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Bio Test III

QuestionAnswer
oxidative phosphorylation two stages: electron transport chain and chemiosmosis
electron transport chain use energy from electrons to make H gradient, pump H against gradient
chemiosmosis flow back with gradient through ATP synthase, uses E to phosphorylate ADP to ATP
electron transport chain 1: electrons from NADH flow through Cl to electron shuttle Q
electron transport chain 2: CI pumps 4 H out against gradient
electron transport chain 3: electron from FADH2 enter through CII to Q CII does not pump H
electron transport chain 4: Q carries electron from CI or CII to CIII
electron transport chain 5: CIII passes electron to cytochrome C (electron shuttle) CIII pumps 2H per electron
electron transport chain 6: Cyto C carries electron to C4 C4 passes electron to oxygen to water
electron transport chain 7: C4 pumps 4H out
Per NADH 10 H pumped
Per FADH2 6 H pumped
oxygen is the... final electron acceptor, need oxygen for this process
chemiosmosis H flow with gradient through ATP synthase use energy to add Pi to ADP- ATP
ATP made by oxidative phosphorylation 1 NADH- 2.5 ATP 1 FADH2- 1.5 ATP
glycolysis results in 7 ATP
pyruvate oxidation 5 ATP
citric acid cycle 20 ATP
fermentation oxygen absent
Process can do without oxygen glycolysis, which could cause a buildup of NADH
fermentation convert NADH- NAD allows glycolysis to continue
2 types of fermentation yeast and mammals
yeast ethanol
mammals lactic acid
pyruvate- no oxygen fermentation
pyruvate- oxygen pyruvate oxidation, citric acid cycle, and oxidative phosphorylation
catabolism for ATP production 1 carbohydrates
catabolism for ATP production 2 fatty acids by betaoxidation- CAC
catabolism for ATP production 3 proteins- amino acids- glycolysis and CAC
regulation of catabolism key enzyme: phosphofructokinase AMP, ATP, Citrate
phosphofructokinase in glycolysis, allosteric enzyme
AMP low energy, activates it
ATP high energy, inhibits it
Citrate CAC intermediate, inhibits it
yeast mating 2 mating types- a and alpha
yeast mating factors bing receptors on opposite cell type, response of mating/cell fusing, new cell a/ alpha
local signalling types direct contact, release ligand
direct contact gap junctions, plasmodesmata, recognition molecules
release ligand autocrine, paracrine, synaptic endocrine
gap junctions cytoplasmic communication
plasmodesmata plant cell communication
recognition molecules cell surface- ligand and receptor on outside of cells
autocrine ligand acts on cell secreting it
paracrine ligand secreted locally and act on nearby cells
synaptic neurotransmitter (specific type of ligand) is released into a synapse
endocrine long distance signalling- ligand travels through the blood
receptors highly specific for a ligand changes shape when ligand binds
GPCR g-protein coupled receptors
bound to GTP active
bound to GDP inactive
GPCR activation step 1: inactive G protein is bound to GDP
GPCR activation step 2: ligand bings GPCR, activates G protein by removing GDP and replacing it with GTP
GPCR activation step 3: G protein activates target molecule- initiates a cellular response
GPCR activation step 4: G protein converts GTP to GDP to become inactive (hydrolyzes)
RTK activation step 1: RTK exists as monomers on cell surface
RTK activation step 2: Ligand bind and RTK dimerize
RTK activation step 3: RTK transphosphorylate tyrosine on the receptor
RTK activation step 4: PTyr- allows target molecules (proteins) to bind and activate- cell response
Ion Gated Channels allow ions to flow through with concentration gradient, ligand controls open/closing of channel
Ion Gated Channel step 1: no ligand- gate is closed ions cannot move through
Ion Gated Channel step 2: ligand binds channel- opening it ions move through- cell response
Ion Gated Channel step 3: ligand leaves- closes the channel
intracellular receptors nucleus/cytoplasm small/hydrophobic ligands- enter cell via diffusion
ligand hormone
signal transduction multiple step pathways, amplify signals, regulation
kinase cascade kinase a phosphorylates kinase b phosphorylates kinase c
phosphatase dephosphorylate proteins-removes P used to shut off signalling pathway
second messengers small nonprotein water soluble molecules or ions spread out in cell by diffusion
examples of second messengers cyclic AMP cAMP, Calcium, IP3, DAG
GPCR- PKA Pathway Step 1: steps of GPCR activation (write out)
GPCR- PKA Pathway Step 2: GTP bound G protein activate adenylyl cyclase (target enzyme)
