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Seabury 3

QuestionAnswer
constitutive a gene that is on all the time and thus does not respond much to the environment
inducible enzymes are produced only if substrate is present (e.g. lac)
repressing if the substrate exists, no need to produce the enzyme (e.g. tryptophan)
negative control gene expression (GE) occurs unless regulator molecule shuts it off
positive control GE occurs only if regulator directly stimulates it (CAP/cAMP in lac operon)
I+ gene in lac operon needed for lock-and-key fit of repressor and operator; if bacteria is I-, lac genes will undergo transcription/translation WITHOUT lactose constitutive
O+ gene in lac operon affects repressor chape; if gene is mutated (Oc), then no lock-and-key fit --> makes enzymes w/o lactose
I^s mutation in lac operon causes the inducer to lack lactose binding site --> doesn't make enzymes repressed
effect of glucose on lac operon represses lac operon by CAP-cAMP complex binding at promoter inducible condition cAMP exerts positive control
tryptophan operon attenuator biosynthesis when trp absent, the cell needs to make it
cellular localization pattern where the protein goes after it is produced
Dscam gene encodes protein that giudes axon growth, uses alt. splicing
types of regulatory RNA short RNA RNA interference, RNAi (animals) post transcriptional gene silencing, PTGS (plants) short interfering RNA, siRNA (plants)
short RNA regulates CYTOPLASMIC gene expression by repressing translation or degrading mRNA
post transcriptional gene silencing (PTGS, plants) dsRNA is cut every 21 nucleotides by DICER to make short interfering RNA (siRNA), which unwinds to sense and antisense strands; the antisense strand combines with a protein coplex (RISC), which recognizes, binds, and cleaves mRNA
microRNA ssRNA that binds w/ internal or 3' untranslated mRNA and either -blocks translation -targets RNA for degradation
cyclin a protein that checks conformation before cell enters next phase of cell cycle cyclin B must be bound to CDK1 for mitosis to continue
G1/S CDK4-cyclin D
G2/M CDK1-cyclin B
tumor suppressor genes halt passage through cell cycle
proto-oncogenes promote cell division
RB1 retinoblastoma 85% of those born with mutation get it (fam) 55-60% who develop mutation -> tumor (sporadic)
TF, EF2 normally tell cell to stop, but in mutated form, cell cycle always on -->retinoblastoma
WT1 Wilms tumor gene kidney cancer, child gene on HSA11p encodes TF
p53 tumor suppressor gene TF for 20 genes normal action shut down by carcinogens negatively regulated by MDM2 Li-Fraumeni disease
BRCA1-HSA17 predisposition inherited as a dominant trait 85% w/ one mutation develop another increased risk of breast and ovarian cancer
BRCA2-HSA13 autosomal dominant breast cancer ONLY
Rous sarcoma 1st oncovirus described SRC gene encodes for tyrosine kinase
Ras proteins signal transduction proteins that reg. cell growth/division; transmit extracellular signals to cytoplasm single aa substitution to -> mutation 30% of cancers have mutation
HRAS on chromosome 11 regulates cell division in response to growth factor
NRAS chromosome 1 control of cell growth
Philadelphia chromosome result of reciprocal translocation between 9&22 Chronic Myelogenous Leukemia
metalloproteins encode matrix cutting enzymes for metastasis to occur
colon cancer -benign->malignant (95%) -familial 1.Familial adenomatous polyposis 2.Hereditary non-polyposis colorectal cancer
Familial adenomatous polyposis related genes: FAP, APC, HSA5 slow progression, rapid initiation many polyps
Hereditary non-polyposis coleorectal cancer related genes:HSA2, HSA3, MSH6, MLH3 slow initiation, rapid progression few polyps
top cancer killers, men and women men: lung, prostate, colon/rectum women: lung, breast, colon/rectum
solid tumors derived from epithelium
requirements for good vector -independently replicate -restriction enzyme cleavage site -selectable marker (antibiotic resistance, lac) -easy to recover
pUC18 commonly used plasmid vector has polylinker site, lac Z gene as selectable marker for blue-white screening
BACs Bacterial artificial chromosome 200Kb
YACs yeast artificial chromosome 230-1900Kb
Southern blotting allows us to determine which DNA clones contain the DNA fragment of interest
roche 454 pyrosequencing relies on detection of phosphate release during nucleotide incorporation
categories of genomics -structural -functional -comparative
shot-gun sequencing isolate genome->fragment by sonication->clone fragments into vectors->prepare clone library->clones selected at random and sequenced
c-value paradox genome size (in eukaryotes) does NOT correlate with genome complexity (polyploidic plants)
human genome first discovered by Venter (2007) 50% transposable elements (LINEs, SINEs)
chimp vs. us differences: -indels -regulation of gene expression -recombination hot spots
paralogs arise from single gene duplication in SAME spp
orthologs homologous genes in DIFFERENT spp
alpha and betablobin sequances are similar, reflecting some common elolutionary history
HSA 14 heavy chains
HSA2, HSA22 light chains
break-nibble-add mechanism joining of V (variable region) and J (joining region) is imprecise, subject to adding or removing a few bases (rearranging the gene)
proteomic tech -2D electrophoresis: separate by charge then MW -mass spec
FGF-10 component of signal pathway controlling outgrowth in turtles
development, basic 1. maternal effect genes establish gradient 2. gap genes, pair-rule genes, and segment polarity genes divide organism into segments (determination) 3. homeotic/selector genes specify the identity of each segment (differentiation)
runx2 pair-rule gene mutation in this causes 'runt', cleidocranial dysplasia
HOMEOBOX shared sequence of selector/homeotic genes among many spp.
things that activate responsible hox genes -retinoic acid -fibroblast growth factors -Wnt proteins -bone morphogenic proteins (deer antler) -hedgehog proteins
HOX-D13, HSA2q cause synpolydactyly in humans autosomal dominant
HOX-A13 autosomal imcomplete dominance frameshift
PAX paired box genes nervous system mutations -> cancer, 'splotch', Waardenburg syndrome (autodom)
ced 3, 4, 9, 1 bcl2 cell death genes 3&4 -> cell death in many ways 9 -> protects cell from destruction 1 -> activates 9 bcl2 -> prevents apoptosis (cancer causing gene)
Created by: Jessica S Jessica S on 2013-03-29



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