cells final Flashcards
HeLa cells immortality
overactive telomerase never shortens allowing indefinite replication and division
gene regulation
chem modifications to chromatin and histones, during transcription or translation
chromatin
dna, rna, proteins packed to give chromosome shape
methylation
reversible PTM in nucleus of cytosines occurs in CpG islands near gene promoter and silence transcription, cause gene inactivation
restricts DNA access
histones
proteins that provide structural support to chromosomes and bind with DNA to form nucleosome
belong in nucleus
have nuclear localization tag
RNA processing
RNA transcript to mRNA by splicing introns, add 3’ polyAtail and 5’ cap. to cytoplasm
srRNA
inhibits translation, cause degradation of RNA, silence and inhibit, chromatin remodeling
HAT
acetylation makes histones more negative and loosens DNA packing so transcription factors can bind to promoter TATA box
+ control lac operon
CAP activation in response to glucose
active/inactive based on glucose - cAMP/CAP levels
- control lac operon
induced or repressed operator
induced by presence of lactose which relieves repressor, promoter recruits RNA polymerase
controls cAMP levels in lac operon
rate of bacterial growth
high lactose and high glucose lac operon
induced and inactive
negative cell cycle regulators
p53, p21, Rb tumor suppressors
positive cell cycle regulators
cyclin CDK
EGF binding
Upregulating proliferation
Down regulating apoptosis
ZO-1
tight junction protein
ZO-1 knockout has increased F actin expression→ actin is a component of microtubules
qRT-PCR
dna expression; further left = more transcription/translation
separation experiments
TLC, centrifugation, electrophoresis
siRNAs
knock down gene in experiments
silencing
repress transcription by change gene dosage and rate of transcription
proximate
mechanisms
ligand
signaling molecule binds to receptor causes activating change
membrane composition
TLC by polarity, freeze fracture lipid bilayer, FRAP, pulse chase?
pulse chase
trafficking and movement proteins
evolution
by natural selection reqs variation that is heritable and results in differential reproductive fitness success
protein destined for ion channel
amino-terminal and signal anchor peptide seq
rough ER
studded w ribosomes; protein synthesis destined as transmembrane, secreted out, or lumen organelles
default is secretion
COP II move from ER to golgi
lysosomal enzymes
vesicles that break down protein; synthesized on rough ER, processed in golgi
Golgi apparatus
synthesizes carbs, sorts protein and lipids to final destinations.
PTMs like glycosylation occur here by enzymes
cargo arrives at cis-golgi and exits trans-golgi face
COP I move from golgi to ER
COP I vesicles
move golgi to ER
COP II
move ER to golgi
ER resident proteins
amino terminal sequence
amino terminal sequence
ER (lumen) proteins, ion channel protein, secreted
rough ER
Coat proteins
make vesicles
destined for mitochondria/chloroplast, ER, secretion
amino terminal signal sequence
SRP
signal recognition particle is rna-protein complex
no signal peptide
free ribosome in cytosol
Sar I GTPases
trafficking
controls coat assembly on coat protein complex II (COPII)-coated vesicles, which mediate protein transport from the endoplasmic reticulum (ER) to the Golgi.