GPCR- PKA Pathway Step 3: AC convert ATP- cAMP
GPCR- PKA Pathway Step 4: cAMP binds and activates PKA- P targets and trigger cell response
Calcium as second messengers High Concentration of Ca- in ER, mitochondria, outside cell Low Concentration of Ca- in cytoplasm, ligand gated ion channel- opening results in high Ca solutions in cytoplasm
GPCR to Calcium Pathway Step 1: ligand bind GPCR
GPCR to Calcium Pathway Step 2: GPCR activates G protein by removing GDP- GTP
GPCR to Calcium Pathway Step 3: G protein activates phospholipase C
GPCR to Calcium Pathway Step 4: phospholipase C cleaves the phospholipid PIP2 into DAG and IP3
GPCR to Calcium Pathway Step 5: IP3 bind to an IP3 gated calcium channel in ER membrane
GPCR to Calcium Pathway Step 6: Calcium channel opens and calcium flows out with gradient
GPCR to Calcium Pathway Step 7: Calcium binds to proteins to activate them cellular response
Regulation of Cell Response- 4 aspects of control amplification, specificity, scaffolding for effiency, termination
amplification each step increases number of molecules activated
specificity each cell type- different proteins present- different response to one ligand
scaffolding for effiency scaffold proteins- bind molecules in a signalling pathway together- increases speed of signal
termination shut off signal
phosphotases counteract kinases
CAD trigger protein to hydrolyze the GTP- GDP
apoptosis programmed cell death
apoptosis 1: chop up DNA and proteins in cell
apoptosis 2: package contents
apoptosis 3: immune cells eat the packages
C elegans apoptosis: capases- enzyme that cleave and activate proteins for apoptosis normal condition- no death ced 9 active- inhibits ced 4- pathway shut off
proteases chop up protein
nucleases chop up DNA
Regulation of Gene Expression DNA transcribed into RNA which is translated into protein
Regulation 1: DNA packaging/ chromatin structure
Regulation 2: Transcription
Regulation 3: RNA processing
Regulation 4: RNA transport out of nucleus
Regulation 5: Translation
Regulation 6: Degrade the mRNA
Regulation 7: Protein Processing
Regulation 8: Transport protein to cell location/activate
Regulation 9: Degrade protein
Chromatin Structure packaging of DNA
Heterochromatin tightly packaged, transcription is inhibited, deacetylation of histone and methylation
Euchromatin loosely packaged, transcription is more active, acetylation of histone and demethylation
packaging is regulated by _______ in nucleosome histones
histones have tails that can be modified
Acetylation of histones euchromatin add an acetyl group
Deacetylation of histones heterochromatin remove acetyl group
Methylation heterochromatin add methyl
Demethylation euchromatin remove methyl
Epigenetics inherit histone/DNA modification- gene expression patterns can be passed down
Transcription initiation components of a gene- codes for a protein all sequences of DNA
promoter site of where general transcription factors and RNA polymerase bind
transcription start site RNA polymerase starts making mRNA
exons expressed regions code for protein
introns noncoding removed during RNA processing
poly A seq codes for translation
termination region codes for stop of transcription
enhancers location where transcription activates proteins
control elements sequence bound by transcriptional regulators
Transcription is controlled by: general transcription factor and RNA polymerase bound to promoters combination of activators/ repressors binding control elements
Nuclear Localization of gene: gene is near nuclear envelope (outside)- transcription is inhibit gene is near middle of nucleus- transcriptionally active
mRNA processing step 1: add a 5 inch methyl Gcap
mRNA processing step 2: removal of introns by splicing
mRNA processing step 3: add poly A tail to the 3 inch end
Alternative Splicing make different proteins from one gene by changing exons included
Transport to Cytoplasm only processed mRNA can leave- look for 5' cap, exons, and poly A tail- leaves through a nuclear pore
Translation use mRNA to make protein
mRNA degradution determined by 3' UTR- untranslated region controls half-life
half-life time it takes to break down half of the mRNA
Protein Processing protein cleavage, covalent modification
Protein Cleavage activate zymogens- inactive form of enzyme that gets cleaved to be activated digestive enzymes
Covalent Modification add functional group to protein
Transport to all Location transport protein to correct cellular compartment signal sequence in the protein aa that tells it where to go
