Microbiology2 – Flashcards
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| Macrophages |
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| -antigen presenting cell-fixed in tissue-present antigen to helper T cells via MHC2 |
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| Dendrite Cells |
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| -antigen presenting cells-best at presentation to naive T cells-present antigen via MHC2-transport antigen to lymph nodes |
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| B Lymphocytes |
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| -may serve as antigen presenting cells-recognize free antigens via antigen receptors on surface-differentiate into plasma cells |
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| T lymphocytes |
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| -helper T cells -TH1 cells -TH2 cells -Cytotoxic T cells |
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| helper T cells |
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| -helper T cells:express CD4 on surface,bear specific antigen receptors, recognize antigens presented via MHC2,secrete cytokines to regulate immune function |
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| TH1 cells |
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| pro inflammatory |
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| TH2 cells |
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| humeral response(antibody response) |
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| cytotoxic T cells |
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| -express CD8 on surface -bear specific antigen receptors(t cell receptors) -target and destroy injected or cancerous cells -secrete degradative chemicals:perferins, granzymes |
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| human leukocyte antigens |
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| -discovered during transplantation in mice -transmembrane proteins important for: allowing immune cells to recognize self and presenting foreign antigens to T cells -highly polymorphic (only identical twins have exact same) -located on chromosome 6 |
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| MHC1 |
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| -synthesized in ER-viruse protein replicating in cell are degraded into peptides, peptides shuttled into ER-peptines loaded into MHC1 and transported to surface -interact with cytotoxic t cells |
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| MHC2 |
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| -synthesized in ER-APC's phagocytose antigen-degrade antigens into phagosomes-phagosome and post-golgi vesicles fuse-degraded peptides loaded into MHC2 and transported to cell surface to interact with helper t cells |
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| artificially acquired active immunity |
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| vaccines |
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| naturally-acquired active immunity |
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| natural exposure to pathogen |
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| artificially-acquired passive immunity |
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| anti-toxin, anti-venom |
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| naturally acquired active immunity |
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| maternal antibody transferrance |
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| adaptive immunity |
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| -peptides (MHC) are best antigens-polysaccharides are good antigens-a memory response to a specific antigen developes (secondary exposure) |
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| Humoral immunity |
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| production of antibodies by B cells-cells mediated immunity-cytotoxic T cells activated to destroy infected cells CD8 |
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| Humoral response |
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| -billions of different B cells (antibodies attach to membrane, each cell binds to diff antigen) -colonal selection (cells that bind to antigens replicate, differentiate to plasma, secrete antibodies) |
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| antibody structure |
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| -5 isotopes of antibody(differ in heavy chain constant regions)-IgM:first antibody produced in immune response-IgG:primary circulating antibody in blood-IgD:on surface of mature B cell -IgE:bound by mast cells and basophils-IgA:secreted across mucosa (Peyer's patch) |
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| Antibody Response |
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| Primary exposure:antibodies appear in serum after several days (B cells bind with antigen create antibodies)-some B cells become memory cells Secondary Exposure: antibodies appear in blood within hours |
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| How cytotoxic T cell is activated |
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| -TH0 binds to MHC2 on antigen presenting cell-SIGNAL 1: T cell receptor binds to antigen,CD4 binds to MHC2 -SIGNAL 2:(constimulation)CD28 on T cell bind B7 on APC, cell is activated to TH1 or TH2 |
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| Cell Mediated immune response |
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| activated Tc binds to MHC1, T cell receptor binds antigen,CD8 binds MHC1, T cell secretes degradative chemicals(perforins-preforate membrane & granzymes-induce programmed cell death apoptosis) |
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| effector cell |
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| does not need second signal |
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| STD |
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| horizontal transmission; CAUSATATIVE BACTERIUM -chlamydia trachomatis:most frequent -neisseria gonorrheae:men get dysuria and pyuria -treponema pallidum(syphilis):primary-chancre,secondary-disseminated rash,tertiary-inflammatory lesions:gummas, congenital:mother to baby CAUSATATIVE BACTERIUM |
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| staphylococcus aureus |
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| localized infections -furuncles(boils) -coagulase (clot former) |
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| Human Microflora |
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| -humans colonized with many microbes -normal flora=commensal org. -change constantly and vary with types of tissue,condition:pH,moisture,microbes present -can cause disease if reach abnormal location |
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| Human Microflora: Skin |
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| difficult to colonize:dry, salty,acidic, protective oils -billions microbes in moist areas -mostly anaerobes |
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| Microflora:Nose, mouth |
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| -Nasopharynx & oropharynx -dangerous if enter bloodstream -can form biofilm around teeth (plaque,gum disease, streptococcus) |
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| Microflora: Stomach |
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| -very high acidity -few microbes survive(helicobacter pylori) -loss of acidity:achlorydira (malnourishment, allows pathogens to grow) |
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| microflora: Stomach |
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| -contains vast majority of human microflora -bacteria ferment ingested food -provide nutrients, inhibit pathogens |
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| Human Genitourinary Microflora |
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| -kidney and bladder are sterile -urethra and vagina contain bacteria -probiotic treatment |
