What is the function of the spindle apparatus during mitosis?
What is the apparatus made of?
Spindle apparatus separates chromosomes during mitosis pulling them to opposite ends of a cell
The apparatus is made of microtubules (tubulin dumers)
What is cancer? Name 3 hallmarks of cancer
Cancer is the result of uncontrolled proliferation and phenotype changes in individual cells
Hallmarks include: Increased proliferation, increased cell growth, decreased apoptosis, loss of contact inhibition, ability to migrate/colonize, escape immune response, increased telomerase and metabolic activity
What is the function of the Sepal (outermost), Petal, Stamen and Carpel (innermost) for a plant?
What is the function of Meristems?
Sepal: enclose/protect flower
Petal: attract pollinators
Stamen: male gamete production
Carpel: female gamete production
Meristems: stem cells found at the ends of shoots that allow for continuous cell growth and division even after embryonic development
Describe how information flow through neurons?
What is the flow of information through the entire nervous system?
Neurons: Dendrites collect electrical signals, cell bodies integrate and generate signals, axons pass signals to the dendrites of postsynaptic neurons
Nervous system: Sensory Neuron (Afferent), Interneuron, Effector Neuron (Efferent), Effector (Response)
What are synapses and where do they interact?
What is the difference between pre and post synaptic neurons?
Synapses are places of communication in which an action potential is integrated and affects a target cell. Synapses interact with other neurons, specifically dendrites, cell bodies, other axons and non-neuron cells
Pre: the signaling neuron (where the signal is traveling from)
Post: receiving the signal (where the signal is traveling to)
Name and Describe the 4 stages of Interphase
What is the phase where no cell division happens?
G1: Organelles are replicated and cells grow in size. Nutrients accumulate for DNA replication
S: Replication of Chromosomes, Centromeres (genetic material) and Organelles
G2: Organelle biosynthesis and cell growth
G0: permanent state of no dividing
Explain the role of apoptosis and the immune system in preventing cancer phenotypes from occurring in individual cells?
Apoptosis promotes programmed cell death and removes cells with abnormal proliferation/metabolisms
Immune responses screen cells for abnormalities and can trigger apoptosis/phagocytosis, killing the pre-cancerous cells
Growth: plants do not experience the cell migration animals do, plant organs are formed post-embryonically
Reproduction: plants dont have germ cells, shoot meristems convert vegetative development to reproductive development during flowering and gametogenesis, plants have mechanisms to limit self fertilization
What is the mechanism and effect of toxins such as Lidocaine and Tetrodotoxin on generating an Action Potential?
These toxins affect voltage gated Na+, keeping them in a continuous refractory period. When the membrane reaches threshold potential these Na+ vg channels cannot open to depolarize the membrane, meaning no AP will be generated
What are the two types of synapses?
What are neurotransmitters and how are they packaged for rapid release?
Electrical: direct cytoplasmic connections so that the membrane depolarization continues into the target cell through an Na+ influx
Chemical: release of neurotransmitters into the synaptic cleft and recognition by the pre/post synaptic neurons
NT: compounds made by metabolic pathways; synthesized ahead of time, loaded into vesicles, docked at the membrane
Explain the process of cyclin degredation
Enzymes called ubiquitin ligases tag cyclins with ubiquitin leaving CDKs inactive. The tagged cylins then are taken to Proteasomes for proteolytic degredation
What is a Loss of Function Mutation?
What is a Gain of Function Mutation?
What is a Tumor Suppressor gene and are these active in cancer cells?
Whats the difference between an proto-oncogene and an oncogene
A LOF Mutation is complete inactivity of a molecule/process
A GOF Mutation is hyperactivity of a molecule/process
A Tumor Suppressor Gene blocks cancer phenotypes; inactive in cancer cells
Proto-oncogenes promote regulated cell proliferation. When mutations occur proto-oncogenes are hyperactivated and become oncogenes which drive unregulated cell division
What is the ABC Model? What genes are antagonistic and what does this mean in regards to organ development?
What wild type organ does each gene correspond to in the model:
Gene A (Whorl 1)
Gene B + A (Whorl 2)
Gene B + C (Whorl 3)
Gene C (Whorl 4)
The ABC model involves four unique signals and gene combinations specifying four organ types, forming concentric whorls. Genes A and C are antagonistic meaning that when Gene A is mutated Gene C takes its place and organs corresponding to Gene C develop
Gene A: sepal
Gene B + A: petal
Gene C + B: stamen
Gene C: carpel
What are the two function of myelineation of nerve cells? What accessory cells produce myelin? What disease is associated with myelin damage and what are its effects?
1) help electrical signals travel from nodes faster
2) help cell save energy bc the membrane potential is only maintained at nodes
Schwann Cells
Multiple Sclerosis: signaling is slower and impaired, causing weakened muscles and loss of coordination
How does a post-synaptic neuron integrate multiple excitatory and inhibitory signals to decide whether to fire an action potential?
A post-synaptic neuron receives many inputs from different presynaptic neurons, including both excitatory (which depolarize) and inhibitory (which hyperpolarize) signals. These inputs are summed at the cell body.
If the overall effect of the combined signals reaches the threshold potential, voltage-gated Na⁺ channels will open and trigger an action potential. If inhibitory signals dominate or the combined excitatory input is too weak, the neuron will not fire.