GTPases
on or off
protein switches regulate cell responses to EC signals
cause cell survival, proliferation
in nucleus to start transcription and gene expression
Ras
GTPase activates RAF kinase and MEK/MAP growth signal kinase and ERK/MAP
activated by EGFR to cause cell proliferation
signaling molecule
polar ligand on cell surface like EGF
MDM2
degrades p53 (- regulator, ubiquinates)
p53
antagonistically pleitropic bc p21 path allows for apoptosis beneficial early on or stores away and causes aging/senescence
checks for DNA mutations or triggers apoptosis
Rb
tumor suppressor binds to transcription factors and genes NOT transcribed
life history characteristics
lifespan
litters/year
reproductive age
maturity
# offspring
parental care
(hemi)desmosomes
bind to IM filaments and connect w integrins
Integrins and hemidesmosomes bind to ECm basal lamina
desmosomes
adhesive junction for mechanical stress stability containing cadherins
e cadherin
uvomorulin
desmosomes
connects epithelial cells to each other
B-catenin
in nucleus as transcription factor or peripheral junction
loss of e-cadherin
invasion
B-catenin leaves cell junction, moves to nucleus to act as proliferative transcription factors
more e-cadherin/uvomorulin
limits cell invasion by contact inhibition
B-catenin at junction
cadherin
transmembrane glycoprotein synthesized on rough ER that mediated Ca2+ adhesion
tight junctions
adherins junctions form 1st
limit paracellular diffusion
composed of claudin
prevent EMT
connect/link to actin MF microfilaments
ZO-1 tethers cytoskeleton
belt-like
claudin
composes Tight junctions
adherens junctions
bind actin MF - cytoskeleton
plasmodesmata
in plants; intercellular channels span cell walls and facilitate exchange of signaling molecules;
most similar to GAP junctions
gap junctions
allow exchange
integrins and cadherins
transmembrane proteins w a cytoplasmic domain connected to their cytoskeleton
integrins
interact with ECM and actin cytoskeleton cytoplasmic domain.
growth factors stored in ECM can bind w integrins and activate proliferative signaling pathways and ECM invasion
cells gain function to invade assisted by focal adhesions and integrin dimers
focal adhesions
integrin-ECM migration by actin polymerization
linked to the actin cytoskeleton
anchorage dependent growth
grow attached to surface ECM as good neighbors
Hayflick limit
telomere function and senescence limit doublings of cells
retrotransposons
via reverse transcriptase from mRNA to DNA
NO introns
EMT
invasion and metastisis
integrin activation increases cell adhesion to ECM
integrin activation
increase cell adhesion and create focal adhesions linked to actin cytoskeleton
barriers to MC
- cheaters - specialization
- nutrient transport by bulk flow
- adhesion by integrins
- communication by junctions
snowflake yeast
mutation in cytokinesis = incomplete binary fission
clonal
heterogeneity in growth form from additional mutations
cost of MC overcome by specialization
MC phenotype has fitness advantage and maintained
angiogenesis
hypoxia HIP1a by low O2 releases VEGF
terminated by Dll4 and PDGF
invasion and metastisis
EMT by loss of uvomorulin/e-cadherin
integrin activation
replicative immortality
telomerase constitutively overactivated
sustain proliferative signaling
Ras jammed accelerator or activated EGF receptors by AKT or MAP/ERK kinase pathway
resisting cell death
damage to TP53, mutated AKT
pericytes
connect by integrins and gap junctions
stabilize new capillary
AKT
protein blocks apoptosis (phosphorylation by kinases)
evade growth suppressors
loss of TP53 or mutations or MDM2 overexpression, RB
genomic instability
no cell cycle checkpoints, mutations damage DNA
telomere shortening
senescence and apoptosis
metabolism
warburg effect of glycolysis via HIF1a
commensalism
1 benefits, 1 neutral
ammensalism
negative from 1 pop onto other
sprouting angiogenesis
- tip cell selection of high delta expression, low notch expression
- tip cell migration
- stalk elongation
- capillary fusion
- blood flow perfuses new capillary
- pericytes stabilize new capillary
tip cell selection in angiogenesis
high delta expression, low notch
diffusion
eletron transport chain
ficks 1st law
axelrod
tumor progression facilitated by cooperation in form of by-product mutualism in genetically diverse tumor cells
VEGF
angiogenesis
triggers tip cell formation
fibroblasts and endothelial cells bind VEGF
endothelial cells express Dll4 delta on surface
endothelial cells express notch on surface
TME
cytoskeleton stiffens
non-cancer cells use alternative metabolic pathways
cancer cells avoid immune system
actin
polymerize to form MF
