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114 Cards in this Set

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  • Back
caps (+) end of actin filament; keeps it a constant length
Only made up of actin (thin) filaments
Middle (- end) of sarcomere that is only myosin filaments
Section where actin and myosin overlap in sarcomere
goes from z-line to z-line & has myosin on it. also keeps muscles from stretching too far (over-relaxation)
connected to z-line preventing over-contraction of muscles
globular protein complex composed that contacts the thin filament and tropomyosin
elongated molecule that fits into the grooves within the thin filament
Troponin & Tropomyosin in muscle contractions
When calcium levels rise, the interaction between calcium and troponin leads to a movement of the tropomyosin from position b to position a, which exposes the binding site on the thin filament to the myosin band
ATP in muscle contraction/ absence of ATP
ATP causes myosin II to detatch resulting in a power stroke. In the absence of ATP, myosin can't detatch leading to rigor mortis
Transporter Plug
checks to see if material is supposed to come into the nucleus (NLS)
Histones on DNA
green fluorochromes stick to the histones in order to view the DNA
Wild-type vs. Mutated nuclear import signal
microinjection of a normal protein-NLS using s micromanipulator shows the antigen accumulating in the nucleus. the same procedure with a mutated NLS shows the antigen accumulating in the cytoplasm since it can't gain access to the nucleus.
NLS protein entering nucleus
1)importin aplha & importin beta grab onto the NLS protein
2)They bring it towards the nuclear pore & bind to the cytoplasmic filament
3)The filament bends in and the transporter plug checks the protein
4)The transporter plug moves in along with the protein
5)Ran-GTP breaks the complex apart
6)The transporter plug checks importin alpha & beta, and Ran-GTP to get out of the nucleus
7)The address on the protein is cut off & hydrolyzed
What enters the nucleus
-DNA polymerase
-RNA polymerase
-rRNA proteins
-about 300 proteins enter the nucleus for specific functions
problems with nuclear matrix -> age very quickly
-DNA & 8 molecules of histones
-DNA wraps around histones twice & held together by the H1 histone
-nucleosome core particle consists of 146 base pairs
help organize large amount of DNA in small spaces (interphase)
DNA being compacted
Double helix -> wraps twice around 8 subunit histone (interphase) -> looped domains on chromosome (metaphase)
Cell Cycle
-G1:cell grows and carries out normal metabolism; organelles duplicate
-S:DNA replication and chromosome duplication
-G2:Cell grows and prepares for mitosis
3)Cytokinesis (ends M-phase)
1)Chromosomal material condenses to form compact miotic chromosomes. Chromosomes are seen to be composed of two chromatids attatched together at the centromere
2)Cytoskeleton is dissasembled & mitotic spindle is assembled
3)Golgi complex and ER fragment. Nuclear envelope disperses.
1)Chromosomal microtubules attatch to kinetochores of chromosomes
2)Chromosomes are moved to spindle equator
Chromosomes are aligned along metaphase plate, attatched by chromosomal microtubules to both poles
1)Centromeres split, and chromatids separate
2)Chromosomes move to opposite spindle poles
3)Spindle poles move farther apart
1)Chromosomes cluster at opposite spindle poles
2)Chromosomes become dispersed
3)Nuclear envelope assembles around chromosome clusters
4)Golgi complex and ER reforms
5)Daughter cells formed by cytokinesis
Pulse label in cell cycle with
Cells in M-Phase & G1-Phase fused
both cells go into M-Phase
Cells in M-Phase & S-Phase fused
both cells go into M-Phase with pulverized chromosome fragments
Cyclin B triggers what and causes what?
