cell final Flashcards
lec 20-27
1
Q
what does cell division refer to
A
the creation of two daughter cells from one parent cell
2
Q
what are daughter cells identical to
A
each other and to the parent cell
3
Q
why is cell division tightly regulated
A
to prevent the overproduction of cells
4
Q
what does the term cell cycle refer to
A
a series of stages that a cell progresses through before cell division can occur
5
Q
what are the 4 sequential stages of cell division
A
G1, S, G2, M
6
Q
what does the G2 phase do
A
prepare the cell for DNA replication
7
Q
what happens during the G1 phase
A
The cell grows, makes mRNA and proteins for DNA replication, and produces energy. It commits to the cell cycle at the START point.
8
Q
what is START
A
a process where the cell is committed to progress through the remainder of the cell cycle
9
Q
what happens during the S phase
A
the parent cell’s DNA is replicated
10
Q
what are sister chromatids held together by
A
cohesions
11
Q
what is a centromere
A
the region where the
kinetochore will form and microtubules will bind
12
Q
what is a centrosome
A
a microtubule organizing center
13
Q
what happens during the G2 phase
A
The cell checks for DNA replication errors, finishes centrosome duplication, and starts forming microtubules for mitosis.
14
Q
What are the stages of mitosis and their functions?
A
Prophase: Chromosomes condense, nuclear envelope breaks, spindle forms.
Metaphase: Chromosomes align at the center.
Anaphase: Cohesins are degraded, and chromatids are pulled apart.
Telophase: Chromosomes decondense, nuclear envelope reforms.
15
Q
What causes the chromosome number to double during anaphase?
A
Sister chromatids are separated into individual chromosomes.
16
Q
What cells enter G0 permanently?
A
ostmitotic cells like neurons
17
Q
Can any cells leave G0 and re-enter the cycle?
A
Yes, some dividing cells temporarily enter G0 and can rejoin the cycle later.
18
Q
what is the difference between G1 and Go phases
A
G1 is part of the cycle where the cell grows and prepares to replicate DNA. G0 is a resting phase where cells exit the cycle and do not divide (often permanently).
19
Q
What two proteins form the complex that regulates the cell cycle?
A
Cyclin (regulatory subunit) and CDK (cyclin-dependent kinase, catalytic subunit).
20
Q
How does cyclin control CDK?
A
It activates CDK and determines which proteins it can phosphorylate.
21
Q
How is cyclin level regulated?
A
Through transcriptional waves (increased production) and proteasomal degradation (breakdown after phase completion).
22
Q
What are mitogens and anti-mitogens?
A
Mitogens promote G1 entry by increasing cyclin/CDK levels. Anti-mitogens do the opposite and inhibit entry.
23
Q
What enzymes regulate CDK through phosphorylation?
A
CAK (CDK-activating kinase): Activates CDK
Wee1 kinase: Inhibits CDK
CDK inhibitors: Bind to and block cyclin-CDK complexes
24
Q
What triggers the transition from G2 to M phase?
A
Dephosphorylation of CDK (by inactivating Wee1 and activating phosphatases).
25
How is the cycle reset after mitosis?
M phase cyclins are degraded, CDK inhibitors are produced, and CDK targets are dephosphorylated.
26
What are the components of a checkpoint pathway?
A sensor (detects error), signaling cascade (alerts the cell), and effector (halts the cycle and activates repair).
27
What happens if DNA damage is detected?
CDKs are inactivated, the cell cycle is halted, and repair is attempted. If damage is unfixable, the cell undergoes apoptosis
28
What does the spindle assembly checkpoint do?
It ensures all chromosomes are attached to spindle fibers before anaphase, preventing chromosome mis-segregation.
29
How do cells contribute to tissue and organ formation?
Cells of the same type aggregate to form tissues, tissues combine to make organs, and organs associate to form organ systems.
30
Give an example of this organizational hierarchy.
Myocytes form muscle fascicles → fascicles combine with other tissues to form skeletal muscle → skeletal muscles associate with bones to form the musculoskeletal system.
31
What is a key hallmark of metastatic tumors?
The breakdown of cell-cell adhesion.
32
Why is cell adhesion important in multicellular organisms?
It allows cells to associate with one another and the extracellular environment, which is essential for tissue structure and function.
33
What mediates cell-cell adhesion?
Cell-adhesion molecules (CAMs) on the plasma membrane.
34
What mediates cell-matrix adhesion?
Adhesion receptors such as integrins that bind to extracellular matrix proteins.
35
What are CAMs and what do they do?
CAMs are membrane proteins that extend into the extracellular space and bind to other CAMs (same or different) on neighboring cells.
