cell structure and function Flashcards

Question

cyanide effect on ETC

Answer 1

blocks passage of e- to O2 --> cells die

Answer 2

rate limiting for glycolysis INHIBITED by - atp, citrate STIMULATED by - amp (prod. atp being used rapidly)

Answer 3

``` insulin = hyperglycaemia. beta cells of islets of Langerhans --> blood --> glucose uptake to cells (--> storage, atp prod.) glucagon = hypoglycaemia. alpha cells in islets of Langerhans --> blood --> breakdown of glycogen --> glucose --> blood (higher blood sugar) ```

Answer 4

function of insulin lost TYPE 1 = insulin dependent. autoimmune (beta cells destroyed). genetic/environmental factors onset in children/teens, 5-10% of diabetics TYPE 2 - insulin resistance. body prod. insulin, receptors non-functional. most diabetics, onset >40 yrs can be linked to other pathologies and obesity.

Answer 5

local = signals act on nearby target cells eg neurotransmitters long distance = signals act from distance eg. hormones prod. by specialised cells --> travel via circulatory system --> act on specific cells

Answer 6

1. RECEPTION - signalling protein (primary messenger) bind to receptor --> change shape/chemical state change 2. TRANSDUCTION - receptor protein activates another protein --> relay of changes (relay molecules = secondary messengers) - proteins activated via phosphorylation 3. RESPONSE all activates proteins --> 1< functions occur

Answer 7

only target receptors interact with ligand 3D molecular shape of proteins - STRUCTURE DETERMINES FUNCTION can have different receptors at diff times --> transmission of signal only when needed intracellular = primary messenger hydrophobic, small (lipid soluble) can enter cell. least common membrane bound/cell surface = primary messenger large, hydrophilic, most common

Answer 8

transmembrane - pass 7x many diff types; many diff ligands; diverse functions 1. receptor unbound, rest, G protein bound to GDP, enzyme inactive 2. ligand binds to receptor, binds GP. GTP displace GDP, enzyme still inactive 3. active GP disassociates from receptor, enzyme activated --> cell response 4. GP has GTPase activity (hydrolysed to GDP + Pi) - release from enzyme, resting shape

Answer 9

binding of ligand --> change shape (open/close gate) --> ions can pass membrane protein, specific ions can travel in response to ligand binding 1. rest, gate closed 2. ligand bind --> gate open --> ions into cell 3. ligand dissassoiates --> gate closes

Answer 10

p kinase transfer Pi group (from ATP) to another protein --> activated --> series of ( now active) proteins adding phosphate to next kinase phosphatases = dephosphorylate --> inactive, recyclable. for control

Answer 11

secondary messengers = not proteins, small cAMP - activates downstream protiiens - can start phos. cascade - prod by adenylyl cyclase (activated by GP) - converts ATP to cAMP CALCIUM - low Ca in cell; high outside maintain conc. of Ca via Ca pumps - high Ca in cell = damage so OUT of cell, int ER, into MITOCHONDRIA - phospholipase C activated (GP) --> cleaves PIP2 into DAG, IP3 - IP3 diff --> cytosol --> bind to gated channel in ER - Ca+ out of ER --> activate other proteins --> cascade

Answer 12

amplifying response - eg. 1 adrenalin molecule --> 10^9 glucose-1-phosphates multiple control points specificity of response despite molecules in common coordination of other signalling pathways RESPONSE = gene expression, open/close ion channel, alter protein --> gain/lose activity, movement of cytoskeleton

Answer 13

signals for limited time; activation promotes start of deactivation --> signal short = homeostatic equilibrium, cell ready to respond again phosphodiesterase (PDE) breaks down cAMP inhibition of specific PDEs - therapeutic eg. viagra

Answer 14

through GPCR --> activates cAMP + 2 p kinases in cascade | active glycogen phosphorylase = convert glycogen --> glucose-1-phosphate --> glycolysis --> ATP when needed

Answer 15

process of going from DNA to functional product

Answer 16

1. transcription of RNA from DNA 2. processing of pre-mRNA transcript 3. translation of mRNA --> protein

Answer 17

transcription factors (TF) assemble, DNA needs to be accessible regulatory proteins - block translation specific proteins assist in nuclear export in DNA capping, splicing

Answer 18

temporal (time) and spatial (place) control - achieve right thing at right place at right time housekeeping proteins - continually made, mRNA available in large quantities, longer half life other proteins - prod in response to stimuli as req. cell signalling --> nucleus --> activate transcription. short lived

Answer 19

INITIATION ELONGATION TERMINATION

Answer 20

INITIATION - template strand 3'-5' = inverse of non-template strand - TATA box = promoter, upstream (around 25nt) -TF inc. TATA box binding protein (TBP) assembly - RNA pol bind, more TFs bind --> transcription initiation complex ELONGATION - complimentary RNA nt add to 3' end of growing transcript - h bonds between bases, phosphodiester bonds between nt - double helix reforms, transcript leaves template strand TERMINATION - after trans of polyadenylation signal --> enzymes release pre-mRNA; RNA pol dissociates - fidelity (proofreading) is less than for DNA rep

Answer 21

