Exam 5
Quiz yourself by thinking what should be in
each of the black spaces below before clicking
on it to display the answer.
Help!
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| show | promoter region (CAP + RNA polymerase), operator, and structural genes; inducer of lactose operon is lactose
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| gene z | show 🗑
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| gene y | show 🗑
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| gene a | show 🗑
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| show | 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
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| gene o | show 🗑
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| show | inducer; lactose (allolactose) binds repressor product, which no longer binds operator;
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| p | show 🗑
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| show | catabolite activator protein; binds promoter region to activate transcription of structural genes (positive gene regulation); insure that glucose is used before lactose
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| show | cyclic adenosine monophosphate; complexes with CAP to allow efficient complexing to promoter region
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| CAP-cAMP complex | show 🗑
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| negative regulation | show 🗑
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| show | I P O lacZ lacY lazA
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| show | the regulator protein (a repressor) binds to the operator and inhibits transcription
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| show | 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
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| positive regulation | show 🗑
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| show | 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
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| when levels of cAMP are low and glucose is high | show 🗑
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| glucose present (cAMP); no lactose; no lac mRNA | show 🗑
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| glucose present (cAMP low); lactose present | show 🗑
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| show | maximum transcription because CAP and cAMP can readily bind
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| show | when a base is replaced with a similar base (ex: A is swapped for G)
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| transversion mutation | show 🗑
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| frameshift mutation | show 🗑
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| when a tautomeric shift occurs | show 🗑
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| base analogs | show 🗑
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| show | donate an alkyl group to amino or keto groups in nucleotides to alter base-pairing affinity
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| Intercalating agents | show 🗑
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| UV radiation | show 🗑
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| show | removes thymine dimers caused by UV light; depends on the activity of a protein called the photoreactivation enzyme (PRE).
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| PRE system of UV repair | show 🗑
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| Base excision repair (BER | show 🗑
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| show | 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;
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| show | Individuals with xeroderma pigmentosum have lost the ability to undergo nucleotide excision repair; faulty XPA system
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| show | 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
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| Insertion sequences (IS elements) | show 🗑
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| show | ~50% of the human genome
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| cancer | show 🗑
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| show | stops replication and it is responsible for genomic stability and DNA repair (signals what strand was the original strand)
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| Chronic Myelogenous Leukemia | show 🗑
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| HNPCC | show 🗑
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| show | 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
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| show | are resistant to chemotherapies and radiation therapies
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| show | induces transcription of BAX and inhibits transcription of Bcl2, leading to cell death.
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| show | 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
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| Ras pathway | show 🗑
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| Ras mutation | show 🗑
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| show | 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
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| show | 50%
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| show | 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;
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| show | 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
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| show | Histone deacetylases and histone acetyltrasnferases; responsible for remodeling chromatin
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| show | Parts of cancer cells that will entice vascular cells to grow towards the cancerous cells (induce blood supply)
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| What % of cancers are hereditary? | show 🗑
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| show | 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
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| show | anaphase promoting complex cause the cells to divide
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| What % of cancers are associated with viruses? | show 🗑
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| show | 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
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Created by:
JacobGant
Popular Genetics sets