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AP Bio Unit 4: Cell Communication and Cell Cycle Cheat Sheet by

AP Bio Unit 4: Cell Communication and Cell Cycle

Overview of Cell Signaling

local regula­tors:
~ paracrine: on site release and response of signal molecules
~ synaptic: neurons use ACH
~ cell to cell joining
~ long distance regula­tors: carry commun­ication factor to tissue group far from source
~ endocrine: pituitary gland
~ animals: hormones / HGH
~ plants: ethylene CH2 = CH2
~ ex: one bad apple ruins the bunch

Cell Commun­ication

Paracrine: target cells lie near the secreting cell
Juxtac­rine: a ligand on one cell surface binds to a receptor on the other
Autocrine: the secreted molecules act on the secreting cell itself
Endocrine: secrete specific hormones into the bloods­tream

Tyrosi­ne-­Kinase Steps

1) Tyrosine Kinase is separate when inactive
2) Ligand attaches to a receptor
3) Tyrosine Kinase comes together (dimer)
4) Tyrosine Kinase is phosph­ory­lated with a (P) from ATP
5) The activated Tyrosine will activate relay proteins

Transd­uction Pathways

regulation
specif­icity
amplif­ication
termin­ation

C. Elegans (Apopt­osis)

nemotodes
apoptosis occurs when specific proteins that accelerate apoptosis override the proteins that "put the brakes­" on apoptosis

Why Should a Cell Program its Death?

needed for proper develo­pment:
~ metamo­rphosis
~ removes fetal webbing between fingers / toes
~ menstr­uation
~ synapse formation
~ eliminates T cells that cause autoimmune
destroy cells that pose a threat:
~ infected with virus
~ DNA damage
~ cancer cells

Fever

when the phagocytes are overwh­elmed:
~ release a signal to the hypoth­alamus
~ body temper­ature increases
~ increase in metabolism

Inflam­matory Response

"­che­mical alarm"
redness, swelling, heat, pain
mast cells release histamine:
~ vasodi­lation occurs
~ increase temp = increase in metabolic rate
~ attracts phagocytes

Cell Cycle

life cycle of the cell
functions: reprod­uction, growth, repair
Interp­hase:
1) G1: first gap / growth
2) S: DNA synthesis / DNA is copied
3) G2: second gap / prepar­ation of cell contents for division
mitotic division:
4) the m phase: cell division
~ prophase
~ metaphase
~ anaphase
~ telophase
5) cytoki­nesis: completes division of cytopl­asmic contents

G1 Checkpoint

checks for:
~ cell size
~ nutrients
~ growth factors
~ DNA damage

Internal Controls

CDKs: cyclin dependent kinases (proteins)
cyclins: regulatory proteins (must be present)
~ increases as the cell goes through interphase
MPF: mitosis promoting factors in G2
~ cyclin + CDK
APC-An­aphase promoting complex
~ kineto­chore fiber connection

Causes of Cancer

mutations
carcin­ogenic chemicals
UV light
viruses
oncogenes
p53 genes

What Causes Uncont­rolled Cell Growth?

defects in proteins that control the cell cycle
mutations that knock out key genes

Basic Types of Cancer

carcinoma: arises from body's outer coverings and inner linings
sarcoma: arises from body's supporting structures
lymphoma: arises from lymph system
leukemia: arises from red marrow in bone, spleen

Proto-­onc­ogenes

initiate each phase of the cell cycle
active when conditions are approp­riate for growth
mutations cause growth to occur at all times
oncogenes promote cancer develo­pment
 

Steps of Cell Signaling

1) signal reception
~ a cell detects a signaling molecule
2) signal transd­uction
~ a series of chemical reactions that creates a response
3) signal response
~ the signal triggers a cell response

G-Protein Steps

1) Ligand attaches to receptor
2) Activates the G-protein
3) G-protein moves across membrane
4) G-protein interacts with another protein in the cell membrane

Ion Channel Steps

1) the ion channel is closed
2) ligand attaches to a receptor
3) the ion channel opens
4) ions pass through

Cell Response to Signal

regulation of activities or transc­ription initiation = signals sent to turn on a gene
ex: testos­terone enters directly into the cell
elaborate pathways amplify and specify responses to signals

Apoptotic Pathways and Signals that Trigger them

caspases are the main proteases (enzymes that cut up proteins) that carry out apoptosis
apoptosis can be triggered by external or internal factors
examples:
~ an extrac­ellular death-­sig­naling ligand
~ DNA damage in the nucleus
~ protein misfolding in the ER

