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PCB 3063

Exam 5

TermDefinition
operon promoter region (CAP + RNA polymerase), operator, and structural genes; inducer of lactose operon is lactose
gene z structural gene; b-galactosidase controls lactose catabolism, breaks down lactose into galactose and glucose
gene y structural gene; galactoside permease concentrates lactose in the cell
gene a structural gene; thiogalactoside transacetylase is not in the pathway
gene i repressor gene; product (R) binds to operator to inhibit transcription (negative gene regulation); makes the protein that is the repressor - sits on the gene and stops transcription
gene o operator gene; controls transcription of the three structural genes
i inducer; lactose (allolactose) binds repressor product, which no longer binds operator;
p promoter region; RNA polymerase and CAP-cAMP binding
CAP catabolite activator protein; binds promoter region to activate transcription of structural genes (positive gene regulation); insure that glucose is used before lactose
cAMP cyclic adenosine monophosphate; complexes with CAP to allow efficient complexing to promoter region
CAP-cAMP complex allows you to bind the promoter or operator and it induces production of a lot of mRNA; transcription stimulator by bending the DNA
negative regulation regulator control that is mediated by a repressor that binds to the operator and inhibits transcription
order of the lac operon I P O lacZ lacY lazA
in the absence of lactose the regulator protein (a repressor) binds to the operator and inhibits transcription
when lactose is present some of the lactose is converted into allolactose, which binds to the regulator protein thus making it inactive and unable to bind to the operator; transcription can then occur
positive regulation regulatory protein is an activator that stimulates transcription
When levels of cAMP are high and glucose is low cAMP binds to CAP and the complex binds to DNA, which increases the efficiency of polymerase binding; this results in high levels of transcription and translation of the structural genes to break down lactose into glucose
when levels of cAMP are low and glucose is high cAMP and CAP are less likely to bind, which causes RNA polymerase to bind less efficiently causing the transcription rate to be low
glucose present (cAMP); no lactose; no lac mRNA no transcription because repressor binds to the operator
glucose present (cAMP low); lactose present minimal transcription because CAP binds less efficiently since cAMP is low
no glucose (cAMP high); lactose present maximum transcription because CAP and cAMP can readily bind
transition mutation when a base is replaced with a similar base (ex: A is swapped for G)
transversion mutation when a base is replaced with a dissimilar base (ex: A is swapped for C); causes buckling of DNA and change in geometry
frameshift mutation when a number of bases (not multiples of 3) are added or deleted which disturb the initial frame of reading
when a tautomeric shift occurs the rare form of C can bind with the normal form of A; the normal form of T can bind with the rare form of G
base analogs are molecules that have similar structures to the bases such as 5BU but can cause big problems if incorporated into DNA
Alkylating agents donate an alkyl group to amino or keto groups in nucleotides to alter base-pairing affinity
Intercalating agents are polycylic ringed structures that can squeeze in between the bases of DNA causing a frameshift mutation
UV radiation creates pyrimidine dimers that distort the DNA conformation in such a way that errors tend to be introduced during DNA replication
UV repair removes thymine dimers caused by UV light; depends on the activity of a protein called the photoreactivation enzyme (PRE).
PRE system of UV repair The bond creating the thymine dimer is cleaved by the photoreactivation enzyme (PRE), which must be activated by blue light in the visible spectrum; useful for small lesions
Base excision repair (BER DNA glycosylase recognizes and removes the incorrect base to form an AP site; AP endonuclease cleaves the phosphodiester bond on the 5' side and removes the sugar; DNA polymerase and DNA ligase come in to fill and seal the gap
Nucleotide excision repair (NER); prokaryotes DNA damage causes distortion that is recognized by an enzyme complex; the DNA is then separated and ssDBP stabilize the ssDNA; An eynzyme cleaves the strand on both sides of the damage and removes it; DNA polymerase and DNA ligase fill and seal the gap;
Xeroderma Pigmentosum; eukaryotes Individuals with xeroderma pigmentosum have lost the ability to undergo nucleotide excision repair; faulty XPA system
Homologous recombination repair (HRR) fixes a dsDNA break by digesting back the 5' ends to leave overhanging 3' ends that interact with a region of an undamaged sister chromatid to allow DNA polymerase to copy the undamaged DNA sequence into the damaged strand; uses BRCA genes
Insertion sequences (IS elements) have a transposase gene and inverted terminal repeats; ex: Alu elements
transposons make up ~50% of the human genome
cancer occurs predominantly in somatic cells with only ~1% occurring in the germ-line; normally 6-10 mutations occur in DNA repair, apoptosis, cell cycle, etc. in order for the cell to become cancerous; monoclonal (originating from a single cell)
geminin stops replication and it is responsible for genomic stability and DNA repair (signals what strand was the original strand)
Chronic Myelogenous Leukemia When chromosomes 9 and 22 translocate to form a new Philadelphia chromosome where bcr and abl are next to each other, a new protein is formed, which shouldn’t be there;
HNPCC hereditary nonpolyposis colorectal cancer; affects 1 in 200 people; 9 known genes associated with DNA repair; causes genomic instability and accumulation of mutations
apoptosis conditons when there is a balance of Bcl2 and BAX, they form inactive heterodimers; when there is an excess of Bcl2, they form homodimers and prevent apoptosis; when there is an excess of BAX, they form homodimers and stimulate apoptosis
Cancer cells with Bcl2 overexpression are resistant to chemotherapies and radiation therapies
In normal cells, activated p53 protein induces transcription of BAX and inhibits transcription of Bcl2, leading to cell death.
Ras proto-oncogenes a G-Protein, critical to cell signals linked to nuclear transcription; controlled by GTP; When Ras is constantly turned on, it turns on a pathway for transcription, which will alter protein levels; if not turned off, the cell will turn malignant
Ras pathway RAS→RAF→MEK→MEK→MAP→MAP→MAP→Transcription
Ras mutation When Ras is mutated at position 12 (Gly-->Arg) or 61 (Gln-->Aarg), it will promote tumor formation
p53 A protein that can stimulate or repress transcription of more than 50 genes; p21 cell cycle arrest at G1/S checkpoint via cyclin D arrest; can also halt G2/M; Activates DNA repair pathways and if that fails apoptosis
What % human cancers have mutated p53? 50%
Retina blastoma a protein that controls the G1/S checkpoint (tumor suppressor gene); those affected are born with 1 mutated copy and the other copy mutates within 6 months; kids with this disease will have their pupils turn white when exposed to light;
Retina blastoma (Rb) pathway RB binds E2F and keeps it inactive; increasing concentrations of cylcin D and E phosphorylate RB, which activates it and releases E2F, which then binds to DNA and stimulates transcription; works in the nucleus and cytoplasm
HDAC and HAT Histone deacetylases and histone acetyltrasnferases; responsible for remodeling chromatin
Metaloproteinases Parts of cancer cells that will entice vascular cells to grow towards the cancerous cells (induce blood supply)
What % of cancers are hereditary? ~10%
pathway for colon cells to becoming cancerous loss or inactivation of one of the APC alleles (c5); mutation of the K-ras oncogene (c12); loss of DCC (c18); loss of p53 (c17); some people may only go partway through this pathway
APC anaphase promoting complex cause the cells to divide
What % of cancers are associated with viruses? ~15%
environmental agents can cause cancer smoking causes transitions/transversions; UV damage causes thymine dimers; chemicals may not initially be harmful but may degrade into a harmful substance; radiation can be fatal enough to cause spontaneous abortions
Created by: JacobGant
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