Cyclin B triggers cdc-2 to open & start MPF activity (all three proteins together), this then triggers mitosis. Interphase is underway when Cyclin B is destroyed
Cancer Cells make what fast?
make cyclin fast = short/fast cell cycles
cdc2 also known as
cdc2 activity through cell cycle
1)During G2, cdc2 kinase interacts with cyclin B, but remains inactive due to the phosphorylation of Tyr15 by Wee1
2)kinase CAK transfers a phosphate to Thr161, which is required for cdc2 kinase activity later in the cell cycle
3)When the cell reaches critical size, enzyme Cdc25 phosphatase is activated removing inhibitory Tyr15 phosphate, activation of cdc2 kinase drives cell into mitosis
4)By end of mitosis, stimulatory phosphate on Thr161 is removed.
5)The free cyclin is degraded and the cell begins another cycle
Cyclins needed throughout cell cycle
1)Cyclin D's + Cdk4/Cdk6 -> G1
2)Cyclin E + Cdk2 -> G1-S transition
3)Cyclin A + Cdk2 -> G1-S transition
4)Cyclin B/A + Cdk1 -> G2-M transition
allosteric activator
Cell Cycle Checkpoints
-Protein stops cell to make sure everything is happening correctly
1)G1 Checkpoint: checks for correct growth or initiate DNA repair if it is damaged
2)G2 Checkpoint: checks if chromosomes are completely copied and if enough cyclin was made to initiate MPF
3)M Checkpoint: is chromosome attatched to microtubules on both sides for anaphase (biattatchment)
Chromosome and microtubule connection
Chromosome (active) grabs the microtubule (passive)
joins chromatids
outer surface of centromere functions as site of attatchment of the chromosome to the dynamic microtubules of the mitotic spindle
______ is responsible for moving the chromosome to the poles (Anaphase A), while _______ is responsible for seperating the poles from each other (Anaphase B).
Dynein; Kinesin
How are microtubules connected to kinetochore
Dynein and CENP-E (member of kinesin family) hold microtubule to the corona fibers of the kinetochore
moves toward minus end
part of kinesin family which moves toward the plus end
associates with cdc20 to check if there is equal tension from both sides of the chromosome (part of M checkpoint)
associate with cdc20 & contact microtubule to make sure it is there (part of M checkpoint)
Chromosome Alignment
Also known as jockying -> moves chromosomes into the correct position
What causes chromosomes to move
microtubules don't actually touch kinetochore -> lengthening = kinesin (CENP-E) -> shortening = dynein
astral spindle fibers
star like pattern around centriole
polar spindle fibers
go out towards chromosome, but don't make contact. play a role in jockeying & seperation of chromosomes
chromosomal spindle fibers
make contact with chromosomes
Pericentriolar material
Surrounds centrioles
Anaphase Promoting Complex
1)APC-Cdc20 -> hydrolyzes securin -> releases separase -> separase cleaves cohesin seperating chromatids and entering anaphase
2)APC-Cdh1 -> destroys mitotic cyclins -> stops activity of mitotic Cdk -> moves out of mitosis and into the G1 phase
Experimental demonstration of checkpoints
1)laser used to destroy a microtubule creating monoattatchment
2)imbalance arrests cell in metaphase
3)monoattatched chromosome is pulled to the pole by and attatched glass needle
4)artificially applied tenison mimics the natural tension and cell proceeds into anaphase
one chromatid falls off of microtubule when it is shortening towards minus end
actin filaments form underneath the plasma membrane and contract to pinch off the two cells. contractile ring sets up wherever the microtubules overlap at metaphase. (contractile ring also made up of myosin II)
Synaptonemal Complex
ladder-like structure with transverse protein filaments connecting the two lateral elements
Prophase I
1)leptotene: chromosomes become visible in light microscope (long & thin)
2)Zygotene: visible pairing of homologues -> synapsis -> synaptonemal complex (SC) formation
3)Pachytene: fully formed SC holds homologues close together
4)Diplotene: dissolution of SC -> chromasomes attached to one another at chiasma (where crossing over occurs)
5)Diakinesis: meitotic spindle is assembled & the chromosomes are prepared for seperation
6)Metaphase I: kinetochores of sister chromatids are connected as a unit to microtubules form the same spindle
Point of recombination or crossing over
Cohesion (Meiosis I)
cohesin does not break down (no APC)
-If connected, considered one chromosome
-When broken apart, they are individual and behave independently
Cohesin (Meiosis II)
breaks apart in presence of APC
Trisomy 21
Down's Syndrome -> Egg has two maternal copies of chromosome 21 + one paternal copy = 3 copies
