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PCB 3063
Exam 5
| Term | Definition |
|---|---|
| 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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