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| 580393497 | Do Eukaryotes have operons? | NO. Have Euchromatin (stretched out( and Heterochromatin (bundled up) | |
| 580393498 | Problem encountered with Eukaryotic gene regulation | in a mutlicellular organism there are MANY TYPES oF CELL types. -They differ through VARIABLE GENE EXPRESSION -Genes must be able to be turned on/off at right times (luxury genes) | |
| 580393499 | Transcription factors with motifs bind where? | to enhancer sequence -activator (pair of proteins)& TFs interact with mediator complex --> forms bridge arrangement | |
| 580393500 | Insulators | can bind in bend of dsDNA which silences the gene downstream - bind between enhancer and promoter sequence | |
| 580393501 | Enhancer sequences | - have ability to bind certain proteins in MAJOR GROOVE - Proteins= Transcription factors | |
| 580393502 | Why are Transcription factors the ones that bind to major groove of enhancer sequences? | because they have motifs -motiffs are sequence specific on DNA -Major groove causes high affinity for a certain motif to bind | |
| 580405601 | Activators | help bridge hap - engage protein in major groove | |
| 580405602 | Enhancer sequences in SV40 | - enhancer sequences are 72 base pairs -cell has 2 enhancer sequences ( but ONLY NEEDS 1) - enhancers right-ward transcriptions 200X when it has right transcription factors bound to it | |
| 580405603 | How do we know that TF are what cause enhancement of transcription and not enhancer itself? | Because if enhancer sequence is put in backwards it still works | |
| 580405604 | histone acetyl transferase | acetylates lysines (basic) of histone tails | |
| 580405605 | Bromodomain sections of proteins interact with what? | interact with acetylated histone tails -found in many proteins that act to initiation transcription | |
| 580405606 | Chromodomain sections of proteins interact with what? | interact with methylated histone tails | |
| 580405607 | H1 histone | - known as linker histone - not in histone core | |
| 580405608 | Histone core is composed of? | H2A, H2B, H3, H4 (2 copies of each) = 8 subunits | |
| 580405609 | Which subunit usually makes the histone tail? | -H3 because it has regulatory ability in transcription -has 3 lysine residues (can be acetylated) | |
| 580405610 | Acetylation | removes positive charge on histones, thereby decreasing N termini of histone tails with negative charges of phosphate groups on DNA -->condensed chromatin structure becomes more relaxed and is associated with greater levels of transcription | |
| 580405611 | Lysines can be...? | -methylated: turns transcription off (locally) or -Acetylated= turns transcription on (Locally) | |
| 580440652 | What allows Nucleosomes to be repositioned/rephased? | because they are wound loosely around DNA | |
| 580440653 | What happens if one nucleosome moves downstream? | the others move downstream as well - this provides entry in transcription bubble - For RNA polymerase to enter, TATA region must open up | |
| 580440654 | ATP- Dependent Remodeling Complexes | Nucleosome rephasing can be driven by ATP -Proteins (wall proteins around region of DNA/ chromatin) must have ATPase to make nucleosome travel | |
| 580440655 | Example of ATP driven Nucleosome remodeling complex | "SWI/SNF" in yeast and "BAF" in vertebrates are associated with ATP dependent chromatin remodeling. | |
| 580440656 | SWI/SNF is associated with? | activating transcription of genes at chromosome targets by causing sliding and/or transferring of nucleosomes. - has a bromodomain (interact with acetylated histone tails) | |
| 580440657 | BAF is associated with? | usually repressed chromosomal gene targets | |
| 580440658 | Why are ATP-dependent Chromatin remodeling complexes important? | - they are responsible for remodeling tissue - in mammals, 1 out of 12 subunits may be modified and results; this subunit determines which kind of cell will be made (muscle cell -> cardiomuscle cell) | |
| 580440659 | Homing | ex) joining of a muscle tissue will "home" to a dead tissue of the heart -occurs because cells know where they are going; driven by remodeling complexes | |
| 580440660 | Chromatin remodeling is carried out by? | Purpose: allow access to condensed genomic DNA to regulatory machinery proteins of transcription 1.) histone modifications 2) ATP driven chromatin remodeling complexes (move, eject, restructure nucleosomes) | |
