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Bio test 11/12/13
| Question | Answer |
|---|---|
| what is a signal transduction pathway? | a series of steps by which a signal on a cells surface is converted into a specific cellular response |
| What is quorum sensing? How is it related to biofilms? | a chemical communication system bacteria use to monitor their local population density and coordinate group behaviors., helps with formation of biofilms |
| paracrine signaling | a cells releases signaling molecules that effect nearby target cells (ex: growth factors) |
| synaptic signaling | occurs in nuestras, an electrical signal triggers release of neurotransmitters that cross a synapse to a target cell (ex: dopamine) |
| How is long-distance signaling different from local signaling? | long distance signaling use hormones and proteins in vascular/body fluids while local signaling uses gap junctions or plasmodesmata and are regulators that travel short distances from secreting cells. |
| 3 stages of a signal transduction pathway | reception transduction response |
| reception stage of cell signaling | a signaling molecule binds to a receptor protein, causing it to change shape |
| transduction stage of a signal signaling | cascades of molecular interactions relay signals from receptors to target molecules in the cell |
| response stage of a signal signaling | cell signaling leads to regulation of transcription or cytoplasmic activities |
| what is a ligand | the binding between a signal molecules and receptor (highly specific) |
| components of a protein coupled receptor, describe them | G protein coupled receptor (largest fan of cell surface receptors) G protein (works with G protein coupled receptor, acts as an on/off switch) GDP (if it is bound to a G protein, the G protein is inactive) |
| what happens in a protein coupled receptor process | ligand binds to receptor, changes its shape, activates G protein causing GDP to be replaced with GTP, activated G protein activates enzyme, triggers a cellular response. G protein hydrolyzes GTP back to GDP - inactivates G protein = prevents overaction. |
| What is a receptor tyrosine kinase? | membrane receptors that attach phosphates to tyrosines |
| explain what happens in a receptor tyrosine kinase reaction? | ligand binds to receptor tk, receptor changes shape, 2 receptor tks form a dimer, receptors phosphorylate each other, activating receptor tks, inactive relay proteins bind to tyrosines, get activated, activates signaling pathways = cellular responses |
| what happens in ion channel receptors? | a ligand binds to a closed gated ion channel receptor in plasma memb, when ligand binds, the ion channel opens, allows specific ions to flow into cell, the flow of ions triggers a cellular response, when ligand unbinds from receptors, ion channel closes |
| what channels does the nervous system use? | ligand gated ion channels, voltage gated ion channels |
| where are intracellular receptors found, what do they bond to | cytoplasm or nucleus, they bond to chemical messengers that are hydrophobic or very small, like nitric oxide |
| explain how intracellular receptors work using testosterone (T) | diffuses through plasma memb, binds to intracellular receptor forming a hormone receptor complex, enter nucleus, binds to DNA, acts as a transcription factor, Mrna is transcribed, Mrna exits nucleus, translated into new protein in cytoplasm |
| explain the function of transcription factors in the cell | regulate gene expression by binding to specific DNA and controlling transcription of genes into Mrna. |
| 2 benefits of multi step pathways | a few molecules can amplify the response quickly, more opportunities for coordination and regulation of the cellular response |
| explain the role of protein kinases in transduction | the enzyme transfers phosphates from ATP to proteins (tags), phosphorylation |
| explain the role of protein phosphates in transduction | removes phosphates from proteins (untags), dephosphorylation |
| What is the difference between a first messenger and a second messenger? | first- extracellular signal molecule that binds to the receptor second- small non protein, water soluble molecules/ions that spread throughout the cell by diffusion. (calcium/ camp) participate in pathways initiated by G proteins and Tyrosine Kinases |
| explain role of 2nd messenger cAMP | adenylyl cyclase converts ATP into cAMP which acts as a 2nd messenger that activates protein kinase which produces a cellular responses. cAMP = BROADCASTS |
| how could cAMP response be inhibited | block/inactivate G protein, block an enzyme from functions (get a med/ treatments to block adenylyl cyclase |
| explain the mechanism of disease in cholera. | it locks the g protein into active form casing continuous activation or adenylyl cyclase= exces cAMP= opens ion channel which pumps chloride ions out of intestinal cell= water flows= dehydration/ diarrhea |
| Calcium ions are another secondary messenger commonly used by cells. Where are Ca+2 ions typically stored in cells? What happens to the cytoplasmic concentration of calcium when it is used as a second messenger? | stored in ER outside cell, cytoplasmic concentration of calcium concentration increases which activates proteins that trigger a cellular response |
| what are and How do scaffolding proteins enhance a cellular response? | large relay proteins to which other relay proteins are attached increase signal transduction efficiency, they support and help all proteins respond quickly. |
| What is apoptosis? | programmed or controlled death, proteins are involved in this process |