36
How are CAMs linked internally in the cell?
They are connected to the cytoskeleton and can initiate intracellular signaling.
37
Where do CAMs cluster?
In structures called cell junctions.
38
What are the three major types of cell junctions?
Tight junctions
Anchoring junctions
Gap junctions
39
What is the function of tight junctions?
They form a seal that prevents molecules from passing between cells (paracellular pathway), forcing substances to go through cells instead (transcellular pathway).
40
What proteins make up tight junctions?
Occludin, claudin, and junction adhesion molecules (JAMs).
41
What do anchoring junctions do?
They create stable links between cells and their cytoskeletons, providing structural support and allowing force transmission.
42
What are the two types of anchoring junctions?
Adherens junctions: Act like zippers
Desmosomes: Act like spot welds
43
What is the function of gap junctions?
They allow direct passage of ions and small molecules (like second messengers) between neighboring cells.
44
What proteins form gap junctions?
Connexins — 6 from each cell align to form a continuous channel.
45
What is the ECM composed of?
Proteoglycans: Form gel-like substances that resist compression
Collagen: Provides strength and structure
Multi-adhesive matrix proteins: Help organize and stabilize ECM (e.g., laminin)
46
What are integrins and what do they bind to?
Integrins are transmembrane receptors that bind to ECM components like collagen, laminin, and fibronectin.
47
How strong are integrin interactions, and how is strength achieved?
Individually weak, but strong when many integrins cluster together at junctions.
48
What are focal adhesions?
Junctions that connect ECM proteins to cytosolic microfilaments.
49
What are hemidesmosomes?
Junctions that connect ECM proteins to intermediate filaments inside the cell.
50
What are stem cells?
Unspecialized cells that can differentiate into other cell types and self-renew to maintain their population.
51
What is self-renewal?
The ability of stem cells to divide and produce more stem cells throughout an organism’s life.
52
What are pluripotent stem cells?
Stem cells that can become any cell type in the body (e.g., embryonic stem cells).
53
What are multipotent stem cells?
Stem cells that can differentiate into several, but not all, specialized cell types (e.g., hematopoietic stem cells in adults).
54
What is asymmetric division in stem cells?
A type of division where one daughter cell remains a stem cell and the other becomes a differentiated cell.
55
What triggers asymmetric division?
Polarity signals—signaling molecules on one side of the cell lead to reorganization of the cell's contents before division.
56
What is symmetric division in stem cells?
A division where both daughter cells either remain stem cells or both become differentiated cells.
57
What is a stem cell niche?
The environment containing signals required for stem cell maintenance, division, and differentiation.
58
What happens when stem cells are removed from their niche?
They may lose some of their stem cell properties.
59
What are intrinsic regulatory signals in stem cells?
Internal mechanisms that help maintain stem cell identity and behavior.
60
What are extrinsic signals?
External cues (like signaling molecules) from the niche that influence stem cell division and differentiation.
61
What are progenitor cells?
Cells that are partially differentiated, have limited self-renewal, and can only become one or a few cell types.
62
How are progenitor cells related to stem cells?
Many stem cells first become progenitor cells before becoming fully differentiated.
63
What are iPS cells?
Differentiated cells that are reprogrammed to become pluripotent stem cells using synthetic biology.
64
What is the source of all blood and immune cells?
Hematopoietic stem cells.
65
What is the role of Notch signaling in stem cells?
It regulates stem cell fate decisions and homeostasis.
66
How does Notch signaling influence cell outcomes?
High Notch activity pushes cells toward differentiation; low Notch activity maintains stem cell identity.
67
What is optogenetics used for in stem cell research?
To control and study cell fate decisions by manipulating light-sensitive signaling pathways during division
68
What are the two main types of cell death?
Necrosis and apoptosis
69
What distinguishes necrosis from apoptosis?
Necrosis is a passive form of cell death caused by injury, releasing cell contents and inducing inflammation. Apoptosis is a programmed process that avoids inflammation by packaging cell contents into fragments that are phagocytosed.
70
Name two environmental factors that can affect cell lifespan.
Infections and toxic substances
71
What endogenous molecules influence a cell’s survival or death?
Trophic factors promote survival, while other endogenous signals stimulate cell death.
72
What family of enzymes is central to apoptosis?
Caspases
73
How are caspases activated?
They are synthesized as inactive procaspases and activated by proteolytic cleavage.
74
What is the difference between initiator and effector caspases?
Initiator caspases activate other caspases, while effector caspases cleave cellular proteins to carry out apoptosis.
75
What triggers the extrinsic pathway of apoptosis?
