Cells

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countchocula58
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283988
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Cells
Updated:
2014-09-25 18:25:42
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foundations fnd1 cells tubberly
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Cells are small and therefore unimportant
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  1. 3 cytoskeleton networks
    • actin filaments (microfilaments)
    • intermediate filaments
    • microtubules
  2. Actin filaments
    • Most rigid and takes a lot of force to break (but still flexible)
    • Polarized, can treadmill depending on actin concentration (needs ATP)
    • Cell movement, muscles, microvilli, contractile ring, cortecal ring to hold together and form epithelium in intestine
    • Myosin walks on it for muscles, vesicles and movement (always to plus except in muscle)
    • Deficiencies cause deafness, skeletal and cardiac muscle myopathies and listeria infection
  3. Intermediate filaments
    • Starts flexible and gets stiff
    • monomer helix to dimer to tetramer to tetramer bundle (no polarity)
    • Hold cells together
    • Defects cause blistering and progeria
  4. Microtubules
    • Most flexible, break easily
    • Heterodimers of α and β tubulin monomers (polarized), minus end at centrosome (MTOC)
    • GTP level controls growth/shrink from plus end
    • For cilia and flagella
    • Dynein to minus kinesin to plus
  5. Motor Proteins
    • Myosin (plus)-actin fillaments, ATP causes it to let go, ADP causes binding, usually unbound but work together
    • Kinesin (plus)-microtubules
    • Dynein (minus)-microtubules, ATP causes it to swing, 50/50 attached time
    • Move organelles and are cargo specific
  6. Endoplasmic reticulum
    • Synthesis and glycosylation of integral membrane proteins
    • 3D non static structure
    • Stores calcium and synthesizes lipids and steroids
    • Drug detoxification
  7. Golgi apparatus
    • 3D part of network
    • Glycosylation and sorting to different parts
  8. Signal Sequence
    Targets protein during synthesis to ER where it can be cleaved and attached to a GPI anchor or inserted into the membrane
  9. Protein Folding
    • Glycosylation modification and trimming acts as a timer and to identify misfolded proteins
    • Chaperones assist and require ATP
  10. Misfolded proteins
    • Transported by chaperones to be degraded in cytosol (marked by ubiquitin)
    • Too many misfolded cause the unfolded protein response
  11. Unfolded protein response
    • Sometimes caused by viruses making lots of protein
    • Sensors interact with chaperones to recognize
    • Regulated mRNA splicing activates more folding proteins
    • Phosphorylation inactivates translation initiation factor so only proteins that help with folding are entering ER
    • Release of proteolysis
  12. Vesicular Transport (budding)
    • Different vesicles are coded differently depending on the target
    • Cargo molecules bind to coat to cause clustering and budding
    • Microtubules frequently assist
    • Coat can leave for recycling once budded
  13. Clathrin Coated
    • Golgi to plasma membrane
    • Plasma membrane to endocytotic pathway
  14. COP coated
    • ER to golgi
    • Golgi to Golgi
    • Golgi to ER
  15. Vesicular Transport (fusion)
    • Rab is a protein on the vesicle that a tethering protein on the target membrane can bind to (targets)
    • v-snares are on the vesicle and associate t-snares on target to help dock then are recycled
  16. ER to golgi
    • Uses COP coat with receptors that only bind correctly folded proteins for further processing
    • Resident proteins stay behind because they do not have receptors
    • These are usually recycled back to ER by binding KDEL proteins
    • Microtubules can assist by positioning golgi
  17. Golgi compartmentalization
    • Each compartment has different functions as far as packaging and processing is concerned
    • cis Golgi is where it trafficks with the ER
    • trans golgi is where it trafficks with endocytotic pathway
  18. Golgi to early endosome
    • Can turn it into a lysosome by sending hydrolases
    • The signal to do this is the oligosaccharide attached to the hydrolase by the ER to target to specific lysosome
    • Recycle!