| How is apoptosis utilized in embryonic development in humans? | if cell detects something is wrong it can kill it off, can kill off things they don't need (humans don't need tail or webbed feet that were born with so our bodys kill it off) |
| adenylyl cyclase | an enzyme in the plasma membrane, converts ATP to cAMP in response to an extracellular signal Involved in fight or flight response |
| hormone receptor complex | can act as a transcription factor, turning on specific genes in the nucleus |
| gap junctions | protein-lined channels connecting the cytoplasm of adjacent animal cells |
| plasmodesmata | crucial microscopic channels that pass through plant cell walls, directly connecting the cytoplasm of adjacent cells for intercellular transport and communication, |
| Meiosis 1/2 and mitosis, interphase | G1- growth S- DNA replication (no S phase between Meiosis 1 and 2) G2- growth, prep for division |
| meiosis, prophase 1 | crossing over occurs homologous chromosomes pair |
| meiosis, metaphase 1 | independent assortment homologous chromosomes line up |
| meiosis anaphase 1 | homologous pairs are separated |
| meiosis telophase 1 / interkinesis | 2 haploid cells are created interkinesis= rest before meiosis 2 |
| meiosis, prophase 2 | spindle forms, chromosomes condense |
| meiosis, anaphase 2 | sister chromatids are separated |
| meiosis, telophase 2 /cytokinesis | 4 unique haploid cells form |
| mitosis prophase | nuclear membrane breaks down nucleolus breaks down DNA/chromatid is condensed into chromosomes centrioles separate + produce spindle microtubules centromere begin to move to poles |
| mitosis prometaphase | chromosomes attach to spindle microtubules at kinetochore |
| mitosis metaphase | chromosomes line up in the middle of cell at metaphase plate (like the equator of the cell) |
| mitosis anaphase | spindle MT shorten @kinetochore, pulls sister chromatids apart to separate poles |
| mitosis telophase/cytokinesis | nuclear membrane and nucleolus reaper, spindle microtubules disintegrate, chromosomes decondense cytokinesis occurs - cytoplasm divides into 2 identical diploid cells (1 chromosome in each cell) both new cells enter interphase |
| differences between gametes and somatic cells | gametes are sperm and egg, somatic cells are any cells other than a gamete (23 chromosomes are somatic cells)- are diploid |
| how are offspring different in sexually reproducing organisms form asexually reproducing organisms | sexually reproducing organisms 2 parents give ride to offspring which inherited genes from both parents asexually reproducing is when a single individual passes genes to its offspring without fusing a gamete (faster, produces more offspring) |
| homologous chromosomes | same type of chromosomes from mom and dad |
| sister chromatids | joined copies of the original chromosome, separate during cell divison |
| centromere | is a crucial constricted region on a chromosome that acts as the attachment point for spindle fibers during cell division, ensuring that replicated chromosomes (sister chromatids) are accurately pulled apart into two new daughter cells |
| chiasmata | x shaped regions that each chromosome has |
| sex chromosome combo in males vs females | males- xy females- xx |
| autosomes (how many in somatic and sex cells) | remaining pairs of chromosomes of non sex chromosomes (somatic- 44) (sex cell- 22) |
| diploid vs haploid | diploid- when a gamete contains a single set of chromosomes |
| why do sex cells have half the number of chromosomes as somatic cells/ why is meiosis important in sexually reproducing organisms | because meiosis halves the chromosome number during special cell division which helps create gametes preventing chromosome doubling |
| crossing over | genetic rearrangement between non sister chromatids (during prophase 1) homologous chromosomes exchange corresponding segments of DNA. |
| independent assortment | during meiosis 1 homologous chromosomes pairs line up randomly at the metaphase plate. this means maternal and paternal chromosomes are assorted independently into gametes producing many combos |
| maternal vs praternal | maternal- mom paternal- dad |
| chromosomes vs chromatids | chromosomes are DNA packaged and chromatin are DNA unwound. (chromatids separate and become chromosomes as cell division occurs) |
| cytokinesis (animals vs plants) | division of the cytoplasm animals- cleavage furrow plants- cell plate |
| what happen in G0 phase of mitosis | cells exit the cell cycle, don't divide, usually nerve, muscle, liver cells this happens when a cell receives a signal to differentiate, when resources are insufficient to grow/divide and its stage and development |
| kintetochore | protein complex at the centromere of each chromatids, where spindle fiber attach |
| what are non kinetochore microtubules of the spindle | overlap with microtubules from the opposite pole and help push poles apart, elongating cell |
| binary fission and how its different from mitosis | replication of bacterial chromosomes, different from mitosis because it occurs in prokaryotes and doesnt include spindle or nucleus. |
| check points / diff ones in the cell cycle | where the cell cycle stops until a go ahead signal is received m, g2, g1 (most important) |
| cyclins | regulatory proteins |
| cdks | enzymes that activate cell cycle proteins when bound to cyclins |
| mpf | cyclin cdk complex that triggers cells passage into mitosis |
| what happens when cycling combine with mpf | mpf becomes active and initiates mitosis by phosphorylating target proteins |