Signal Transduction
transferring signal from outside to inside
1)Activation of enzyme activity
2)Change in cytoskeletal organization
3)Change in ion permeability
4)Activation of DNA synthesis
5)Activation of RNA synthesis
toxins that stop g-proteins from working properly
How Glucagon Hormone Signal Transduction Pathway affects Glycogen metabolism in muscle cell
1)glucagon binds to the N-terminus of the receptor (7 alpha helix through PM)
2)C-terminus comes into contact with alpha subunit of G-protein
3)GDP turns into GTP (on) position
4)alpha subunit slide over and contacts the N-terminus of Adenylyl Cyclase
5)Active Site of effector opens
6)ATP + H2O enter -> cAMP out
7)cAMP then activates Protein Kinase A, which activates Glycogen Synthase & Glycogen Phosphorylation
8)Pathway turned off-> PDE destroys cAMP & c-subunits go back to inactive form
cAMP -> PKA activates
1)mictotubule (assembly/disassembly)
2)Endoplasmic Reticulum (protein synthesis)
3)Nucleus (DNA synthesis & differentiation, RNA synthesis)
4)Phosphorylase Kinase -> Phosphorylase (glycogen breakdown)
5)Glycogen Synthase (glycogen formation)
6)Triglyceride Lipase (lipid formation)
Free calcium in response to hormone stimulation
Exposure of cell to vasopressin leads to controlled spikes in the concentration of free calcium at periodic intervals.
How receptor transduces the primary signal into the cytoplasm when Insulin interacts with the Insulin Receptor
-Insulin Receptor 2 alpha subunits, 2 beta subunits, and 2 alpha helices
1)insulin comes into contact and binds to the alpha subunits of the receptor
2)This causes the beta subunits to undergo autophosphorylation which places phosphates on the tyrosine kinase domains.
3)The receptor then attracts IRS proteins which bind to the phosphates by their PTB domain
4)This attracts certain subunits to attach to the phosphates on the IRS
5)This causes an activation cascade by activating PI3K which activates PDKI which activates PKB
6)PKB is then able to stimulate enzymes for maikng glycogen in the cytoplasm
7)This in turn activates glycogen synthase
-regulates glucose levels
-mitogen: causes mitosis in cells
Anything that binds to tyrosine phosphate
has an SH2 domain
Explain signal transduction pathway if you added EGF to a culture medium with fibroblast cells
1)The EGF would bind to a growth factor receptor (2 ligands would be needed)
2)The receptor would then autotransphosphorylate to add phosphaes to the tyrosine kinase domain
3)Grb2 would then bind to a phosphate which would then have an Sos bind to it.
4)The Sos would then contact Ras-GDP activating it to Ras-GTP
5)The Ras-GTP would then act as an allosteric activator for Raf (MAPKKK)
6)Raf would then phosphorylate MEK (MAPKK) which would activate it
7)MEK would then phosphorylate ERK (MAPK) which would activate it
8)ERK could then phosphorylate a transcription factor
9)The TF would then be able to increase the transcription of specific genes involved in the growth response
Extrinsic (receptor-mediated) apoptosis
1)TNF bindsto TNF receptor (TNFR1)
2)Activated receptor binds two different cytoplasmic adaptor proteins (TRADD & FADD) and procapase-8 to form a multiprotein complex
3)TNF receptor, FADD, and TRADD interact with one another by homologous regions called death domains
4)Once assembled in the complex, the procapase molecules cleave one another to generate and active caspase-8 molecule containing 4 polypeptide segments
5)Caspase-8 is an initiator which cleaves the executioner caspases to carry out the death
(TNF & TNFR1 are also known to activate signal pathways, one of which leads to cell survival rather than death)
Death Domains
act as docking sites
Executioner Capase
does most of the damage, but not all
Intrinsic (mitochondria-mediated) apoptosis
1)Internal cellular damage -> Activation of proapoptotic Bcl-2 family member (Bad or Bax)
2)Bad or Bax inserts into outer mitochondrial membrane, releasing cytochrom c from intermembrane space
3)Cytochrome c molecules form a multisubunit complex with Apaf-1 (cytosolic protein) and procaspase-9
4)Procaspase-9 molecules are activated due to association with Apaf-1
5)Caspase-9 molecules cleave and activate executioner caspases -> apoptosis
DNA damage
1)p53 levels rise -> G1 arrest -> repair before division or Bax/Cytochrome-C pathway causing apoptosis
2)no p53 -> no G1 arrest -> mitotic failure and cell death or division with damage leads to tumor
When a cell moves, it extends a structure called a ________ at the leading edge and forms several _________ with the substratum such as collagen.