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| risks, benefits of microflora |
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| -makes vitamins -digest food -prevents colonization by pathogens -makes immunomodulins -opportunistic pathogens:surface breach allows bacterial entry |
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| innate immunity |
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| -barriers to infection -nonspecific reaction to destroy invaders |
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| adaptive immunity |
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| -reaction to specific antigens -body reacts to antigens when exposed (retains memory of those antigens) |
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| Neutraphils |
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| phagocytic cells- 60/70% of WBC |
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| manocytes |
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| phagocytic cells -5% WBC -in tissues differentiate into macrophages and dendritic cells |
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| Basophils and Eosinophils |
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| -leukocytes -release toxins to posion microbes -inhance inflammation |
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| lymphocytes |
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| -T cells:modulate specific immune responses -B cells:produce antibodies to bind antigens |
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| innate host defense |
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| -skin: keratin, oil, cells that phagocytose microbes,dead skin cells, washing -mucous:trap/destroy pathogens, mucous layers slough off -cillia:removes microbes from lungs -toll like receptor proteins on tissues (gut-m cells, skin-langerhans cells) |
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| chemical barriers to infection |
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| -acidic pH-high salt content-lysozyme-bile,antimicrobial peptides |
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| accute inflammatory response |
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| -infection releases microbes to tissue -macrophages phgocytize bacteria-capillary cells express selectins(slows macrophage movement)-macrophages/neutrophils:squeeze between capillary cells,leave capillary and attack bacteria -damaged tissue secretes bradykinin, mast cells degranulate(release histamine, stimulate blood vessels to open further), prostaglandin stimulates nerve cells(signal itching, pain) |
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| Phagocytosis |
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| -phagocytes must avoid attacking host cells(CD47 prevents attack),phagocyte toll like receptors bind bacterin and bind opsonized bacteria(cells coated with antibodies) -phagocytes kill, digest engulfed bacteria with oxidative burst (produce peptide to kill bacteria) |
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| innate defense by interferon |
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| -interferons produce d by infected host cells(infected with viral/bacterial path. secrete interferon proteins) -nearby cells respond to interferons -type 1:IFN arms recipient cells to resist virus(inhibit protein synthesis) -type 2:IFN modulates adaptive immune function(nearby immune cells become more sensitive) |
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| natural killer cells |
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| -destroy injected/cancerous cells -healthy cells make surface MHC1 protein(infected cells stop making MHC1) -antibodies bind viral proteins on surface-NKC kill antibody bound or MHC1 less cells(secretes perforin protein into target cell( |
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| complement |
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| -series of 20 serum proteins -activated by Ag-Ad complexes(classical pathway) -cell wall(polysacch,alt pathway) -mannose or other sugar on bact. cell wall(lactin pathway) |
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| Functions of Complement |
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| -lyses cell membranes -opsonization(coats cell wall) -enhanced inflammation(mast cell and basophil degranulation) |
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| Fever |
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| -pyrogens induce temperature rise(exogenous pyrogens (LPS)) -endogenous pyrogens (interferons,TNF,IL-6,IL-1) -signal brain to raise temp -high fever stresses invading microbes (non optimal growth temp and reduces iron availability) |
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| Bacteria vs. eukaryotic genes |
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| -replication is same -E. genes are much larger |
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| DNA |
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| -linked chain of sugar and phosphate(covalent linkage) -5` to 3`(add to 3`) and need available OH group to continue replication |
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| replication |
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| -semiconservative(each next generation has one old and one new) |
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| bacteria nucleoid |
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| condensed bacterial DNA. (30-50 loops of DNA) |
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| super coiling of nucleoid |
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| circular DNA(has no free end;break in the loop will cause DNA to be relaxed) |
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| super coiling stress |
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| constraining the supercoils involves wrapping the DNA around proteins in the cell |
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| topoisomerase |
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| binds to DNA breaking one or both strands and passes the DNA strands through the break before resealing it. the enzyme holds the cut ends of the DNA so it doesnt rotate |
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| topoisomerase type 1 |
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| cuts one strand and passes the other strand through the break before resealing the cut-changes DNA one supercoil at a time |
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| topoisomerase type 2 |
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| cuts both strands and passes them from somewhere else in the DNA or even another DNA through the break before resealing it. -changes 2 supercoils at a time |
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| gyrase |
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| a type 2 toposiomerase that adds negative supercoils (allows DNA strand to unwind) |
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| primosome |
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| structure of protein that initiate replication at the origin |
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| DNA helicase |
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| unwinds the helical DNA at replication forks (melts DNA) (recruits primase) |
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| Primase |
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| lays down the primers that are necessary for DNA polymerase activity. the primers are composed of RNA |
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| DAN polymerase 3 |
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| does most of the replication using 5`-3` polymerase activity. uses clamp to bind to strand |
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| DNA polymerase 1 |