| growth factors | proteins released by certain cells that stimulate other cells to divide |
| how does pdgf made by platelets affect fibroblasts | stimulates fibroblasts to divide helping heal wounds |
| what is density dependent inhibition | crowded cells stop dividing (cancer cells cant exhibit this) |
| anchorage dependence | they must be attached to a substation in order to divide (cancer cells cant exhibit this) |
| what characteristics do cancer cells exhibit | don't respond normally to the body's control mechanisms, need growth factors to grow/ divide make their own growth factors, abnormal cell cycle control system, higher protein translation |
| difference between benign and malignant tumor. | benign- abnormal cells remain at original site malignant- invade surrounding tissues/ can metastasize (move)/ form more tumors |
| how does radiation work to treat cancer | damages DNA to prevent cancer cells from dividing, leading to cell death |
| when/ how is chemotherapy used? | targets and kills cells that divide frequently by interfering with cell division (cause side effects) also effects hair gut and immune cells |
| what does it mean when cells differentiate | cells stop dividing to specialize in structure and function |
| cell cycle regulators | molecular signals that may stimulate or half cell division, instruct cell to differentiate or initiate cell death. |
| harmless results of too little/ too much cell division | too little- hair loss too much- warts |
| stimulating proteins | protein that regulates the cell cycle encoded by proto-oncogenes |
| inhibitory proteins | protein that regulates the cell cycle encoded by tumor suppressor genes |
| tumor suppressor genes | are essential genes that act as the "brakes" for cell growth, preventing uncontrolled division, repairing DNA damage, and triggering programmed cell death (apoptosis). |
| kinase | enzymes that add a phosphate to other proteins to activate or inhibit it |
| G1 (events, checkpoints, regulatory processes) | events- growth factors stimulate signals in cells which causes rises in cyclin concentration. cyclins bind to cdks which phosphorylate other proteins which then goes to s phase checkpoints- is there damage in dna? go- cyclins stop- p53/ rb |
| S phase (events, checkpoints, regulatory processes) | when s phase cyclins reach threshold, cdk cyclin complexes signal cell to duplicate DNA, grown factors stimulate rises in s phase cyclin concentrations check points- make sure DNA is fully replicated stop- cyclin/cdk go- ATM/ BRCA1, p53 |
| G2 phase (events, checkpoints, regulatory processes) | conc of mitotic cyclins rise, bind to cdks, if DNA damage/ incomplete replication, inhibitory proteins prevent activation of cdk cyclin complex, when fixed, cdk cyclin complex activated check- make sure everything is copied stop- p53 go- cycline |
| M (mitosis) (events, checkpoints, regulatory processes) | the process of mitosis check- check if things are properly attached go- cyclins/cdks stop- mad proteins (inhibit things when protein aren't properly attached to the mitotic spindle) |
| to cause cancer what is requires what is requires of tumor suppressors and proto oncogenes | proto oncogenes require 1 allele to be mutated (dominant) which results in a gain in function OR a tumor suppressor genes requires 2 alleles to be mutates (recessive) which results in a loss of function. |
| explain impact of 1 mutated tumor suppressor genes vs 2 mutated tumor suppressor genes | 1- cell cycle can still function 2- cell cycle proceeds inappropriately |
| explain impact on the cell cycle of a proto oncogene vs an oncogene | Proto-oncogenes- normal genes, promote controlled cell growth/division, when mutated, are oncogenes, causing uncontrolled cell proliferation, bypassing checkpoints, leading to tumor formation, promoting excessive cell division/ inhibit normal apoptosis. |
| p53- role | encoded by a tumor suppressor gene stops cycle when things are damaged while they get fixed |
| explain why people who have mutated brca1 genes are more likely to get breast cancer | cell death and repair won't be controlled and can cause build up |
| potential outcome of a mad protein | cause damaged cells that aren't pulled apart properly |
| negative feedback | returns the system back to steady state end product decreases the pathways |
| positive feedback | moves the system further away from its set point end product increases the pathway (ex: labor, ripening fruit) |
| synapsis | the fusion of chromosome pairs at the start of meiosis. |
| viberio fisheri- when do they glow and how | glow when in a colony, using a signal transduction pathway causing them to produce a protein |
| how does the adrenal gland produce the fight or flight response | cells inside secret epinephrine which sets up a signal transduction pathway, liver responds and makes cells release glucose from glycogen |
| Phosphorylation cascade | is a signal transduction pathway where one protein kinase activates the next by adding a phosphate group, creating a chain reaction that amplifies a small initial signal into a large cellular response |
| steps of signal transduction pathway | adenylyl cyclase becomes activated with an alpha subunit from g protein. converts ATP into cAMP which activates protein kinase which can then active other proteins/ enzymes in cell, phosphorylase is now activated and converts glycogen into glucose. |
| how do bacteria communicate | have species specific language receptors and other species receptors |
| meiosis metaphase 2 | chromosomes line up singly |
Created by:
Lilyhowes