``` capping = modified G add to 5' tailing = 50-250 A add to 3' c & t = facilitate export & ribosome binding, stability splicing = remove introns from transcript exons = coding regions (inc. UTR) introns = non-coding regions UTR = untranslated parts at 5' & 3' SPLICING spliceosome (large complex of proteins & small RNAs in nucleus introns removes, exons rejoined --> mature mRNA alt. splicing = diff combinations of exons toned together --> multiple forms of mRNA from single pre-mRNA --. multiple gene products from same gene ```

Answer 22

mRNA binding site on small subunit A site = holds next in line tRNA (w anticodon carrying aa - physical link between RNA and aa seq.) P site = holds tRNA carrying growing polypep (middle) E site = exit

Answer 23

INITIATION - GTP (energy) req. initiator tRNA (methionine) small ribo w initiator tRNA ALREADY BOUND, bonds 5' cap of mRNA small R scnas DOWNSTREAM --> find translation site (aug) h bonds between mRNA & initiator big R binds ELONGATION 1. codon recognition - bp w complimentary anticodon, GTP invested --> increase accuracy/ efficiency 2. peptide bond formation - large R catalyses, removes polypep chain from tRNA in P 3. translocation - tRNA from A --> P, P --> E exit. GTP needed empty tRNA reloaded in cytoplasm TERMINATION 1. ribo reaches stop codon (A), --> release factor bind 2. release factor = promote hydrolysis - bond between P tRNA and last aa --> release polypep 3. ribo + others dissociate (can be recycled), 2 GTP hydrolyses

Answer 24

side chains determine properties (amino group, carboxyl group, side chain) PRIMARY DNA seq. covalent bonds (relatively strong) between aa N terminus = 5'; C terminus = 3' leave ribo --> 2º structure SECONDARY = weak H-bonds--> alpha helix and beta sheets TERTIARY = 3D shape stabilised by SIDE CHAIN interactions QUATERNARY = multiple proteins associated together --> functional protein (not all)

Answer 25

proteins for function in cytosol --> complete translation on free ribosomes - ALL translation starts here --> many processed & sorted through RER & GOLGI proteins go through endomem. system = complete trans. at RER

Answer 26

direct ribosomes to RER; at N terminus; signal recognition particle binds to SPs 1. polypeptide synth 2. SRP binds to SP 3. SRP binds to receptor on RER 4. SRP detaches --> polypep synth. resumes (now in RER) 5. signal cleaving enzyme cuts off SP 6. complete polypep --> fold. SECRETORY proteins = solubilised in LUMEN; MEMBRANE proteins = anchored to mem; BOTH = go to GOLGI (via vesicles) --> maturation

Answer 27

translation complete but protein (may) not (be) yet functional phosphorylation; methylation; acetylation, carboxylation some in golgi; others cytosol confer activity ability to interact w/ other molecules direct to particular locations