lamellipodium; integrin adhesion
When a cell stops dividing, it usually arrests in ________ phase of the cell cycle. The time from S-Phase to M-Phase can be determined by pulse labeling cells with _________.
G0; [^3H]Thymidine
CDK1 and ________ are required for entering M-Phase, while CDK2 and ________ are required for entering S-Phase during the mitotic cell cycle.
Cyclin B; Cyclin E
The checkpoint proteins in late G1 check the cell for any ________, while the checkpoint proteins in late G2 check the cell for _________.
improper growth; successful replication
When the mitotic spindle forms, the microtubules are "captured" by the _________ on the chromatids with the _______ end of the microtubules facing this structure.
kinetochore; plus
_______ is responsible for moving the chromosomes to the poles (Anaphase A), while ______ is responsible for seperating the poles from each other (Anaphase B).
Dynein; Kinesin (CENP-E)
Abnormal chromosome seperation such as Primary Non-disjunction takes place during _________ of meiosis, while Secondary Non-disjunction of chromosomes takes place during _______ of meiosis.
first meiotic division; second meiotic division
Cytokinesis requires the function of ________ filaments.
Phopholipase C (PLC-beta) hydrolyzes PIP2 within the Plasma Membrane into two second messengers. They are ______ & _______.
Genes coding for components of some signal transduction pathways may become mutated and they become cancer causing oncogenes. Two examples of abnormal signaling oncogenes are _______ & ________.
ras; raf
Growth factor oncogene
PDGF -> sis
Growth Factor Receptor Oncogene
EGF -> erbB
Protein Kinase (signaling) Oncogenes
1)Src -> src
2)Ras -> ras
3)Raf -> raf
Protein Oncogene that affects apoptosis
Bcl-2 -> bcl-2
Transcription Factor Oncogene
Myc -> myc
What happens when and M-phase cell + G1 phase cell fused? M-phase + G2-phase cell fused?
1)M-phase cell fused with G1-phase cell, the chromatin in the nucleus of the G1-phase cell showed premature chromosome compaction forming sets of elongated partially compacted chromosomes.
2)When M-phase cell is fused with a G2-phase cell, the G2-phase cell showed premature chromosome compaction in its nucleus forming compacted elongated chromosomes that are doubled since they already went through duplication in the S-phase. The results suggest that transitions from G1 or G2 towards M-phase is induced by a stimulatory agent. This is also known as positive control.
How is MPF activated?
1)inactive cdc2 kinase interacts with cyclin B during G2
2)cdc2 kinase remains inactive as a result of the phosphorylation of Tyr15 by Wee1
3)CAK is a seperate kinase that transfers a phosphate to Thr161 which is required for cdc2 kinase activity later
4)When the cell reaches a critical size, and enzyme Cdc25 phosphate is activated removing the inhibitory phosphae on Tyr15
5)This activates cdc2 kinase driving the cell into mitosis
6)At the end of mitosis, the stimulatory phosphate is removed from Thr161
7)The free cyclin B is destroyed and the cell begins another cycle
Which substrates are phosphorylated by MPF and what events do they cause during M-Phase of the cell cylce?
