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133 Cards in this Set

  • Front
  • Back

gibbs free energy

amount of energy available to do work; describes spontaneity of reaction

enthalpy

dH; total energy in a molecule

exothermic

releases heat; products have less energy than reactants; dH negative

endothermic

absorbs heat; products have more energy than reactants; dH positive

entropy

dS; amount of disorder in system

2nd law of thermodynamics

in isolated system, entropy always increases & d-S is always positive

how are gibbs free energy, enthalpy, & entropy related?

dG=dH - T(dS); T in K

exergonic

describes entropy; reaction is spontaneous & has -dG

endergonic

describes entropy; reaction is non-spontaneous & has pos. dG

non-spontaneous reaction

neg. dG

spontaneous reaction

pos. dG

mechanisms for energetic coupling of reactions

1. redox reactions


2. atp transfer of phosphate groups

redox reactions

- type of energetic coupling


- reduction: become negative (gains electrons)


- oxidation: become positive (lose electrons)

energetic coupling

occurs b/t endergonic/non-spontaneous rxns & exergonic/spontaneous rxns

reduction

- become negative


- electrons move closer to atom being reduced (bond length shorter)


- gain potential energy


- increased number of C-H bonds (more C-H bonds = more potential energy)

oxidation

- become positive


- electrons move further away from atom being oxidized (bond length longer)


- lose potential energy


- increased number of C-O bonds

electron carriers

electron acceptor; readily donates high-energy molecules to other molecules




ex. NADH, FADH2

NAD+

oxidized form of NADH; less energy than NADH

NADH

reduced form of NAD+; more energy than NAD+

FADH

oxidized form of FADH2; less energy than FADH2

FADH2

reduced form of FADH; more energy than FADH2

atp hydrolysis

- type of energetic coupling


- ATP reacts w/ water


- bond b/t outermost P group & rest of molecule broken --> high energy P released


- extremely exergonic

enzymes

lowers activation energy (Ea) for rxn; doesn't change dG

do enzymes make endergonic reactions spontaneous?

no; doesn't change dG

low substrate concentration (enzyme-catalyzed)

speed of rxn increases quickly

medium [substrate] (enzyme-catalyzed

increase in speed of rxn slows down

high [substrate] (enzyme-catalyzed)

rxn rate reaches plateau at max speed

factors affecting enzyme function

-temperature


-inhibition


-pH

temp/pH effects (enzyme)

enzyme less effective outside of ideal temp/pH; can become denatured if temp/pH gets too high/low

competitive inhibition

regulatory molecule binds in active site on enzyme & substrate can't bind

allosteric activation

active site becomes available for sub. binding when regulatory molecule binds to different site on enzyme; beneficial conformational change

allosteric inhibiion

active site becomes unavailable for sub. binding when regulatory molecule binds to different site on enzyme; detrimental conformational change

how are enzymes regulated?

covalent & noncovalent modifications

covalent modifications

-reversible or irreversible depending on type of modification


-ex. phosphorylation

non-covalent modifications

-reversible or irreversible depending on type of modification


-ex. cleavage of peptide bonds in 1* structure; allosteric regutlation

glycolysis (location)

cytosol

pyruvate processing (location)

matrix of mitochondria

citric acid cycle (location)

matrix of mitochondria

electron transport chain/oxidative phosphorylation (location)

intermembrane space of mitochondria

inputs (glycolysis)

2 atp (needed to get process started), 2 nad+, 4 adp, glucose

outputs (glycolysis)

2 adp, 2 nadh, 2 h+, 4 atp, 2 pyruvate




net: 2 atp

inputs (pyruvate processing)



2 pyruvate, 2 nad+, 2 coenzyme a (CoA-SH)

outputs (pyruvate processing)

2 nadh, 2 acetyl coa, 2 co2)

inputs (citric acid cycle)

2 acetyl coa, 6 nad+, 2 fadh, 2 adp, water

outputs (citric acid cycle)

4 co2, 6 nadh, 2 fadh2, 2 atp, h+

where in cellular respiration does feedback inhibition occur?

citric acid cycle

feedback inhibition (citric acid cycle)

-rxn rates high when atp needed


-rxn rates low when atp surplus

what would happen if feedback inhibition was removed (citric acid cycle)?

excess of cac product/atp would be made

in aerobic respiration, does inhaled o2 chemically combine w/ c to make co2?

