an error in the chromosome separation. This could lead to apoptosis.
The drugs bind the tubulin, thereby inhibiting their division in S-phase. This inhibits cell division.
The drugs bind the spindle fiber and hinder the separation of chromatins. This promotes the division spontaneously.
26.
(credit: modification of work by Andrew K. Joe, et al./American Association for Cancer Research)
The two graphs show the results of a study on a cancer drug. The left graph shows the results control group, untreated cancer cells. The right graph shows the results for the cells treated with the drug.
What can be said about this drug?
The drug does not have an effect on cancer cells.
The drug causes the cells to go through the G1 phase slower.
The drug causes the cells to go through the G1 phase faster.
The drug arrests the cell cycle at the G1 phase.
27.
Describe the general conditions that must be met at each of the three main cell cycle checkpoints.
checkpoint - assessment of DNA damage, - assessment of new DNA, M checkpoint - segregation of sister chromatids in anaphase.
checkpoint - Energy reserves for s phase, checkpoint - assessment of new DNA, M checkpoint- attachment of spindle to kinetochore.
checkpoint - assessment of DNA damage, checkpoint - energy reserves for DNA, M checkpoint - attachment of spindle to kinetochore
checkpoint - Energy reserves for S-phase, S checkpoint - synthesis of DNA, checkpoint - assessment of new DNA
28.
Explain the roles of the positive cell cycle regulators compared to the negative regulators.
Positive regulators promote the cell cycle but negative regulators initiate apoptosis.
Positive regulators block the cell division in cancerous cells but negative regulators promote in such cells.
Positive regulators promote the cell cycle but negative regulators arrest the cell cycle until certain events have occurred.
Positive regulators show positive feedback mechanisms but negative regulators show negative feedback in the cell cycle.
29.
Describe what occurs at the M checkpoint and predict what would happen if the M checkpoint failed.
The M checkpoint checks for proper attachment of sister chromatids and if it fails, then cells may undergo nondisjunction of chromosomes.
The M checkpoint checks if the DNA is damaged and promotes its repair. If it fails, then the daughters end up with damaged DNA.
The M checkpoint ensures the proper duplication of DNA and if it fails, the cells may undergo nondisjunction of chromosomes.
The M checkpoint ensures that all the components required for cell division are available and if it fails, the cell cycle will be inhibited.
30.
List the regulatory mechanisms that might be lost in a cell producing faulty p53.
assessment of damaged DNA, recruiting repair enzymes, and binding of spindle to kinetochore
quality of DNA, triggering apoptosis, and recruiting repair enzymes
quality of DNA, binding of spindle to kinetochore, and assessment of DNA repair
triggering apoptosis, recruiting repair enzymes, and proper binding of spindle to kinetochore
31.
p53 can trigger apoptosis if certain cell cycle events fail. How does this regulatory outcome benefit a multicellular organism?
The apoptosis helps in controlling the consumption of energy by the extra cells.
The apoptosis inhibits the production of faulty proteins, which could be produced due to the DNA damage.
The process of apoptosis stops the invasion of viruses in the other cells.
The cells are killed due to the production of reactive oxygen species produced, which could harm the organism.
32.
Name the processes that eukaryotic cell division and binary fission have in common.
DNA duplication, division of cell organelles, division of the cytoplasmic contents
DNA duplication, segregation of duplicated chromosomes, and division of the cytoplasmic contents
formation of a septum, DNA duplication, division of the cytoplasmic contents
segregation of duplicated chromosomes, formation of a septum, division of cell organelles
33.
The formation of what structure, which will eventually form the new cell walls of the daughter cells, is directed by FtsZ?
