Cell Bio Long Answer Flashcards
(30 cards)
Polar auxin transport + gravitropism
- Directional movement of auxin. Amyoplasts respond to gravity, changing the location of PIN3. Auxin IAAH, which is uncharged, diffuses into the cell. It dissociates into IAA and H, but IAA can’t diffuse over the lipid bilayer, so it is trapped inside the cell. The only way for IAA to get out is through PIN proteins. This polar localization determines the direction of Auxin transport from cell to cell and gravitropism.
- Other facts: Interestingly, high auxin causes the PIN1 protein signal to transport toward the cells with high auxin. Auxin diffuses, and this could be behind the spiral pattern in plants
Adult vs. juvenile plants
They have different structures. Cuttings from an adult plant will create adult plants, and cuttings from a juvenile plant will create a juvenile plant. Unlike adults, juvenile plants do not have flowers or fruit. They often produce aerial roots and climb, while adults don’t. Their leaf arrangements are alternating as opposed to adults, which are spiraling. In some species, the leaf shape is different for adults and juveniles. These differences are regulated by hormonal changes and transcription factors. In juvenile plants, the SPL protein is repressed by miR156. In adults, miR156 decreases, so SPL is not repression declines. SPLs activate miR172, which represses AP2-like pathways that were inhibiting adult traits such as flowering.
Plant cell wall vs animal extracellular matrix
Both the ECM and the plant cell wall support the cell and help with signaling, but there are many differences between them. The plant cell wall is rigid around each cell to resist turgor, while the ECM is flexible. The plant cell wall is mainly made up of cellulose microfibrils and carbohydrates. It is made up of the middle lamella, the primary cell wall, and the plasma membrane. The ECM is made of fibrous proteins, proteoglycans and glycoproteins. The plant cell wall helps with cell shape and strength while the ECM helps with cell differentiation and migration.
Selective pressures and multicellularity
- Multicellularity:
- Selective pressures: factors that influence survival and reproduction
- Explain this: “A hen is only an egg’s way of making another egg.”
This quote looks at genes instead of an organism as a whole. It looks at how genetics are a means of reproduction and evolution. It makes one think of how genetics are formed in a way to continue into reproduction, meaning there is a germline and somatic cells. This division of labor is important in the concept of multicellularity.
CDKs and how their activity is regulated by the cell
Cdks are important for the regulation of the cell cycle. The MPF consists of cdk and cyclin and drives the cell from G phase into mitosis. The MPF can regulate spindle/microtubule formation, activation of condensins, etc. To activate the MPF, there is an activating kinase and an inactivating kinase. When a phosphatase removes the phosphorylation at the inactivation site, which is at the top, it causes the MPF to be active. The cdk activity can be regulated by the cell in many ways. For example, if the cell needs to inhibit the cell cycle rapidly, cdk inhibitors will become activated. These inhibitors will attach to (like a hug) the cdk and rapidly stop the cell cycle. This is important when something goes wrong (such as the possibility of cancerous cells). Another way it is impacted is through the regulation of the MPF. The cyclin degradation can cause negative control of the cell cycle by inhibiting an already active MPF.
Microtubules
accessory proteins
- One accessory protein of microtubules includes MAPs. These are microtubule-associated proteins that help stabilize the microtubules and organize microtubule bundles.
- Another accessory protein is stathmin. Stathmin regulates microtubule assembly by depolymerization, preventing tubulin assembly.
Microtubles Transport
Motor proteins on microtubules are kinesins and dyneins. They both use their heads to move along the microtubules, almost as if they are walking. Kinesins move toward the plus end and dyneins move toward the minus end (the MTOC). They help recognize and transport material on microtubules.
Microtubles Structure + function
Microtubules are a type of protein filament in the cytoskeleton. Microtubules play a large role in cell division, making up the spindle fibers. Microtubules are hollow structures made of tubulin. They are a heterodimer of beta and alpha subunits of tubulin. They are more rigid than actin. At one end, they are attached to MTOC, also known as the centrosome, which organizes the microtubules. They grow at the plus end. GTP regulates the stability of the microtubules; for example, low GTP can cause a catastrophe, and microtubules shrink.
Apoptosis
Intrinsic (know BLC-2 path)
Internal stress signals trigger the intrinsic pathway. This triggers MOMP, which is when holes are made in the outer membrane of the mitochondria, regulated by Bcl2. When this occurs, cytochrome c is released from the mitochondria. Apaf-1 in the cytoplasm is activated by cytochrome c. On the apaf1, there is a CARD region, which stimulates recruitment. They connect with each other to create a wheel formation and recruit caspases. This is called the apoptosome. Finally, executioner caspases are recruited, and cleavage occurs.