Positive and Negative Feedback

homeos­tasis: mainta­ining stable internal conditions
negative feedback:
~ shuts off original stimulus
~ ex: thermostat
positive feedback:
~ speeds up the original stimulus
~ ex: gossip

Chemical Signals and Cells (Phago­cytes)

neutro­phils:
~ engulf a pathogen and self-d­estruct
macrop­hages:
~ grabs pathogens with cytopl­asmic extensions
~ engulfs pathogen
~ digests pathogen
~ removes pathogen through exocytosis
natural killer cells:
~ kills cells infected with a class 1 MHC protein
when a cell is infected:
~ the cell stops making MHC
~ NK cells poke the infected cell with enzymes
~ triggers apoptosis

Mitosis

Interp­hase: 46 chromo­somes
Prophase: 92 chromo­somes
Promet­aphase: nucleus dissolves and microt­ubules attach to centro­meres
Metaphase: chromo­somes align in the middle of the cell
Anaphase: separated chromo­somes pulled apart by spindle fibers
Telophase: microt­ubules disappear and cell division begins
Cytoki­nesis: two daughter cells formed

Meiosis Image

Spindle Fibers

centrosome
kineti­chore fibers:
~ attach to chromo­somes
~ movements
nonkin­eti­chore fibers:
~ attach pole to pole
~ support

G2 Checkpoint

checks for:
~ DNA damage
~ DNA replic­ation comple­teness

M (mitosis) Checkpoint

the spindle checkpoint
checks for:
~ chromosome attachment to spindle at metaphase plate
~ 92 spindle fibers
~ 46 chromo­somes

External Factors

chemical factors:
~ nutrients
~ PDGF
physical factors:
~ density dependent
~ anchorage

Disrupt Cell Cycle and Trigger Cancer

genes that stop or slow the cell cycle
~ ex: tumor suppressor genes
genes that trigger cell growth and division by initiating different stages of the cell cycle
~ ex: proto-­onc­ogenes
 

Steps of Cell Signaling Image

EpiPen (Cell Signaling)

epinep­hrine (adren­aline) is released
hormone / neurot­ran­smitter
endocrine / nervous system
initiates a flight or fight response
triggered by stressors
secreted from adrenal gland

Secondary Messengers

small molecules and ions are key signaling components
cyclic AMP /adenyl cyclase / phosph­odi­est­erase
calcium ion and inosital tripho­sphates IP3

Apoptosis

programmed cell death
"cell suicid­e"
evolved early

Apoptosis Cell Death (ways cells die)

injury:
~ mechanical damage
 
~ toxic chemicals
suicide:
~ shrink, bleb, fragment
 
~ chromatin degrades
 
~ mitoch­ondria breaks down
 
~ "find me" / "­engulf me" signal

Innate (nonsp­ecific) Immune System

physical and chemical barriers that protect the body
1st line of defense:
~ skin (physical barrier)
~ mucous membranes (chemical and physical barrier; enzymes and defensins)
2nd line of defense:
~ fever
~ chemical signals
~ inflam­mation

Humoral Response

identi­fic­ation of specific antigens in body fluid
antigen:
~ bacteria
~ virus
~ fungus
~ toxin
~ diseased cell

Antibodies

protein receptors on the surface of B cells
some antibodies travel freely
antibodies connect with a comple­mentary antigen

Cytoki­nesis

animal cells: cleavage furrow
~ contra­ctile ring of actin involved
plant cells: cell plate

Mitosis Image

Cell Cycle Control

cells should only divide when needed
internal and external controls
cell cycle control systems (internal control):
~ series of checkp­oints
~ must pass all checkp­oints to divide
example: cellular inspection station

S (synth­esis) Checkpoint

checks for:
~ DNA damage
~ prevents redupl­ication of DNA

Cell Cycle Image

Cancer

defini­tions of cancer:
~ neoplasm of prolif­erating cells (new tissue growing out of control)
~ cell division out of control
~ cells produced are useless
~ compete with healthy cells for nutrients and oxygen
benigns (not moving) versus malignant (moving)
~ benign is a sedentary mass of cancerous cells
~ malignant is a moving mass of cancerous cells - metastasis

Tumor-­Sup­pressor Genes

p53 (guardian of the genome)
~ p53 protein increases in cells exposed to UV radiation
p53 mode of action­"
1) DNA damage
2) p53 increases
3) p53 bind to DNA (not at damage site)
4) transc­ription of genes that stop cell cycle or lead to cell death
 

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