Cell cycle and apoptosis Flashcards
what is mitosis required fro
normal growth development and maintenacne
cell cycle properties
ordered set of events leading to growth and divison
- coordinated across different tissues
results in two identical daughter cells
DNA duplicated and divided equalyl
main phases in cell cyel
mitotic phase (when cell divided) interphase
what is interphase divided into
G1
2 phase
G2
interpahse
chromosomes are formed by condensation of chromatin
nuclear envolpe breaks worn
prophase
chromosomes attached to mitotic spindle
metaphase
line up at equator
tension on spindle fibres
anaphase
chromosomes pulled apart to poles
telophase
actin forms here and congrats them to physically divide the cell
cytokinesis physically separates them
what are the crital check points of cell cel
G1 G2 M phase
which phases influences the cell cycle
s phase
mitotic phase
what triggers transitions in the cell cyle and what with
cyclins
cyclin dependant kinases
what do cyclins do
trigger cell cycle transititions
what happens to the cyclins in cell cyel
levels rise and fall depending on stage of cell cycle
clycins correspond to which phase
G1 cyclin (D) S phase (E and A) M phase (B and A)
what binds to cyclin
cyclin dependant kinases
what do cyclin dependant kinases do
phosphorylate proteins that control cell cylle
when is cyclin dependant kinase active
when bound to kinase
what is cyclin dependant kinase activity controlled by
Cdk inhbitorss
cell cycle is regulated by
1) Cyclin and Cdk synthesis
2) Cyclin degradation, Cdk phosphorylation, Cdk inhibition
promoting factors for the cell cycle
- cyclin and CDK complex
- eg mitosis promoting factor
- phosphorylates and activates proteins involved in chromatin condensation, nuclear envelope breakdown, spindle assembly
when do cyclin levels dall
due to degradation
checkpoint G1/s
check for growth factors
nutritional state of cell
size of cell
complex Cdk drives this through
s phase
DNA replicated
G2 checkpoint
before entering mitotic phase
checks replication is completed
DNA integrityyy
anaphase promoting compelx
degrades cyclin
allows cell cycle to complete
makes sure chromosomes are aligned so they separate evenly
growth factor extraceullar signals lead to
bind to receptor strucural change cascade of phosphorylation substance enters nucleus transcription/translation could lead to product of Vdk
what is stage G0
cells permanently or temporaly leave cell cycle
what stage are most cells in the body in
G0
what can cells do in Go
resting
but can secrete
what is terminal differentiation
permanent left cell cycle
cell cycle synchronisation
cells can be at different phases
if serum removed and re-added, cells will then start at G1
what does dysregualted cell growth lead to
cancer
what are many cell regulatory genes involved in
tumour suppressor genes
what can chemotherapy taret
DNA replication
mitosis
cytokineis
blood vessel growth
what is p53
tumour suppressor gene
what does p53 do if DNA damaged
initiate DNA repair
arrest cell cyel
initiate apopsosis
defective p53
allows abnormal cells to prliferation
unable to monitor DNA through cell divison
replication with damaged DNA
apoptosis
programmed cell death
destroys cells that may be a threat
apoptosis initiation
may be initiatied by withdraw of positive signals
or repeat of negative signals e.g. UV
apoptosis
break down of nuclear envelope
blebbing
phagocytosis
apoptosis vs necrosis
apop - contrlled energy dependatn cells shrink membrane in tact non inflammatory no scarring nucelar fragmentation physillogical Necrosis - uncontrlled no ATP reqrueid cellls swell membrane not maintained swelling scarring large cell groups nucelar dissolution pathological
what is apoptosis related by
intrinsic/extrinsic mehcanisms
many steps
bcl-2 inhibits the initiation of the intrinsic mechanism (cancer)
caspases
proteolytic enzmes
what do cascades present as
inactive proenzymes /zymogens
apoptosis in disease
- Human papilloma virus inactivates p53
- Epstein barr virus protein similar to Bxcl- 2
- Melanoma inhibits expression of Apaf 1
- Fas antagonists – block T cell cytotoxicity
- Autoimmune eg SLE, Rheumatoid arthritis
- Increase in apoptosis eg HIV
mitosis and apoptosis in dental physiology
- Craniofacial growth and development
- Homeostasis in mucosa, skin and pulp
- Tooth development
- Bone remodelling (eg in orthodontics)
- Wound healing (proliferation of keratinocytes to protect, apoptosis of immune cells )