  19. Ways to get stuff into the cell
    • Receptor mediated endocytosis (clathrin coated pits) with adaptors for certain receptors
    • Phagocytosis engulfs large things and forms a complete membrane
    • Pinocytosis pinches off very small amounts of extracellular fluid in bags called cavaeolae. No receptor or clathrin. Used in prions, placenta, immuno etc
  20. Fates of endocytosis
    • An early endosome can bud to various fates
    • Becoming a lysosome and degrading
    • Trafficking to the other side of the cell is transcytosis
    • Trafficking back to the same membrane is recycling
  21. Multivesicle bodies
    • Somewhere on the pathway to a late endosome or is a late endosome
    • Forms vesicles within the vesicle so that it can degrade transmembrane proteins or dump things outside of cell (transfer to other cells and used by tumors)
    • Also can fuse with lysosome
  22. Types of secretory pathway
    • Regulatory has vesicles stored in cytoplasm awaiting outside signal
    • Constituative is unregulated and goes straight to plasma membrane. This is used for plasma membrane proteins
  23. Cell Cycle phases
    • G0/senescence
    • G1, S, G2, M, cytokenesis
  24. Regulatory mechanisms of cyclin/Cdk
    • Association (cyclin and Cdk)
    • Cdk Inhibitor association (CKI)
    • Inhibitory phosphorylation
    • Activating phosphorylation
    • Cyclin transcription
    • Cyclin/Cdk degradation
    • Cdk Inhibitor (CKI) degradation
  25. Cdk/cyclin degradation
    Proteolysis regulated by APC/C, which is activated by association with Cdc20 to cause ubiquitination of cyclin/Cdk to proteolysis by proteosome
  26. Cdk Inhibitor (CKI)
    • bind to cyclin/Cdk and inhibit despite activating phosphates
    • p27 is an example (but also stabilizes Cdk E
  27. Cdk Inhibitor (CKI) degradation
    SCF complex with F-box protein causes ubiquitination of Cdk Inhibitor (CKI) to proteolysis by proteosome
  28. Inhibitory phosphorylation
    • Despite activating phosphorylation, an inhibiting phosphorylation
    • Activating phosphatases can remove to activate it
  29. Cyclin/Cdk levels
    NOT cyclin levels, these wax and wane in activity throughout phase of cell cycle
  30. G1 regulation (Rb)
    • Rb is the brakes on G1, bound to E2F family when hypophosphorylated and phosphorylation causes disasociation
    • Cyclin D1/Cdk4 first phosphorylates Rb and cyclin D1/Cdk6
    • Cyclin D1/Cdk6 phosphorylates Rb and then cyclin D1/Cdk6 and cyclin D1/Cdk4 both phosphorylate cyclin E/Cdk2
    • Cyclin E/Cdk2 is the final phosphorylator of Rb to cause E2F family release
    • E2F family activates genes for the E2F family and cyclin E/Cdk2 and cyclin A (for S phase) and replication factors
  31. G1 regulation (mitogen)
    • Mitogen binds to mitogen receptor, activating MAP kinase
    • MAP kinase activates genes for cyclin D and E2F family
    • MAP kinase causes degradation of p27
    • MAP kinsae phosphorylates G1 cyclin/Cdks
  32. Cdk Inhibitors (CKI) in G1
    • CIP/KIP family and INK4 family inhibit the cyclin/Cdk
    • Except CIP1/p27 which stabilized cyclin D/Cdk4,5 , but INK4A bumps it off and it stabilizes cyclin E/Cdk2. This allows cyclin
    • D/Cdk4,6 to be active (unbound) and cyclin E/Cdk2 to be active and stabilized for the positive feedback loop
    • This is from mitogen
  33. G1 regulation (p53)
    • DNA damage recognized by ATR/ATM kinase phosphorylates CHK1 and 2 to activate them
    • CHK1 and CHK2 phosphorylate p53 (releasing Mdm2)
    • p53 transcribes p21 (CKI)
  34. S phase regulation
    • Cdc6 is bound to ORC
    • Cyclin A/Cdk (S phase Cdk) phosphoryaltes Cdc6 for degradation
    • ORC is phosphorylated and Mcm starts unwinding
    • At the end, M Cdk maintains phosphorylation at ORC so that you don't rereplicate (Cyclin B/Cdk1)
    • M phase cyclin must be inactivatingly phosphorylated during S phase
    • ATR/ATM kinase travels with replication complex and upon identifying an error, phosphorylates CHK1 which phosphorylates Cdc25 to degradation
    • Cdc25 is the activating phosphatase of M cyclin/Cdk
  35. Telomeres in cell cycle
    • At certain shortness they stop cell cycle even if you remove Rb and p53. Some keep growing (tumors) from genome instability
    • Telomerase can cause indefinite cell growth in cells that have stopped
  36. Mammalian and cell growth
    • In mammals (not humans) predivision cell growth is well regulated
    • Mitogens activate a pathway that activates raptomyocin (cancer drug target)
  37. Mitotic Cyclin/Cdk phosphorylation
    • Cyclin B/Cdk1
    • CAK does activating phosphorylation
    • Wee1 does inhibitory phosphorylation
    • Cdc25 is the phosphatase against Wee1 but it is inactive until phosphorylate
    • One way to phosphorylate Cdc25 is mitotic cyclin/Cdk which also inhibits Wee1 itself
    • This means mitotic cylcin builds slowly until reaching critical level and BOOM!