During interphase, many substrates remain inactive until they are triggered for their specific functions. cdc2 plays a crucial role in activating these substrates. After cdc2 is activated, it begins to phosphorylate multiple substrates that have specific roles throughout M-Phase.
1)cdc2 phosphorylates Lamin A & Lamin B -> the phosphorylated lamins cause the breakdown of the nuclear membrane during mitosis
2)cdc2 also phophorylates Condensin & Histones -> this causes the the condensation of chromosomes to form compact mitotic chromosomes
3)cdc2 also phosphorylates alpha and beta tubulin -> this causes tubulin growth and the assembly of the mitotic spindle
Muscle Contraction
1)Synaptic Signal to the neuro-muscular junction causes depolarization
2)The impulse is relayed along the transverse (T) tubules and then to the Sarcoplasmic Reticulum
3)Action potential causes Calcium Channels in SR to open and Ca2+ diffuses out of the SR compartment (increaes about 100 fold)
4)Ca2+ binds to troponin causing a shift in tropomyosin to expose the myosin-binding site
5)ATP binds to myosin II head
6)Myosin II neck bends back and grabs toward plus end of actin
7)Hydrolysis of ATP energizes the head & it binds to myosin binding site on actin
8)Release of Phosphate causes power stroke to occur moving actin towards center of sarcomere
9)Ca2+ undergoes re-uptake and the muscle relaxes
something that attracts or repels the cell
guides Primordial germ cells
how sperm knows where to go
attracted by chemicals of egg and move towards warmer zones in female body
NLS signal
comes after protein on the C-terminus
Active transport
using GTP is needed to get things in or out of cell
Phosphorylated Lamin A + B
by cdc2 -> nuclear membrane breakdown during M-phase
Condensin & Histones phosphorylated
by cdc2 -> chromosome condensation during M-phase
alpha & beta Tubulin phosphorylated
by cdc2 -> tubulin growth & spindle formation during M-phase
Cytokinesis Contractile Ring
one cell that has many nuclei (no cytokinesis)
Cell -> Cell communicatio
1)Endocrine: Long Distance (starts at 10^-5M, ends at 10^-9 M)
2)Paracine: short distance
3)Autocrine: "talking to self"
Second Messengers
1)cAMP -> PKA (activated)
2)IP3 + DAG -> PKC (activated)
-Vasopressin: antidieretic -> retains water (targets kidney renal tubule)
-PTH: parathyroid hormone -> targets bone/muscle development
-Odorants: Smell
-Light: retina stimulated
-Sperm: binds to receptor
cofactor for PKC (Ca2+ & DAG needed to get PKC to Plasma Membrane)
Phosphorylates enzymes, cytoskeleton, & transcription factors
Unfertilized vs Fertilized Egg
-PKC inactive -> PKC active
-Glycolysis low -> Glycolysis high
-Pyruvate low -> Pyruvate High
-ATP low -> ATP high
-Protein Synthesis low -> Protein Synthesis high
-no DNA synthesis -> DNA synthesis starts
(Egg can be tricked to turn on by increasing Ca2+ & DAG)
Apoptosis highest rate
-highest rate during fetal development
-neurons destroyed if not needed
-"self" Antibody lymphocyte
-Tissue Sculpting (ex. finger)
-DNA damage that isn't repaired
-Anything with lack of growth factor
Apoptosis Phenotype
-Loss of cell adhesion
-cytoskeleton breaks down
-DNA Fragments
-Nucleus Breaks down
-Cell Fragments -> Blebbing
-Phosphotityl Serine Phagocytosis Signal
-Debris Cleared up by macrophages
-procaspase -> caspase (active)
Herceptin Antibody (Ab)
breast cancer drug that blocks EGF receptors so cancer cells die
-problem is it also blocks receptors on cardio myocytes -> no tropic factor -> Bad -> Bax -> Cyt-C -> apoptosis