-no; co2 produced in citric acid cycle, pyruvate processing


-o2 combines w/ h+ in etc --> water

where do the high energy electrons come from that enter etc of mitochondria?

electron carriers (fadh2 & nadh produced in glycolysis, pyruvate processing, & citric acid cycle)

what do fadh2 & nadh do with their high energy electrons?

transfer them to o2 (acts as final electron acceptor) --> o2 able to combine w/ h present (b/c of proton gradient) & make water

complex I

nadh oxidized

complex II

fadh2 oxidized

complex III

electrons passed to cytochrome c then C4

complex IV

o2 combines w/ h+ to make water

does the electron transport chain produce atp?

no; job is to create proton gradient that fuels atp synthase using transfer of electrons

which has more energy: nadh or fadh2?

nadh; each transfer of electrons decreases potential energy present in those electrons

electron transport chain

pumps h+ from mitochondrial matrix out to intermembrane space

chemiosmosis

pumps h+ from intermembrane space back into mitochondrial matrix to generate atp

atp synthase

uses proton gradient from etc & rotational force to generate atp

inputs (etc)

10 nadh, 2 fadh2, 02, h+

outputs (etc)

water, proton gradient

inputs (chemiosmosis)

h's from proton gradient, 25 adp, 25 Pi

outputs (chemiosmosis)

25 atp

net yield of aerobic respiration

29 atp per glucose molecule

purpose of fermentation

regenerate nad+ to fuel glycolysis

fermentation

-occurs in absence of o2 (final electron acceptor) -takes pyruvate from glycolysis & creates lactate (ethanol in yeast)n

net yield (anaerobic respiration)

2 atp per molecule of glucose

what energy sources other than glucose can be used in respiration?

fats & phospholipids, proteins

where do they enter the pathway (fats/phospholipids)?

pyruvate processing

where do they enter the pathway (proteins)?

citric acid cycle

energy source for anaerobic respiration/fermentation (fats/phospholipids)?

yes

energy source for anaerobic respiration/fermentation (proteins)

no, enters at citric acid cycle so no pyruvate made

function (citric acid cycle)

create nadh & fadh2 for etc; create substrates for a.a. synthesis

photosynthesis

-2 sets of reactions: light-capturing & calvin cycle rxn's


-both sets of rxns linked (products of one are sub.'s for other)

inputs (light-capturing rxns)

sunlight, h2o, adp, nadp+, h+

outputs (light-capturing rxns)

atp, nadph, o2

inputs (calvin cycle rxns)

nadph, atp, co2

outputs (calvin cycle rxns)

nadp+, h+, adp, sugars

purpose (light-capturing rxns)

create substrates for calvin rxns

purpose (calvin cycle rxns)

make simple sugars from co2

where do the o2 atoms released from plants come from?

water

how would poisoning etc from light-capturing rxns affect calvin cycle rxns?

no energy source to fuel rxns; buildup of co2; no simple sugars would be made

location (light-capturing rxns)

on thylakoid membrane

location (calvin cycle rxns)

in stroma

mitochondria & chloroplasts (similar)

-energy powerhouses


-double membrane


-use etc to generate atp


-atp synthase

mitochondria & chloroplasts (different)

-etc uses nadp+ & nadph (chloroplasts) vs. nad+ & nadh (mitochondria)


-presence of photosystems in chloroplasts


-chemiosmosis (mitochondria)

location (photosystem II & cytochrome complex)

thylakoid membrane

location (photosystem I & atp synthase)

membranes outside of granum

stages of calvin cycle rxns

1. fixation


2. reduction


3. regeneration

higher energy: 5 g3p or 3 rubp?