External signaling molecules bind to death receptors on the plasma membrane.
76
Which caspases are involved in the extrinsic pathway?
Caspase 8 (initiator) and caspase 3 (effector).
77
What triggers the intrinsic pathway of apoptosis?
Internal cell stress such as infections, radiation, or hypoxia causing mitochondrial damage.
78
What mitochondrial protein is released during the intrinsic pathway?
Cytochrome c.
79
Which caspases are involved in the intrinsic pathway?
Caspase 9 (initiator) and caspase 3 (effector).
80
What are the two main components of the immune system?
The innate immune system and the adaptive immune system
81
What are the general functions of the immune system?
To protect the body from invading microorganisms and promote tissue repair.
82
What are examples of physical barriers in the human body?
Skin and mucous membranes lining the gastrointestinal, genitourinary, and respiratory tracts.
83
What are the characteristics of the innate immune system?
Rapid, non-specific response that acts within minutes. It recognizes common microbial features and contains the infection until the adaptive immune system is activated.
84
How do chemical barriers protect against microbes?
Substances like sweat, tears, and saliva contain antimicrobial enzymes such as defensins. Mucus and earwax trap microbes and limit access to epithelial cells.
85
Which cells are part of the innate immune system?
Monocytes, macrophages, neutrophils, eosinophils, basophils, mast cells, and dendritic cells.
86
What is the function of monocytes and how do they change in tissues?
Monocytes circulate in the bloodstream and differentiate into macrophages once they enter tissues.
87
What are the roles of macrophages?
Detect and engulf pathogens (phagocytosis), destroy them with enzymes, release cytokines and chemokines, and present antigens to T cells using MHC Class II.
88
What is the role of neutrophils?
They are the most abundant white blood cells, engulf pathogens through phagocytosis, and release cytokines.
89
What immune roles do eosinophils, basophils, and mast cells play?
Eosinophils are involved in allergic reactions and parasitic defense; basophils and mast cells release inflammatory mediators.
90
What is a dendritic cell's main function?
Acts as a professional antigen-presenting cell, migrating to lymph nodes to activate adaptive immune cells and secreting cytokines to guide immune responses.
91
What are the defining features of the adaptive immune system?
Specific and delayed response (4–7 days after infection), involving B cells and T cells that recognize specific antigens.
92
What is an epitope?
A specific region of an antigen to which an antibody binds.
93
What are memory cells and what is their function?
Subsets of adaptive immune cells that provide long-term immunity by responding more effectively upon re-exposure to the same pathogen.
94
What are the two main types of adaptive immunity?
active immunity, which includes natural immunity and artificially acquired immunity. The second type of adaptive immunity is called passive immunity
95
What two antagonistic processes regulate cell numbers in tissues?
Proliferation and cell death.
96
What promotes cell proliferation, and what promotes cell death?
Mitogens and growth factors promote proliferation; absence of survival signals promotes cell death.
97
What is a tumor?
A tumor is an abnormal growth of cells that serves no functional purpose in the body.
98
What is the difference between benign and malignant tumors?
Benign tumors: Non-cancerous, well-differentiated, do not invade surrounding tissue.
Malignant tumors: Cancerous, less differentiated, proliferate rapidly, can invade other tissues (metastasize).
99
Do all cells in the body proliferate throughout life?
No. For example, epithelial cells proliferate continuously, while neurons are terminally differentiated and do not divide.
100
How is apoptosis involved in preventing cancer?
It eliminates damaged or genetically unstable cells before they can proliferate abnormally.
101
What are the two main classes of genes mutated in cancer?
Proto-oncogenes and tumor suppressor genes.
102
How do proto-oncogenes contribute to cancer when mutated
They become oncogenes, which drive increased cell proliferation. Example: Ras.
103
What happens when tumor suppressor genes are inhibited?
Apoptosis is reduced and uncontrolled cell proliferation occurs. Example: p53.
104
What are five key characteristics of cancer cells?
1. Enhanced proliferation (even without growth signals)
2. Resistance to apoptosis
3. Less differentiation
4. Induce blood vessel formation (angiogenesis)
5. Increased mobility and invasiveness
105
What is metastasis?
The process by which cancer cells spread from their site of origin to other parts of the body.
106
What steps are required for metastasis to occur?
1. Break cell-cell and cell-matrix adhesions
2. Migrate through tissue
3. Degrade extracellular matrix proteins
4. Enter bloodstream
5. Travel and survive in new tissue
107
What increases an individual's risk of developing cancer?
Exposure to carcinogens
108
What are carcinogens?
Substances or exposures that can lead to cancer by causing mutations in DNA.