Apoptosis Extrinsic
The extrinsic pathway begins from external stress signals. Natural killer cells that have Fas ligands bind to the Fas receptor of the cell. This recruits the FADD protein, which exposes a hidden death domain and triggers pro-caspase. The pro-caspases cleave each other and create the initiator caspase. The caspases connect and they cleave and activate each other, and the caspase cascade and executioner caspase are triggered until apoptosis occurs.
Apoptosis Mutated and ineffective caspase gene- what could happen?
A mutated caspase gene could prevent a cell’s ability for apoptosis, thus causing cancer, autoimmune diseases due to autoreactive cells, etc.
Cortisol + pregnancy
Cholesterol metabolism
LDL on the surface of a cell connects with the LDL receptor and is engulfed into an endosome. It is then delivered to a lysosome, where cholesterol esters are hydrolyzed into cholesterol. It is then transported to the outer mitochondrial membrane. The rate-limiting step then occurs: it is transported from the outer membrane to the inner membrane of mitochondria via the contact site and StAR. It is then turned into pregnolone by P450scc. Cholesterol is then turned into cortisol.
Cortisol’s impact on pregnancy
In pregnancy, CRH is a corticotropin-releasing hormone that is involved in stress responses and the HPA axis between the hypothalamus and pituitary. CRH is also secreted by the placenta. It increases in pregnant women and beta endorphin spikes as a result. What isn’t expected, though, is that beta endorphin levels return to normal, though CRH is still increased. One theory is that there is desensitization of the pituitary by increased CRH. To test this, DEX is used. DEX suppresses cortisol production. The test was done in pregnant and non-pregnant women. In non-pregnant women, cortisol levels dropped, as expected. In pregnant women, cortisol levels were still elevated. This suggests that there is a resistance to suppression due to the increase in CRH by the placenta. This supports the theory and may be an explanation for postpartum blues.
Cancer
Cell and molecular pathways for cancer development
- Usually, the 3 needs for cancer development are loss of growth control, loss of apoptosis abilities, and loss of senescence control. The stages of cancer development are dysplasia, adenoma, non-infiltrating carcinoma, infiltrating carcinoma, and finally metastatic cancer. The mechanisms behind cancer development can occur in many ways.
- First protogones are genes that regulate the cell cycle. When they lose the ability to be controlled, they become cancerous oncogenes. This can happen for a few reasons, including deletion, gene amplification, chromosomal rearrangement, etc. One example of this is Ras. Ras can become an oncogene when the GEF growth factor activates it. If it does not have a GTPase to turn it off, it will take too long to inactivate. It is also possible for GEF to go into overdrive and activate too much. Both these cause oncogenes and increased cell proliferation.
- When apoptosis pathways are repressed, it can also cause cancerous effects. One way this can happen is through the Bcl2 protein. Anti-apoptotic Bcl2 proteins can stop apoptosis by blocking dimer formation and thus blocking pore formation in mitochondrial membranes. If this is overexpressed, cancer could occur.
- When there is a lagging chromosome in mitosis, two things can occur. First, it can cause the wrong number of chromosomes in a cell, which causes aneuploidy. Second, the cell may try to make a micronucleus out of this. It will break it apart and try to reassemble it, but this is not done correctly. This causes a chromothripsis where genes are overactive.
- Finally, the Philadelphia chromosome can occur. This happens where there is a translocation of chromosomes 9 and 22. When there is a kinase in front of the BCR protein, it causes a hyperactive kinase that phosphorylates more than it should, speeding up the cell cycle process and causing hyperactive growth.
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Cancer development of treatments
- Asciminib is a way that scientists are trying to treat cancer. When BCR binds to AC1, it prevents inactivation. Thus, by using asciminib, it could inactivate it.
- Gleevec is another way scientists are trying to treat cancer. When there are oncogenic kinases, ATP activates the kinase. One way to prevent this is by putting Gleevec into the binding site instead, which can prevent leukemia.
- Finally, scientists can use cancer’s instability to their benefit. There are pathways that DNA can be repaired, but cancerous cells do not ‘care’ about this. So for example, when DNA can be repaired in 2 ways, cancerous cells ignore the second pathway. By using a drug that inactivates the first pathway, regular cells can survive via the second pathway, but cancerous cells will eventually die.
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Benign vs malignant (why)
A malignant tumor is when metastasis occurs, which is when the cancer can pick up and spread somewhere else. For example, we can look at epithelial tissues. Epithelial cells are given survival factors. When they are extruded into the lumen, the center, they lose the survival factors and die via apoptosis. If they do not lose these survival factors, they can continue to grow and spread inside. This is a primary tumor, and it is still benign at this point. But if it spreads outside the basal lamina, it will burst and become malignant and metastatic.
