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BZ 310- Final
Question | Answer |
---|---|
Anterograde secretory pathway | secretion or to the vacuole |
Retrograde secretory pathway | endocytosis |
Smooth ER functions (3) | detoxification (cytochrome P450), steroid hormone synthesis, Ca2+ storage |
Rough ER functions (4) | secretory protein synthesis/uptake, N-linked glycosylation, secretory protein folding, phospholipid synthesis |
What does cytochrome P450 do? | oxidizes harmful hydrophobic molecules |
Cystic fibrosis | malfunctioning ER functions |
Nascent polypeptide | Asn-X-Ser/Thr; core oligosaccharide attached to this, then 3 glucose later removed |
O-liked glycosylation | rare; usually n-linked |
Enzymes that remove glucose from core oligosaccharide | glucosidase (I and II) |
ER quality control | final glucose only removed when protein is folded correctly |
Functions of glycosylation (6) | enzyme folding, quality control, sorting, enzyme functionality, recognition at cell surface, protection at cell surface |
Functions of Golgi (4) | protein sorting, modification of N-linked sugar groups, O-linked glycosylation, formation of some cell wall components |
How were the secretory mutants found in yeast? | mutants sunk after centrifugation |
Class I mutants | defect in ER translocation |
Class II mutants | defect in vesicle budding from ER |
Class III | defect in fusion with Golgi |
Class IV | defect in budding from Golgi |
Class V | defect in fusion with plasma membrane |
Two major processes in secretory pathway | coat protein mediated budding & SNARE receptor mediated vesicle docking and fusion |
Clathrin | involved in receptor mediated endocytosis and transport to endosomes/lysosomes |
COP II and COP I | golgi==>ER |
Rab | a small GTPase needed to prime a vesicle |
Transport to lysosome/plasma membrane depends on what? | mannose 6-P |
Polarized cells (4) | epithelia, neurons, fibroblasts, T-cells |
Two types of exocytosis | constitutive and regulated |
V-snares/T-snares | mediate secretion by promoting vesicle docking and fusion |
Female meiosis | only keep 1 cell in meiosis 1, only keep 1 at meiosis II (right before fertilization) |
G1 | 1 chromosome = 1 chromatid = 1 DNA |
G2 | 1 chromosome= 2 chromatids= 2 DNAs |
Interphase | GI, S, G2 |
14.11 | |
SERIOUSLY 14.11 all of the chromosome shit | |
Astral spindle MTs | connect to periphery |
Polar spindle MTs | space spindle poles relative to each other |
Kinetochore spindle MTs | catch chromosome, connect to kinetochore |
Metaphase | chromosomes in center of cell |
Anaphase | chromatids separate |
Telophase | chromosomes de-condense, nucleus reforms |
Most important control point in cell division | START (between G1 and S) |
What is checked at START? (3) | cell size, DNA intactness, nutrient availability |
G0 | cells enter this when don’t need to divide; must enter G1 to divide again |
CdK | cyclin dependent kinase; each checkpoint has its own |
Cyclin | proteins that vary in concentration over the cell cycle |
Example of cyclin and cdk pair | MPF (mitosis promoting factor); conserved |
2 main regulatory mechanisms of cell cycle | phosphorylation (reversible), degradation of cyclins (irreversible) |
p53 | checks for DNA damage at start and G2-M transitions; transcription factor for cyclin inhibiting protein (=cell cycle arrest) |
which 2 cell wall components are secreted and more soluble? | pectin and hemicellulose |
which 2 cell wall components are synthesized in place? | cellulose and lignin *make up most biomass on earth |
___ connect the cytoplasm of plant cells | plasmodesmata |
proteins in connective tissue are secreted by | fibroblasts |
proteoglycans function | cushioning |
collagen | vitamin c dependent, stretching resistance |
4 types of cell-cell connections | adherens, gap, tight, desmosome |
gap junctions | 2x6 connexins= connexon (allow signaling like cAMP thru) |
receptor connection to actin | contraction, crawling |
receptor connection to IFs | stretching resistance |