109
What is the difference between proto-oncogenes and oncogenes?
Proto-oncogenes are normal genes that regulate cell growth. When mutated, they
become oncogenes, which can cause uncontrolled cell proliferation.
110
What is a classical example of a proto-oncogene?
Ras
111
What happens when tumor suppressor genes are inhibited?
Inhibition of tumor suppressor genes reduces apoptosis and increases cell proliferation,
potentially leading to cancer.
112
What is a classical example of a tumor suppressor gene?
p53
113
What is Simian Virus 40 (SV40)?
SV40 is an oncogenic virus that has been associated with cancer development.
114
What receptor does SV40 use to enter host cells?
Ganglioside receptor GM1.
115
Who was Alton Ochsner and what incident is associated with him?
Alton Ochsner was involved in an incident where he injected his grandchildren with a
tainted polio vaccine, resulting in the death of his grandson and polio in his granddaughter.
116
What role did Bernice Eddy play in the context of SV40?
Bernice Eddy discovered the contamination of polio vaccines with SV40.
117
What does the SV40 genome map show?
It illustrates the organization of viral genes and regulatory elements within SV40.
118
What are the cellular targets of SV40 during infection?
SV40 targets regulatory pathways controlling cell proliferation and apoptosis.
119
What are the two main classes of genes mutated during cancer development?
Proto-oncogenes (become oncogenes) and tumor suppressor genes.
120
How can viruses induce tumorigenesis through cellular fusion?
Viral infection can cause fusion of infected cells with healthy ones, potentially leading to
uncontrolled cell growth.
121
What is cellular senescence?
A state in which cells permanently stop dividing but do not die, often acting as a natural
barrier to cancer.
122
What is the role of Ras in cancer development?
Ras is a proto-oncogene that, when mutated, becomes an oncogene that promotes
uncontrolled cell proliferation.
123
How does the loss of p53 contribute to tumor formation?
p53 is a tumor suppressor gene that promotes apoptosis; its loss prevents damaged cells
from dying, leading to unchecked cell growth.
124
What is the significance of SV40’s interaction with host cell machinery?
SV40 can hijack host cell machinery to replicate and interfere with normal cell cycle
regulation, contributing to cancer development.
125
What was the Cutter incident?
A mishap in which a batch of polio vaccine contaminated with SV40 from Cutter
Laboratories caused illness and death.
126
What type of virus is SV40 and how does it package its DNA?
SV40 is a DNA virus that tightly packs its circular DNA genome using host histones,
resembling mini-chromosomes.
127
What is cellular senescence?
A state of stable cell cycle arrest in which cells become resistant to growth-promoting
stimuli, often due to DNA damage.
128
Who first described cellular senescence?
Leonard Hayflick, through his studies on human fetal fibroblasts.
129
What are key features of senescent cells?
Morphological and metabolic changes, chromatin reorganization, altered gene
expression, and SASP.
130
What does SASP stand for?
Senescence-Associated Secretory Phenotype.
131
How can senescent cells be detected histologically?
By β-Galactosidase staining at pH 6.0, which turns cells blue.
132
What DNA marker is commonly used for senescence?
Histone2A.X, which marks DNA damage sites.
133
What is the role of p53 in senescence?
It is activated in response to cellular stress and DNA damage, promoting cell cycle arrest.
134
How does senescence help prevent cancer?
By stopping replication of cells with damaged DNA
135
What unintended effect can chemotherapy have related to senescence?
It can induce senescence in normal cells, leading to fatigue and other side effects.
136
How do senescent cells contribute to aging?
They accumulate over time and are associated with tissue degeneration and
inflammation.
137
Are aging and senescence the same?
No, aging is a time-based decline, while senescence occurs throughout life, even during
development.
138
How do telomeres relate to senescence?
Telomeres shorten with each division; once critically short, they trigger senescence.
139
What is the “end replication problem”?
DNA polymerase cannot fully replicate the ends of the lagging strand, causing telomere
shortening
140
Which enzyme prevents telomere shortening in cancer cells?
Telomerase
141
What happens when telomeres reach a critical length?
They are recognized as DNA damage, leading to cell cycle arrest.
142
What are senolytics?
Therapeutic agents that selectively eliminate senescent cells.
143
What are potential benefits of senolytics in animal models?
Reduced inflammation, better immune function, and slowed age-related disease.
144
Name three senolytic compounds mentioned in the research.
Dasatinib, Quercetin, and Fisetin.
145
What age-related diseases are senolytics being tested for in humans?
Osteoarthritis and chronic kidney disease.
146
How might senolytics affect lifespan?
They can extend lifespan and reduce physical decline in aging models.