Actin polymerization + actin binding proteins and impacts on cell shape and movement
- Actin is made of a single polypeptide chain folded into a structure with 4 subdomains. The process of actin polymerization is when monomers are added to the barbed end, the plus end, of the actin and released from the pointed end, the minus end, at the same rate.
- The actin-binding proteins assist in this process. Profilin promotes actin filament assembly. Thymosin prevents the assembly of actin filaments. Cofilin promotes the disassembly of the actin filaments. Formin assists through FH domains. FH1 delivers actin to the barbed end, and FH2 regulates the binding, almost like a ring. Arp2/3 initiates the growth of the filaments by binding to existing filaments and forming new branches at a 70-degree angle. NPF factors bind to the Arp2/3 and stimulate activity. Myosin acts as a motor protein. It moves along actin filaments in cases such as muscle contraction (myosin II) and transportation (myosin IV).
- Together with binding proteins, actin can influence cell shape and strength. In cases such as crosslinking via filamins, spectrin, alpha actin, etc., actin can increase mechanical strength.
Actin Cell movement and shape
Actin can play roles in protrusion, adhesion, and contraction for cell movement. In protrusion of a cell, actin polymerizes at the leading edge via Arp2/3 and formins, which create lamellipodia and or filopodia to push the membrane. In adhesion, actin connects via integrins at adhesion points. In the process of contraction, myosin II interacts with actin to contract the cell.
Plant cell signalling
There are 3 types of plant cell signaling. The first of them is hormonal signaling. This form of signaling helps with plant growth, development, and the environment. The hormones activate cascades that influence cell processes and gene expression. The second type is calcium signalling, where calcium acts as a second messenger and regulates cell processes such as growth, responses to light and touch, etc.. The final type is protein kinase signalling. These transmit signals from the surface of the cell to the nucleus. This can influence development, cell division, etc.
Plant cell signaling vs animal cell signaling
Both plants and animals use calcium signalling, GPCRs, and monomers ofthe Rho family. In plants, calcium signaling regulates growth, development, responses to light and touch, etc. In animals, calcium signaling regulates muscle contraction and neurotransmitter release. In plants, ,GTP/GDP can be exchanged spontaneously. In animals, a ligand is required.
Phytochrome stimulation and week 9 lab
Phytochromes are a type of photoreceptor in plants. They absorb certain frequencies of red light. When exposed to these given frequencies, they are autophosphorylated. This activates its kinase and gene regulatory proteins. This activation will result in growth. In the lab, we used tobacco seeds to explore this phenomenon. We had two types of light, red at 660nm and far red at 730 nm. We kept tobacco seeds in the dark to keep the photochromes inactive. We found that when the tobacco seeds are exposed to red light at 660 nm, photochromes were activated and gene regulatory pathways were stimulated and germination occurred. On the other hand, it appeared when far red light was presented, it inhibited germination of the seeds.
Cellulose fibrils vs collagen fibrils
- Cellulose fibrils are found in plants, while collagen fibrils are found in animals. Structure-wise, cellulose fibrils direct growth in plants and play a role in the strength of the plant (they have very high tensile strength similar to steel) and the cell wall. Animal collagen fibrils work primarily in a structural role in connective tissue, such as bone. Cellulose fibrils are made of glucose chains, while collagen fibrils are made of 3 polypeptide chains in a helix structure. While cellulose fibrils are very rigid, collagen fibril flexibility depends on the type. Type 1 is rigid, while others, such as type IV, are flexible.
- The function of the filaments differs as well. Cellulose fibrils are important in cell directional growth, while collagen fibrils are important in tissue organization. Type IV has flexibility. Type IX/XII collagen fibrils play an important role in crosslinking and binding to other ECM proteins. Collagen is synthesized by fibroblasts, which help remodel the ECM. They help align collagen via contractile force, form collagen networks, tendons, and heal wounds.
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General cell signaling + endocrinology
The general cell signaling pathway is that an extracellular signaling molecule binds to a receptor on the cell surface. This activates intracellular signal proteins, which impact effector proteins. The effector proteins produce different results, such as metabolic changes, cell shape, gene expression, etc.
Types of cell signalling
There are multiple types of cell signalling.
Contact dependent
* This is when the signalling molecules stay attached to the signaling cell’s surface and signalling requires direct cell-to-cell contact for transmission
Paracrine
* This is when the signaling cell releases molecules that diffuse locally to affect a nearby target cell
Synaptic
* This is rapid neuron-specific signaling.
Endocrine
* This is long distance signalling via hormones in the blood
Cell surface receptor signalling
* This is extracellular signalling that binds to specific receptors, triggering intracellular responses. Since many signaling molecules are hydrophilic and cannot cross the lipid bilayer, they rely on receptors.
Intracellular signalling
* This is activation of receptors inside the cell rather than the plasma membrane. The receptors interact with hydophobic singalling molecules that can cross the bilayer.