  38. Mitotic Cyclin/Cdk compartmentalization
    • Cyclin B/Cdk1 when unphosphorylated can be found in the cytoplasm, but if it gets into the nucleus and phosphorylated it can't leave
    • Cyclin B/Cdk1 can phosphorylate other cyclin B/Cdk1 in the nuclear pool to make a rapid shift into mitosis
  39. Nuclear envelope dissasembly
    • Occurs in prophase through phosphorylation
    • Cyclin B/Cdk1 (M phase cyclin) does this
    • Dephosphorylation rebuilds
  40. Chromosome condensation
    • After nuclear envelope dissasembly
    • Cohesin and condensin help DNA condense into chromatids
    • Kinetochore binds around centromere
  41. Microtubule spindle formation
    • Astral radiate out, contacting plasma membrane
    • Interpolar connect the spindles
    • Kinetochore connect spindle pole to kinetochore
  42. Erroneous chromosome attachment
    • Monotelic, syntelic, or merotelic
    • Checked for by "wiggle" with motor proteins walking and GTP/GDP dependent microtubule dynamics
    • Kinetochores put out negative signal if not attached
    • Cohesins bind sister chromatids and chromatids to kinetochore
    • Cohesins binding sister chromatids are broken by separase, which is inactively bound to securin
    • When the anaphase promoting complex (APC) forms it ubiquitinates securin for proteosome degradation and frees separase to cleave interchromatid cohesins
    • APC is activated by Cdc20
    • APC also ubiquitinates M cyclin/Cdk
  43. Cyclin concentration and Mitosis
    Different cyclins are degraded at each phase of mitosis for transitions
  44. Anaphase A microtubules
    Kinetochore microtubules shorten causing chromatids to be pulled apart
  45. Anaphase B microtubules
    • Centrosomes (spindle poles) pulled and pushed apart by astral microtubule shortening and interpolar microtubule elongation (motor proteins play big role in all of this)
    • The affect of the interpolar microtubules pushing away is not as significant as microtubule shortening (to kinetochore) to pull chromosomes in and appart
  46. Errors in anaphase
    • Lagging causes an unattached chromosome (from monotelic or syntelic) to form micronuclei
    • Merotelic can cause cytokenesis failure and tetraploidy, a bridge, or chromatin cleavage
  47. Cytokenesis
    • Actin with myosin motors form a big ring that contracts
    • Tons of other proteins involved too
  48. Meiosis I v meiosis II
    • Meiosis I is reduction division (2n->1n)
    • Meiosis II is identical to mitosis except it is haploid
  49. Prophase I steps
    • Divided into different steps becuase there is quite a bit happening
    • Zygotene is when they align
    • Pachytene is when crossing over occurs
    • Diakinesis is when homologs separate
    • Dictyotene is special and where female mitosis is arrested (3rd month prenatal)
  50. Meitoic recombination
    • Big chromosomes have more chiasmata and there must be at least one in each arm
    • Chiasmata only occur between two of the four chromatids
    • It is more frequent in oogenesis than spermatogenesis
    • The closer to the telomeres the more frequent it is
    • Sex linked chromosomes can do it because of pseudoautosomal regions PAR1 and PAR2 which express the same genes (X and Y)
    • Causes more randomization in gamete formation than random homologue separation alone
  51. Chromosome abnormalities
    • Cause constitutional abnormalities (as oppoosed to neoplastic aka acquired)
    • Cause 60% of spontaneous abortions
    • Euploid and aneuploidy
  52. Meiosis I nondisjunction
    • More commonly the cause of nondisjunction
    • Results in 2 trisomy 2 monosomy
    • All chromosomes in trisomy are different
    • Monosomy is just the partners chromosome
    • XXY paternal is thus always MI nondisjunction
  53. Meiosis II nondisjunction
    • Less common to be the cause because it results in two normal gametes (unless it occurs for each cell post meiosis I)
    • 1 trisomy results where two of the chromosomes are the same
    • 1 monosomy which is just the partners chromosome
  54. Balanced Translocations
    • Cause problems in meiosis I and can result in partial trisomies
    • Alternate 1-If the normal chromosomes go to the same side and the translocation chromosomes go to the other side, you have a normal offspring or a translocation carrier
    • Adjacent 1-mix of normal and translocated with the centrosomes all going to the right side. Partial trisomies result but can be less severe than adjacent 2
    • Adjacent 2-mix of normal and translocated with centromeres going opposite ways. Partial trisomies are usually worse than in adjacent 1
    • Only 3 trisomies (13, 18, 21) and one monosomy (X) are compatible with life
  55. Roberstonian translocation
    • Translocation between two acrocentric chromosomes, causin loss of p arms and satelite DNA (13,14,15,21,22)
    • A trivalent is formed in meiosis I with six ways to go but only 4 do not result in monosomies (lethal)
    • Normal (both normals), balanced translocation (just robertsonian), and unbalanced with a trisomy of the chromosome that you take with the robertsonian, which can also be lethal
    • If 21 is involved emperical risk for maternal carrier is 10-15%, 0-2% for male carrier
  56. Inversions
    • Paracentric produces acentric or dicentric products, so either a miscarriage or a healthy offspring
    • Pericentric produces duplications and deletions of non inverted region, so either miscarriages, abnormal offspring, or healthy offspring

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