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BSCI 1511 > Evolution & Signal Trans (lect 1&2) > Flashcards

Evolution & Signal Trans (lect 1&2) Flashcards

1
Q

Random processes

A

mutation & sex recombo

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2
Q

non-random processes

A

natural selection

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3
Q

T/F: Not all adaptations are optimally intelligent?

A

T: The human throat is an ex

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4
Q

T/F: Chimps are more related to gorillas than humans are

A

F: chimp and humans are more closely related than chimps and gorillas

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5
Q

What are phylogenetic trees based on

A

mito rRNA seq

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6
Q

what evidence supports the theory of evolution

A

fossil record, artificial selection, phylogenetic similarities

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7
Q

what is adaptive radiation and provide an example

A

opening of many new niches

bats learning how to fly enabled them to eat nectar, blood, or fruits, etc.

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8
Q

what are the 2 facts and conclusion that can be drawn from the theory of evolution

A

1- repro rates of all organisms are high; if mortality rates did not balance repro rates..populations would quickly rise
2- all organisms are variable and offspring are similar to parents due to heritable features
conclusion- diff among individuals influence how well those individuals survive and repro; traits that inc probability that their bearers will repro successfully will get passed on

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9
Q

why don’t “gaps” in the fossil record discredit the theory of evolution

A

gaps are time periods when rapid change occurred–> punctuated equilibrium
cetaceans had gaps, but fossils transitioning from land to see were found

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10
Q

types of phylogenetic similarities

A

morphology/anatomy, vestigial organs, comparative embryology, comparative biochem/genetics

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11
Q

what method of dating fossils is used and why

A

radiometric dating; radioactive decay is not influenced by temp, pressure or other env variables

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12
Q

analogous vs homologous limbs

A

analogous: no common ancestor, convergent evol, shaped by env, diff bones, same function
homologous; common ancestor, diff function same bones

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13
Q

explain “ontogeny recapitulates phylogeny”

A

the steps of an individual’s dev recreates the history of that specie’s evol

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14
Q

provide an ex of comparative embryology

A

we have gill slits and post-anal tail just like chickens do

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15
Q

what is used to date younger fossils?older?

A

carbon-14–> carbon-12;

potassium-40–> argon-40

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16
Q

what are the 3 stages of signaling

A

reception, transduction, response

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17
Q

what are the 2 main groups of receptors. what are the 3 subgroups of receptors?

A

Main: cytoplasmic, transmembrane
Sub: (transmembrane) G protein linked, enzyme linked, ion channel

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18
Q

what are some types of secondary messengers

A

cAMP, cGMP, Ca+2, DAG, IP3

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19
Q

what are the 3 parts to the cell theory

A

1) living organisms are composed of cells
2) cell is basic functional unit of life
3) all cells come from pre-existing cells

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20
Q

describe the 5 main types of signaling

A

1) gap junctions (direct)- small molecules can pass btwn cells that are connected by gap junctions w/o crossing the membrane. cytoplasm is continuous via pores formed by connexon
2) autocrine (indirect)- sending & receiving signals are the same..releases a factor that itself has a receptor for
3) paracrine (indirect)- receiving cells is near sender, ex. histamine, EGF
4) hormonal (indirect)- sim to paracrine but longer distance
5) synaptic (indirect)- electrical signals stimulate neurotransmitter release

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21
Q

how many transmembrane helices do GPCRs, G proteins, and RTKs have respectively

A

7, 3, 1

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22
Q

detail GPCR pathway

A

ligand binds to GPCR, GPCR undergoes conformational change, interacts w an inactive G protein bound to GDP. Interaction stimulates activation of G protein so drops off GDP, picks up GTP, and activates effector protein via alpha subunit

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23
Q

What do Gs, Gi, and Gq proteins stimulate?

A

Gs- stimulates adenylyl cyclase
Gi- inhibits adenylyl cyclase
Gq- stimulates phospholipase C (PLC)

24
Q

detail RTK pathway

A

ligand binding causes dimerization and cytoplasm domains are brought close together. domains are composed of kinases (tyr residues) which transautophosphorylates. When both domains are phosphorylated, can stimulate phosphorylation of next protein

25
Q

describe the 2 methods dimerization occurs

A

1) ligand mediated- one large symmetric ligand that physically brings domains closer when bound to inactive monomers
2) receptor mediated- 2 ligand molecules that causes conformational change when bound to inactive monomers due to hydrophobic regions

26
Q

provide function and ex of ligand-gated ion channel

A

binding of ligand on one part of the molecule that opens a channel for ions to flow
ex. IP3 receptor opens channels for Ca+2
Ryanodine receptor opens channels for Ca+2
ACh binds to extracellular surface of ACh receptor and opens Na+ channels for Na+ to enter cell

27
Q

what does adenylyl cylcase do

A

makes cAMP from ATP by removing the pyrophosphate

takes alpha-beta bond in phosphates and cyclizes it to the hydroxyl group of ribose

28
Q

function of cAMP phosphodiesterase

A

inactivates cAMP by breaking a bond and recycles it to 5’ AMP which is inactive for signal transduction