Protein Degraduation add ubiquitin tag- send protein to proteosome
proteosome cylinder that breaks down proteins in amino acids
micro-RNA small, single stranded RNA molecules that can complementary bind mRNA
if perfect base pair match.... degrade the RNA
If partial base pair match..... blocks the translation
Cancer uncontrolled growth of cells invade other tissue spaces
Metastasis breaks free from original tissue and travels to new tissue
oncogenes cancer causing
protoncogenes normal genes that control cell growth - can be mutated into oncogenes
epigenetic change chromatin packaging to express more
translocate to a new active promoter
gene amplification more copies of the gene- more expression
point mutation changes one nucleotide in the DNA
in a control element... stimulates more transcription
in a coding sequence.... protein constitutively active always on
Ras g protein that signals to cell division- in 30 percent
Tumor Suppressor Genes prevent uncontrolled growth
p53 loss of function
pathogens microbes that cause disease
microbes bacteria, viruses, fungi, protozoans, prions
innate present at birth, no prior exposure, fast (sec to hrs), broad (nonspecific), barriers prevent entry, internal, present in all animals
adaptive develop after exposure, slow (days to week) the first time, second time is fast, specific- every pathogen is a diff response, consists of humeral and cellular, and only found in invertebraes
humeral antibodies
cellular cytotoxic cells
barrier defenses for invertebraes exoskeleton made of chitin, line stomach with chitin, presence of lysozyme
lysozyme enzyme that breaks down bacterial cell walls
internal defenses for invertebraes eliminate pathogens that got through barriers
hemocytes (phagocytes) phagocytose (eat) bacteria/other foreign substances
Process of Phagocytosis 1: pseudopodia surrounds pathogen
Process of Phagocytosis 2: pathogens fully surrounded by membrane and engulfed by endocytosis
Process of Phagocytosis 3: vacoule forms- compartment
Process of Phagocytosis 4: fuse vacuole with the lysosome
Process of Phagocytosis 5: destroy pathogen
Process of Phagocytosis 6: debris released
antimicrobial proteins kill bacteria and fungi
innate immunity- barriers skin, mucus membranes- mucus, ciliated epithelial cell, saliva and tears
mucus membranes any internal surfaces open to environment
mucus trap the pathogen
ciliated epithelial cells push mucus out
saliva, tears has lysozome
cell based defenses innate cells use Toll like receptors to recognize pathogens
key examples of Toll like receptors TLR4, TLR5, TLR3, TLR9
TLR4 bacterial LPS- cell surface- bacteria are extracellular
TLR5 bacterial flagellan- cell surface- bacteria are extracellular
TLR3 diRNA- virus- vesicles- viruses intracellular
TLR9 unmethylated DNA- vesicles- virus intracellular
Innate Phagocytes neutrophils, macrophage, dendritic cells, eosinophils
neutrophils circulate in blood and first cells to respond
macrophages main phagocytic cells- found in tissues
dendritic cells present fragments of pathogens to T cells (adaptive)
eosinphilis attack large parasitic pathogens
Inflammation mast cells recognize damage and release histamine and cytokines
histamine vasodilation- (open/widen), blood vessels- increase blood flow- bring in innate cells
Cytokines activate innate cells
neutrophils arrive first.... macrophages clean up damage and tissue heals
Fever increase body temp to prevent pathogens from growing
Hypothalamus controls temperature
Septic Shock too extreme inflammation throughout the body
vasodilation everywhere.... decrease blood pressure... leads to organ failure
Adaptive Immunity made of lymphocytes, recognize antigens
Lymphocytes B cells- produce antibodies T cells- cellular immunity
antigens small, specific pieces of a pathogen
Antigen receptors BCR- B cell receptor secreted as an antibody
v- variable different for each BCR/ antibody
c- constant same for everyone
disulflide bond hold together
TCR can't directly bind antigen requires antigen presentation MHC binds antigen TCR recognizes MHC antigen complex
4 Major Characteristics immense diversity of BCR and TCR, self tolerance, clonal expansion, and memory
immense diversity of BCR and TCR achieved by gene rearrangement
self-tolerance eliminate cells that recognize self
clonal expansion cell proliferate/divide when activated
memory respond faster and stronger with repeated exposure
Created by: user-2021040
 

 



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