| 580440661 | Chromatin remodeling definition | is the enzyme-assisted process to facilitate access of nucleosomal DNA by remodeling the structure, composition and positioning of nucleosomes. | |
| 580440662 | Argine and Lysine | both residues can be methylated | |
| 580440663 | Define epigenetics | is the heritable change in gene expression (or cell phenotype) caused by mechanisms other than underlying DNA sequence -functional modification to genome that do not alter genetic sequence | |
| 580440664 | Define chromatin | DNA associated with Histone proteins | |
| 580440665 | Post-translational modification | post translational modification to amino acids in histones -shape of histone sphere would be changed -DNA is not completely unwound during DNA rep --> histones would be carried to new copy of DNA *this would ensure that differentiated cell would stay differentiated | |
| 581176674 | What are the purpose of locus control regions? | they allow for ordered transcription of downstream genes *have ability to enhance regions of linked genes to physiological levels in specific tissue cells - they turn on which group of genes are expressed | |
| 581176675 | What is an example of a set of genes under a locus control region? | Globulin genes (constituents of blood plasma/ made immune system) | |
| 581176676 | What is the globulin gene sequence? | E, GAMMA (b), GAMMA (a), S, BETA ( time (fetal) ---> Adult) | |
| 581184473 | what are luxury genes? | -genes coding for specialized cell products, synthesized abundandlty -they are tissue/organ specific (not expressed in all cells) -not constantly expressed/ expressed only when function is needed | |
| 581184474 | What are housekeeping genes? | -genes that manufacture cell products needed for maintenance of basic cell function -expressed in all cells of an organism under normal conditions | |
| 581214613 | how do locus control regions work? | - A signal from outside the cell causes signal transduction into the nucleus - first gene is produced (euchromatic state) and then turns itself off (by altering nucleosome structure) | |
| 581214614 | What is Ligand Signal Trandsuction | Converting chemical/mechanic signal/stimulation into a cellular response -signal from outside of cell will allow a protein to enter nucleus and bind to dsDNA sequence turning on transcption (kinase -> phosphorylation) | |
| 581214615 | NFkappaB pathway | -ligands cause NFkappB to turn on >150 genes in inflammatory/immune/during development 1) in nucleus NFKappaB is attached to & inhibited by IKappaB 2) phosphorylation of IKappaB releases NFKappaB to travel into nucleus and binds to enhancer sequence (turns on transcription) 3) IKappaB is ubiquinated (signaled for proteosome destruction) & *NFkappaB can be activated by growth factors; important in learning and memory (synaptic plasticity) * genes with NFKappaB binding sites have increased expression following learning -growth hormones can cause release of NFKappaB | |
| 581237148 | How can a viral infection can turn on transcription of the human beta-interferon gene? | 1) infection triggers 3 activator proteins (NFKappaB, JUN, IRF) 2) HMG + JUN + ATF bind to Enhancer1 & IRF binds to Enhacer2 & NFKappaB +HMG bind to Enhancer3 3) once all or abound dsDNA bends back on itself so that E1 is next to E3 (E2 is near/in bend) *we need bend to covert heterochromatin -> euchromatin (methyl -> acetyl group_); JUN binding to E3 allows for conformational bending 4) INFkappaB can be activated (once enhancers are bound and bend occurs) 5) INF-Beta gene is turned on and interferons proteins are made | |
| 581246365 | RTKa (Receptor Tyrosine Kinase) pathway | 1) signal molecules (insulin or EGF) binds to RTK 2) Adapter protiens, GBR2 & SOS bind to RTK. -adapter proteins change tertiary structure 3) RAS protein (GTP binding protein) is activated by adapter proteins 4) Activated RAS binds Raf which then phorphorylates MEK which then phosphorylates MAP (serene/threonine kinase) 5) MAP phosphorylates many transcription factors which travel to nucleus and bind to enhancer sequence * insulin is made by beta cells *EGF (epidermal growth factor) = produced in wound healing * RAS can also turn on/quicken cell division synthesis | |