29
Q

what inhibits cAMP phosphodiesterase

A

caffeine

30
Q

What did Earl Sutherland deduce from his experiments

A

found that both intact and extracted liver cells break down glycogen when introduced with epinephrine. Centrifuged extract into pellet (nucleic acids, organelles) and supernatant (cytoplasm, solubles) and found when P+S+E all together, glycogen gets broken down. Took fractionated weights of E+P and added to S and found cAMP was in the fraction that broke down glycogen

31
Q

functions of cAMP

A

activates PKA

32
Q

which proteins are in the pellet fraction

A

receptor, G protein, adenylyl cyclase

33
Q

which proteins are in the supernatant fraction

A

PKA, phosphorylase kinase, glycogen phosphorylase

34
Q

detail activation of PKA by cAMP

A

cAMP binds to regulatory subunits & releases catalytic subunits that are now active to phosphorylate

35
Q

function of PKA

A

PKA phosphorylates phosphorylase kinase, inactivates glycogen synthase, or txn factors like CREB

36
Q

function of phosphorylase kinase

A

activates glycogen phosphorylase by phosphorylation when active

37
Q

function of glycogen phosphorylase

A

breaks down glycogen into glucose through phosphorylation

38
Q

function of PLC (phospholipase C)

A

breaks PIP2 into IP3 and DAG

39
Q

what activates PKC?

A

DAG and Ca+2 together

40
Q

Function of Calmodulin

A

calmodulin has 4 diff Ca+2 binding sites and when they are all bound, undergoes conformational change and can interact w/ portions of other enzymes w/ CaM binding domains

41
Q

how can Ca+2 levels by amplified using IP3 and Ryanodine receptors

A

IP3 binds to IP3 receptor (ligand-mediated ion channel) which releases Ca+2. Local inc in Ca+2 acts on adjacent ER on another ligand-mediated ion channel called Ryanodine receptors. Ryanodine receptors when bound to Ca+2 will open channels to let more Ca+2 out. Leads to CICR–> “waves”

42
Q

what happens after water is depleted in a plant cell

A

ABA is released from the roots

43
Q

detail the process of a stomata opening

A

When ABA is not activating receptor, Ca+2 channel in PM of guard cell stays closed, no CICR, Ca+2 channels closed in tonoplast, Ca+2 pumped into vacuole, cytoplasm Ca+2 dec, K+ efflux channels close, K+ influx channels open, K+ enters guard cell, osmosis and open stomata

44
Q

detail the process of a stomata closing

A

loss of water = release of ABA from roots, bind to ABA receptor in PM of guard cell, Ca+2 channels open and Ca+2 enters cytoplasm & interacts w/ plant version of ryanodine receptor to open a pore for Ca+2 in tonoplast (CICR). Ca+2 levels in cytoplasm is high, ion efflux channel in PM are open, ion influx channels close, net flow out of cell, stomata close

45
Q

detail the Ras /MapK pathway

A

uses RTKs, when growth factor binds and activates RTK, adaptor proteins are activated which activates Ras (GDP–> GTP), which activates Raf, which phosphorylates MEK, which phosphorylates MAPK which phosphorylates txn factors which changes gene expression

46
Q

activation of Ras stimulates…

A

cell division of many cell types

47
Q

Ras is mutated in about 30% of cancers. why does this make sense

A

Ras can’t hydrolyze itself from GTP to GDP so it is always on and stimulating cell division

48
Q

detail blood vessel dilation involving NO

A

ACh receptors on endothelium PM activate opening of Ca+2 channels, Ca+2 enters cell and activates NOS which takes arg and converts to NO gas which diffuses by paracrine signaling to the muscle cell. NO activates guanylyl cyclase in muscle cell which converts GTP to cGMP (new 2nd messenger). cGMP in smooth muscles relaxes muscles–> dilation

49
Q

what does Viagara do

A

inhibits penile isoform of cGMP phosphodiesterase

50
Q

function of CREB?

A

when activated binds to CRE (a specific DNA motif) to turn on gluconeogenesis in liver

51
Q

function of PKA

A

phosphorylate/activate CREB. phosphorylate and inhibit glycogen synthase, phosphorylates and activates phosphorylase kinases that phosphoryalte and activate glycogen phosphorylases that breakdwon glycogen to glucose

52
Q

provide ex of crosstalk btwn pathways

A

PKA activates CREB phosphorylation directly, but inhibits phosphorylation of Raf which activates MEK which activates MAPk which activates a kinase that phosphorylates CREB

53
Q

how do G proteins terminate signals

A

natural hydrolysis ability (GTP–>GDP) now inactive

54
Q

how do GPCR terminate signals

A

(1) ligand falling off

(2) GRK/arrestins- GRK cont patrol for active GPCR, will phosphorylate them which is a recognition site for arrestins

55
Q

how does the cholera toxin turn off the cAMP pathway

A

cholera bacteria secretes a toxin that modifies a G protein so it can’t hydrolyze–> cont. activation of adenylyl cyclase–> cont. high cAMP levels
cAMP in crypt cells regulate secretion of Cl-, Na+, K+, HCO3- that are irreversibly massively secreted into lumen of intestine

BSCI 1511 (23 decks)

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