Name and Describe the 5 stages of Mitosis
Prophase: chromosomes condense, spindle apparatus begins to form
Prometaphase: nuclear envelope breaks down, microtubules connect to chromosomes at kinetocores
Metaphase: chromosomes line up in the middle of cells
Anaphase: Sister chromatids are pulled to opposite poles of the cell
Telophase/Cytokinesis: chromosomes decondense, nuclear envelop reforms, cleavage furrow forms and cytoplasm is divided forming 2 daughter cells
What are chromosomal abnormalities that cause cancer? How do translocations contribute to the development of cancers? How does changes in DNA Methylation Patterns cause cancer
Chromosomal duplications increase gene activity, deletions remove tumor suppressors
Translocations can cause the fusion of two chromosomes, putting enhancers/regulatory transcription factors near cyclin production genes. These regulatory transcription factors are activated and cyclin accumulation occurs promoting cells into uncontrolled cell division (GOF Mutation)
Methylation changes gene silencing. Hyper: LOF mutation Hypo: GOF Mutation
Explain the process of situ hybridization and how it visualizes gene expression
A DNA/RNA probe complementary to the target sequence is tagged with radioactive atoms. The specimen is then treated to the probe and many copies are added. The probe binds to target mRNA and the gene is visualized
mRNA may only be found in certain whorls, for example mRNA corresponding to gene B would be in whorls 2 and 3. Also miRNA can be used as a test, for example if it is found in Whorls 1 and 2, it is blocking transcription in these areas, therefore this must be a miRNA specific for C gene mRNA
The resting membrane potential of a neuron is typically around –70 mV. Describe how this resting membrane potential is established and maintained.
Include role of ion gradients, ion channels involved, the Na+/K+ pump in the answer
Ion gradients work to cause a charge separation across the membrane, while ion channels allow the passive of selective charged ions into/out of the membrane. The Na+/K+ pump puts 3 Na+ out of the membrane for every 2 K+ pumped in, and this is active transport. This causes an overall negative charge inside the membrane, as more positive charge is being pumped out.
Describe the process of neurotransmitter release at the synapse and explain how neurotransmitters affect the target cell.
When an action potential reaches the axon terminal, it causes voltage-gated Ca²⁺ channels to open. Calcium ions flow into the presynaptic neuron and trigger synaptic vesicles to fuse with the plasma membrane, releasing neurotransmitters into the synaptic cleft.
NT bind to specific target cell receptors and change the membrane potential. They can excite (depolarize) or inhibit (hyperpolarize) the membrane
Name and Describe the three major checkpoints in the cell cycle
How do CDK and cyclins regulate cell cycle activity? Are they specific to each checkpoint?
What is MPF and how does it drive mitosis?
G1/S: Doubled in cell size, organelle replication, potential DNA damage, sufficient nutrients
G2/M: chromosome replication, DNA damage
M: Chromosomes attached to spindle apparatus
Cyclins bind to CDKs and activate them. These active Cyclin-CDK complexes then phosphyrolate target proteins that promote cell division. As cyclin accumulates more CDKs are active and more cell division occurs.
Yes, each phase of Interphase/Mitosis has specific cyclins that accumulate for each checkpoint
MPF is a specific cyclin-CDK complex associated with the G2/M checkpoint. It triggers mitosis events through protein phosphorylation
What is the function of Ras G-proteins in cancer development?
What are K-Ras oncogenes? Explain the mechanism of K Ras G proteins in development of these genes and overall cancer phenotypes
Ras G proteins are able to hydrolyze GDP (inactive) to GTP (active). When they are bound to GTP they promote a signaling cascade.
K-Ras G-proteins hydrolyze GDP tp GTP (active) and promote signaling. K-Ras oncogenes occur via missense mutations in the K-Ras gene, creating a GOF mutation. This causes K-Ras G proteins to be UNABLE to hydrolyze GTP to GDP and become inactive. This leaves the K-Ras G Protein in a state of continuous signaling and active conformation (bound to GTP always)
Describe the gene activity and organ development for these homeotic mutants:
a/a mutant:
b/b mutant:
c/c mutant:
How has the B gene evolved within different flower species?
a/a mutant: only carpels and stamen organs would develop, no sepals/petals, A is lost so C expands into whorls 1 & 2
b/b mutant: petals and stamen not develop, only carpels and sepals, B function is lost
c/c: sepals and petals develop only, no stamens/carpels, C is lost so A expands into whorls 3 & 4
Gene B has evolved to either expand/is restricted into different whorls (expansion to control whorl 1 development, restriction to only controlling whorl 3 development)
Describe the process of generating an action potential. Be specific about the steps, channels and ions used
What is the purpose of refractory periods on neurons?
1) Na+ enters the axon via open voltage gated channels
2) Depolarization (positive charge added) to the membrane that is traveling downstream
3) VG Na+ channels close at depolarization of ~ -30 mV, VG K+ channels open
4) Hyperpolarization of membrane
5) VG K+ channels close, and K+ leak channels move the resting membrane potential back to normal ~ -70 mV
Refractory periods: After Na+ vg channels open and propogate the depolarization signal to the next neuron they generate an AP and then close. Once these vg channels are closed they cannot open for a short period of time. This is to keep the DIRECTIONALITY of action potentials and prevent any neuron backflow
Why does a single excitatory synaptic signal not trigger an action potential in the post-synaptic neuron
How can an action potential eventually be activated?
A single excitatory signal typically causes only a small depolarization, which is not enough to reach the threshold required to open voltage-gated Na⁺ channels in the post-synaptic neuron.
To activate an action potential, multiple excitatory signals must be combined through spatial and summation or temporal . If the combined depolarization reaches the threshold (~ -55 mV), it will trigger an action potential