rubp > g3p; but have same amt. of energy b/c energy lies in # c's in molecule

chromosome

single, dna double helix wrapped around histone protein to form dimers

chromatid

replicated chromosome

sister chromatids

replicated chromosomes still attached at centromere; still 1 chromosome though

homologous chromosomes

-chromosomes similar in size, shape, & alleles for same gene; similar not identical


-present in diploid organisms

where during cell cycle are chromosomes duplicated?

s phase

mpf

-m phase-promoting factor


-made of cyclin & cdk subunits

if [mpf cdk] is constant across cell cycle, how can it be a trigger for initiating m-phase?

-mpf cdk + mpf cyclin = active mpf & initiation of m-phase

what causes [mpf] to decline sharply during m-phase?

cyclin subunit marked for destruction by ubiquitins produced in anaphase --> destroyed by proteasomes

where in cell cycle are checkpoints found?

after g1, before m, during mitosis

g1 checkpoint

pass if cell is right size, has right nutrients, social signals present, & no dna damage

g2 checkpoint

pass if chromosomes have replicated correctly, activated mpf is present, & no dna damage

m-phase checkpoints

-pass if chromosomes have attached to spindle apparatus


-pass if chromosomes have properly separated & mpf absent

defects in cancerous cells

1. make cell growth proteins active when they shouldn't be


2. prevent tumor suppressor genes from shutting down cell cyclet

tumor suppressor genes

-regulatory proteins that control cell group & repairs dna damage


-ex. p53

growth factors

polypeptides or small proteins that stimulate cell division

function (growth factors)

needed for healthy cells to pass g1 checkpoint; cancer cells don't need externally supplied growth factors & pass g1 checkpoint anyways

how many different alleles can the same gene of a diploid plant have?

2 alleles

diploid

-2 types of each type of chromosomes


-2 alleles for each gene; one in each homolog

crossing over

-occurs in meiosis 1


-chromatids from chiasma exchange parts of chromosomes b/t mom & dad homologs

chiasma

-forms meiosis 1


-joining of non-sister chromatids at certain locations to form x


-needed for crossing over to happen

why doesn't crossing over happen in mitosis?

non-sister chromatids are never joined

s-phase

chromosomes condense & duplicate; chromosomes now made of sister chromatids

prophase

chromosomes condense; mitotic spindles begin to form

prometaphase

nuclear envelope breaks down; spindles attach to chromosomes at kinetochore

metaphase

chromosomes line up at metaphase plate in middle of cell

anaphase

sister chromatids separate into daughter chromosomes; chromosomes start pulling towards poles; spindles shorten at kinetochore

telophase

nuclear envelope reforms; chromosomes decondense

cytokinesis

action-myosin ring between 2 cells tightens & separates cytoplasm --> 2 daughter cells (2n)

e2f

regulatory protein important for passing g1 checkpoint; triggers expression of genes needed for s-phase when activated

rb

tumor suppressor protein; keeps e2f inactive

1 chromosome =

1 dna double helix

early prophase 1

chromosomes condense; spindles appear; nuclear envelope starts to break down; pairing of homologous chromosomes

synapsis

pairing of homologous chromosomes

late prophase 1

chiasmata visible; nuclear envelope gone (can be multiple chiasmata b/ non-sister chromatids)

metaphase 1

tetrads lined up at metaphase plate

tetrad

pairs of homologous chromosomes; also called bivalents

anaphase 1

homologs separate & start moving towards poles (homologs made of sister chromatids)

telophase 1 & cytokinesis

daughter chromosomes at opp. poles; spindles shorten at kinetechores --> 2 daughter cells (2n)

prophase 2

spindles form

metaphase 2

chromosomes line up at metaphase plate

anaphase 2

sister chromatids separate & start moving to opp. poles

telophase 2 & cytokinesis

nuclear envelope reforms; 4 daughter cells (n)