ap bio u4

ligand

ligand

molecule that can produce signals

receptor

protein that the ligand binds to and can receive signals

4 steps of communication btwn signal & target cell

1. signaling cell receives stimulus
2. cell produced & releases signaling molecules (ligands)
3. ligands bind to receptor proteins
4. target cell responds

endocrine signaling

long distance, but slow
(ex. hormones)

paracrine signaling

faster method, but must be close together
(ex. nerve cells)

autocrine signaling

within the same cell, cells must produce both receptor & signal
(immune cells)

plasmodesmata

channels through cell walls that connect the cytoplasms of adjacent PLANT cells

gap junctions

provide cytoplasmic channels between adjacent ANIMAL cells

positive feedback loop

causes a system to change further in the same direction/change is amplified

(eg. contractions)

negative feedback loop

causes a system to change in the opposite direction from which it is moving/goes back to original state

ligand receptor complex

the structure formed when a ligand and its receptor noncovalently bind (weak interaction)

hydrophilic & polar signaling molecules

- can dissolve and are easily transported in extracellular fluid
- binds to receptor proteins on surface of cell

3 types of receptor proteins (hydrophilic molecules)

g protein-coupled receptors
receptor-protein kinases
ligand-gated ion channels

*all water soluble
*located on plasma membrane as embedded proteins
*responses from target cells are rapid but brief

g protein-coupled receptors

membrane receptors with G protein
- if GDP is bound to G protein, the protein is inactive
- when Gp binds to ligand receptor, forms GTP
- activates second messenger

second messenger

usually small molecules that move quickly to help signal amplify thru cell

cyclic AMP (cAMP)

produced when hormone binds to receptor protein

second messenger: it activates protein kinases

adenylyl cyclase

target protein and converts ATP to cAMP (activating protein kinases)

kinase

enzyme that catalyzes addition of P groups to protein, activating them

(the phosphate groups come from ATP)

signaling cascade

small amt of signal amplified to produce large cellular response

termination of signaling pathway (4 steps)

1. adrenaline (ligand) detaches from receptor, inactivating it
2. G protein deactivates itself (GTP => GDP) & detaches
3. cAMP not produced, stops activation of target proteins
4. P groups are removed from protein

receptor protein kinases (3 steps)

1. signaling molecule binds to domain which brings two halves of the receptor together
2. this activates kinase activity, phosphates are attached
3. replay proteins bind to phosphates and send out cellular responses

ligand-gated ion channels

membrane ion channels that open when specific ligands are bound to it

hydrophobic, nonpolar signaling molecules

1. diffuse into target cells and activates receptor proteins
2. activated ligand-receptor complexes control gene expression/protein synthesis inside nucleus

*slow to start, but usually sustained

process for how G protein-coupled receptors are activated

When a signal binds to the extracellular part of the receptor protein (top), the G protein binds to the signal-receptor complex inside the cell (middle). As a result of binding to the complex, the G protein's GDP is exchanged for GTP. The G protein then binds to and activates a target protein (bottom). The active target protein produces intracellular events, leading to a cellular response.

endo/exogenous ligands

endo: produced by body
exo: produced by outside body

agonists vs antagonists

agonist: stimulates receptors/produces a response
antagonist: inhibits responses

binary fission

form of asexual reproduction in which one cell divides to form two identical cells

mitochondria & chloroplast performs this form of cell division

steps of binary fission

1. circular DNA is copied
2. both DNA loops attach to membrane
3. cell elongates and separates
4. new cell membrane & cell wall are synthesized
5. 2 daughter cells are formed

chromosome

complex of DNA/RNA/chromatin proteins

allows DNA to be accurately copied during cell division

interphase

period of the cell cycle between successive M phases

G1 phase

directly after M phase, preparations to copy DNA

S phase

DNA replication (chromosomes are duplicated into sister chromatids held together by the centromere)

G2 phase

directly after S phase & prep for M phase

GROWTH PHASE aka size & protein content increases

G0 phase

a nondividing state in which a cell has left the cell cycle

mitosis

division of nucleus in eukaryotic cell

mitotic spindle

group of fibers made up of microtubules
pulls the chromosomes to opposite ends of the dividing cell

centrosome

microtubule organizing center (duplicated in S phase on opposite sides of the nucleus)

prophase

chromatin fibers => chromosomes (they are condensed and become visible)
microtubules extend from centrosomes (mitotic spindle)
centrosomes migrate to opposite sides

prometaphase

nuclear envelope breaks down and the mitotic spindle attaches to the chromosomes

centromere

spindle attaches to chromosome here

kinetochore

sites of spindle attachment, allows spindle to guide chromosomes

metaphase

the mitotic spindles lengthen or shorten to move the chromosomes to the middle of the cell

anaphase

centromere separates -> sister chromatids separate & move to opposite poles

*each chromatid is now a chromosome

telophase

nuclear envelope forms and chromosomes decondense (become less visible)

cytokinesis

division of the cytoplasm to form two separate daughter cells

cytokinesis in animal cells

cell membrane is drawn inward until the cytoplasm is pinched into two nearly equal parts

cytokinesis in plant cells

cell wall splits into two and vesicles fuse together to form a new cell wall

cyclins

proteins that regulate the timing of the cell cycle in eukaryotic cells

cyclin dependent kinases

a protein kinase that is active only when attached to a particular cyclin

- cyclin binds to CDK and kinase function is activated
- cyclin-CDK complex transfer P groups to target proteins (promotes cell division)
- cyclin degrades

DNA damage checkpoint

before its copied in the S phase, is DNA damaged?

if so, delay cyclin-CDK function

DNA replication checkpoint

at the end of G2, is all DNA replicated?

spindle assembly checkpoint

before anaphase, are all chromosomes attached to the spindle?

disruption of cell cycle checkpoints can lead to what

cell death or cancer

necrosis

contents of the cell leak out and potentially damage neighboring cells

apoptosis

cells die thru distinct set of cellular changes (specific enzymes are released)

cancer

a group of diseases characterized by uncontrollable cell division

carcinogens

chemicals that cause cancer

p53

when a DNA is damaged by radiation, protein kinase phosphorylates p53

- p53 binds to DNA and turns on several genes
- one of these genes guides production of protein which blocks cyclin-CDK complex formation
- gives the cell time to repair DNA

p53 behavior in cancer

1. inactivation of p53 allows cell to divide in presence of DNA damage
2. second mutation might accelerate this faulty cell division
3.benign cancer might interfere with cell cycle checkpoint
4. malignant cancer might allow these cells to migrate thru body