Answer 28

cells mostly in interphase G1 (growth/gap phase 1) = most cell activities, duration variable (cell specific). G1 CHECKPOINTS = DNA undamaged, correct cell SIZE & NUTRITION, appropriate SIGNALS. if NOT --> exit to G0 S = synthesis of DNA - DNA replication. strands separated (H bonds sep.) new strand of DNA synthesised opposite each of old strands. DNA polymerase G2 = checks for correct DNA synth --> prep for M: synth of proteins, enzymes, reactants, replication of centrosomes completed

Answer 29

mitotic phase = mitosis + cytokineses INTERPHASE = uncondensed, centrosomes PROPHASE = mitotic spindle forming, cms (2 sister cmt), condensed cms, nuclear envelope gone METAPHASE = cms line up ANAPHASE = sister cmt pulled apart, drawn to opposite poles TELOPHASE = cleavage, nuclear envelope reforms

Answer 30

DNA replicated during INTERPHASE condenses to 2 identical sister cmt during PROPHASE (2 sides of cms = identical)

Answer 31

M1 P1 = synapsis - 2 pairs of sister cmt from each pair of homologous cms line up --> TETRAD; chiasma occur - non-sister cms in tetrads cross over --> recombination MET1 = independent assortment A1 = whole (homologous) cms pulled M2 similar to mitosis but not preceded by DNA replication (since cms pulled in M1, not cmt) A2 = sister cmt separate --> haploid

Answer 32

independent assortment at metaphase 1 crossing over/chiasma in P1 fusion between 2 gametes

Answer 33

``` CAN affect structure and function (coding region more likely; introns less likely but still can) germ line = passed to future progeny local/somatic = during cell division (eg. tumours) large scale alterations = chromosomal rearrangements small scale (point mutations) = 1/few nt altered; substitution, insertion/deletion ```

Answer 34

SUB: silent - no effect missense - change in aa --> effect depends of ROLE of RESIDUE (∴major/minor/good/bad) nonsense - stop codon --> truncated protein INSERTION/DELETION frameshift via insertion; frameshift via deletion = extensive missense - downstream residues from point of deletion altered --> catastrophic effect. 3 NT PAIR MUTATION - NOT frameshift - downstream residues in tact * EFFECT of all mutations depend on WHERE mutation happened eg. closer to N terminus = worse (closer to start)

Answer 35

substitution from Glu to Val --> missense substitution mutation val = non-polar; hydrophobic glu = negatively charged; hydrophilic

Answer 36

at G2 checkpoint maturation (m phase) promoting factor = specific cyclin / CDK complex - KEY for G2 checkpoint Cyclin = protein, fluctuates throughout cell cycle cyclin dependent kinase (CDK) = kinase, activated when attached to cyclin MPF function = phosphorylation of (many) other proteins, allows mitosis to occur END of M phase, cyclin DEGRADES --> no MPF until needed again ACTIVITY DEPENDENT ON MANY CELL SIGNALS

Answer 37

gene product is associated with checkpoints - many = stop and go stop = keep cell proliferation in CHECK go = STIMULATE cell proliferation

Answer 38

GENETIC PREPOSITION - all cells of body. inherited by parents, issue/deficiency in a gene ACQUIRED LOCALLY - in one cell initially, eg. UV radiation, smoking, carcinogens, treatments, drugs in BOTH - altered protein function --> (can) loss of cell cycle control

Answer 39

PROTO - ONCOGENES ("go") --(mutate)--> ONCOGENE - over activation --> increased function. eg. Ras (GTPase); Myc (transcription factor) TUMOUR SUPRESSOR GENES ("stop") --(mutation)--> deactivation --> loss of function. eg. TP53, BRCA1, BRCA2 - all inhibitors (stop DNA replication if DNA not good eg. damaged) both --> uncontrolled cell growth (ie tumour)

Answer 40

MULTIPLE DNA CHANGES not just one change (very rare) eg. 1 mutation increases chance of 2nd mutation, 2nd mutation increases chance of 3rd mutation ETC ETC --> malignant cell