4 main cell surface receptor types | cadherin, CAM, integrin, selectin |
adherins junctions | connect cells to cells, Ca2+ dependent |
two cell connections not associated with cytoskeleton | CAMs and selectins |
CAMs | Ig like, tissue specific (cell adhesion molecule) |
Selectins | recruitment of WBCs to infection site (example) |
3 cell connections associated w/ cytoskeleton | integrins, hemidesmosomes, focal contacts |
integrins | connected to actin, important in cancer biology/infection |
hemidesmosomes | connected to IFs, keratin |
4 signal sending ways | autocrine, paracrine, endocrine, direct contact w/ cell receptors |
3 main cell receptor types in membrane | ligand gated, GPCR, tyrosine kinase |
3 major mechanisms of signal transduction | phosphorylation/de, second messengers, GTP switches |
3 types of second messengers | cAMP, phosphatidyl inositol derived, Ca2+ |
cAMP signaling | hunger/stress signals |
PI 2nd messengers | IP3 (Ca2+ from ER), DAG (activates PKC), PIP3 (activates PKB) |
Ca2+ 2nd messenger | activates calmodulin, troponin, etc. |
All second messengers | readily available source, removed quickly |
Well known for short term responses | GPCR |
Well known for long term responses | tyrosine kinase |
PLC -> | IP3 + DAG |
Adenylyl cyclase -> | cAMP |
Gluconeogenesis cAMP example | CREBP binds to CRE (cyclic amp response element) |
Two different types of g proteins | Gs (stimulate), Gi (inhibit) |
Cholera toxin | modifies Gs to cannot hydrolyze GTP, efflux of ions= diarrhea |
Multiple second messengers example | inositol metabolites can raise intracellular Ca2+ and activate PKC (smooth muscle contraction) |
4 major off-switching mechanisms | GTP hydrolysis, cAMP broken down by phosphodiesterase, Ca2+ pumped, phosphatases |
Ras | small GTP binding protein that functions as an on and off switch (MAPKKK) |
EGF signaling | RTK activity, c-fos/c-jun= TFs and proto-oncogenes |
How cells know which cell to be | transient activation of enhancer, protein expressed, positive feedback loop |
Principle of apoptosis | conserved; regulated activation of proteases called capases (zymogen) |
Cancers from mesodermal origin | leukemia, lymphoma, CNS, retinoblastoma, sarcomas |
Characteristics of cancer cells (8) | grow in clumps, altered growth factor response, invasion of other tissues, altered karyotypes, immortal, altered cytoskeleton, altered receptors, less adhesive/more motile |
8 types of proteins that control cell growth | growth factors, growth factor receptors, signaling cascade, cyclin dependent kinases/cyclins, protein kinases, chromatin proteins, transcription factors, proteins in apoptosis |
tumor suppressors | need to both be mutated (recessive); p53 |
oncogenes | dominant, Ras |
retrovirus and cancer | can pick up a proto-oncogene and make it an oncogene |
DNA virus and cancer | interferes with normal replication controls |
3 immune layers of defense | mechanical/chemical, innate, acquired |
innate responses (4) | inflammation, phagocytosis, NK cells, complement |
humoral immunity | B cells -> antibodies, maturation in bone marrow, bursa in birds |
cellular immunity | cytotoxic T-cells, helper T-cells; maturation in thymus |
IgG | main blood antibody; complement activation |
IgM | B-cell antigen receptor or in blood; activates complement (before IgG) |
IgA | in secretions, dimer |
IgD | B-cell activation |
IgE | parasites, allergies |
3 mechanisms of antibody diversity | combine light + heavy chain, imprecise joining, hypermutation |
CD8 | |
CD4 | |
MHC I | all cells (pairs w/ CD8) |
MHC II | professional antigen presenting cells (pairs w/ CD4) |
MHC I peptide binding domain same structure as | HSP 70 (form fits function) |
Tc kill what? | all cells that present a foreign protein |
Coordination of immune response by Th cells | get out of G0 upon activation, stimulate B cells that display antigen on MHC II, then they get out of G0 (positive feedback) |
Negative selection | cells with strong recognition of self MHC (or cells with very weak recognition of MHC) -> cells killed (auto-immune) |