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| removes primers and fills in the gaps during replication |
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| RNASE H |
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| removes RNA strands of a DNA |
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| DNA ligase |
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| seals the nicks by linking3` hydroxyl groups with adjacent 5` phosphate groups. forms new phosphodiaster bond |
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| single stranded DNA binding protein |
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| binds single stranded DNA at replication fork and blocks potential hybridization |
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| where does replication begin? |
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| OriC |
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| Plasmids |
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| -extra chromosomal pieces of DNA -1.low copy number plasmids, segragation similar to chromosome -2. high copy number plasmids,divide continuously and segregate randomly= |
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| plasmid replication |
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| -similar to chromosomal replication -"rolling cirlce" replication with no lagging strand |
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| plasmid genes |
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| -advantageous under special conditions:antibiotic resistance genes, resistance to toxic metals, metabolize rare food sources, virulence genes to allow pathogenesis |
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| restriction enzymes |
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| -cut DNA at specific sites -normally protect bacteria from viral DNA |
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| PCR |
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| -uses short oligonucleotid -primers bind complementary sites -requires primer |
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| sanger method |
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| -determines sequence of up to 1000 bases |
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| Initiation |
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| bind polmerazing machine, first monomer to template(DNA polymerase, RNA polymerase, ribosome) |
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| Elongation |
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| read template, add next monomer(DNA, RNA,Protein) |
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| Termination |
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| -release machine and completed product |
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| RNA polymerase |
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| -4 proteins in one complex -binds to DNA at sigma factor(promoter)(release of factor initiates reaction), reads sequence -does not require a 3` hydroxyl group for initiation (sigma 70:guides to most genes, sigma 32:active when cell is stressed by heat;heat shock response, sigma 32:active when cell is stressed by heat) |
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| Transcription initiation |
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| -sigma factor binds core RNA polymerase which binds to promoter -polymerase unwinds DNA at promoter |
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| Transcription Elongation |
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| -core polymerase adds RNA to 3` end -mRNA is complementary to template and identical to non-template |
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| Transcription termination |
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| -Rho independent termination:series of U residues downstream pause site -does nto require another protein to end transcription based on DNA sequence and structure of RNA |
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| Translation of RNA to protein |
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| -64 codons -Initiation: Initiation factor bind ribosome to 1st codon(AUG:begin) -Elongation:movement of ribosome along mRNA(tRNA carry a.a. to A site),Ribosomes move forward 1 codon at a time shifting the location then leave through E site. -Termination:releasing factors undock ribosome from mRNA, release factors recognize stop codons |
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| Shine Dalgarno |
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| -place where ribosome initially attaches to RNA |
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| Gene transfer |
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| -transformation:direct uptake of DNA from medium -conjugation:bacterial sex, use of pilus -transduction:viruses inject DNA into cell |
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| recombination |
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| -entering DNA replaces chromosomal DNA(if sequence is overall very similar) -used to repair damaged DNA |
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| Mutation |
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| -point mutation:change in one base pair -nonsense point:change codon to stop -frameshift:one or more base pairs is inserted or deleted -Mutagens cause mutations: electromagnetic radiation, chemicals, spontaneous tautomers during replication |
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| DNA Repair |
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| -Mismatch Repair:mispaired base cut out of strand -Thymidine dimers:induced by UV -Damaged bases:excised by specific enzymes -Recombinational repair:occurs just after strand has replicated, undamages strand is copied and replaces damaged one -SOS repair:extensive DNA damage inactivates LexA, activation of many repair genes, rapid polmerization of DNA |
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| Mobile genetic elements |
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| -chromosomal sequence is not fixed -retrotransposon inserts into chromosome(found in all species) -can jump from one site to another -can copy itself to a new site |
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| horizontal gene transfer |
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| -movement of genes between cells(other than through cell division) -transformation, conjugation, transduction -transposons carry genes into chromosome -plasmids carry genes between cells -spreads useful genes among bacteria |
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| pathogenesis |
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| -process by which microbes cause disease in a host |
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| primary pathogens |
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| -"frank pathogens":are disease causing microbes possessing the means to breach the defenses of a healthy host - |
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| opportunistic pathogens |
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| cause disease in a compromised host |
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| pathogenicity |
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| an organisms ability to cause disease |
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| virulence |
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| measure of the degree of severity of disease |
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| infection cycle |
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| the route an organism takes to spread |
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| fomite |
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| inanimate object through which pathogens can be transferred |
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| vector |
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| insects (mosquitos) horizontal transmission |