| 581291322 | JAK/STATs pathway | 1) ligand (cytokine) binds to surface recepotors 2) squeezes together a pair of cell-membrane JAKs (is a kinase); become activated 3) JAks phosphorylates STAT "pairs" proteins (STAT= signal transduction activator) 4) STAT proteins dimeraize 5) Dimer enters nucleus 6) homodimer STAT binds dsDNA enhancer sequence -> activates transcription/ increases rate of transcription * Can have different types of JAKs --> lock and key fit for ligand * Dimer diversity is increased by formation of STAT heterodimers + homodimers | |
| 581484609 | What is the different between 7-spanner receptors and RTK receptors? | no adapter proteins are needed | |
| 581484611 | 7-spanner receptors | 7 turns within phospholipid bilayer hence "7 spanner" -activate trimeric g-proteins (alpha, Beta, and gamma units) 1) signal= light, epinephrine, seratonin, oderants 2) GTP, when bound toa alpha subunit activates Adenyll cyclase to ATP->cAMP. cAMP binds to Kinase A which phosphorylates many proteins (serines and tyrosines) to turn on nuclear transcription -GAP (GTPase activting protein) is required for alpha subunit to convert GTP->GDP -GI= g-protein inhibitor -> inhibits adenyl cyclase | |
| 581484613 | Bacteria that cause cholera produce what? and How? | they produce toxins that lead to increased cAMP 1) cholera has toxin that catalyzes ADP to bind to alpha-subunit -> this disables GAP -> which disables GTPase -> GTP will build up b/c adenyl cyclase will be active 2) cAMP builds up in lump of interstitial cells 3) water follows cAMP concentration (osmotic balance) --> diarrhea | |
| 581484615 | Bacteria that causes pertussis produce what? and How? | - they produce toxins that lead to constant turn on of adenyl cyclase 1) pertussis toxin is produced that binds to GI (g protein inhibitor) -> prevents Gi from binding to adenyl cyclase (alpha subunit) 2) prevents release of GDP from GTP, which prevents the inhibition of adenyl cyclase (GTP activates alpha subunit) 3) therfore continue to have adenyl cyclase 4) increases cAMP 4) leading to whooping cough (respiratory tract infection) -increase in cAMP causes delay in recruitment of phagocytes | |
| 581554243 | NRPs (nuclear receptor proteins) | 1) steroids -steroids bind to NRP homodimers which travel into nucleus and bind to inverted repeat enhancer sequence - Ex) estrogen, gluccorticoids 2) non-steroidal Hormones (vitaminD) -enters cytoplasm -froms heterodimer (zince-finger/Ns-NRP) -binds to DIRECT REPEAT | |
| 581554244 | The specificity of hormone turn on depends on what? | the spacer between the direct repeat/ inverted repeat | |
| 581554245 | Why is it hard to tapper of drugs? | -drugs are usually analogs of steroids there is a gradual decrease of dimer bound to enhancer ( causes bad side effects) | |
| 581554246 | How does CG methylation turn of transcription? | -GC sites are upstream from gene -DNA is methylated after DNA strand is made (5-methyl cytosine) 1) methylatase adds methyl to C of 5' CG 3'. 2) MeCP2 recognizes methyl group -> recruits histone deacetylase 3) this causes change from euchromatin -> heterochromatin | |
| 581554247 | What happens if a NRP does/does not carry a hormone? | -does not= deacetylation of histone tails in nucleosome -Does=cause acetylation of histone tails | |
| 581554248 | What is the way of preserving a silencer that remains the exactly same? | 1/2 methylation --> full methylation -silencing works because repressor protein sees fully methylated CG site after both strands are made (both sites) -turns of transcription but does not change genetic message (can be demethylated) | |
| 581554249 | How to decrease affinity of MeCP2 for CG sites? | -phosphorylated MeCP2 has less affinity for methylated CG sites -in brain neurons BDNF phosphorylates MeCP2 -BDNF is made when neurons are depolarized (rising phase) | |
| 581554250 | Retts Syndrome | - is caused by mutation in MeCP2 gene --> BDNF cannot deactivate MeCP2 and therefore have less access to genetic information (remains in heterochromatin); MeCP2 helps stop transcription | |
| 581601052 | RNAi | -gene silencing process 1)droscher attaches to dsRNA (in nucleus) & reduces length of long dsRNA -droscher=nuclear bend 2) dsRNA goes to the nucleus where dicer attachers -dicers RNA -creates 2 base pair 3' overhang on each end -creates 21-23 base pair dsRNA 3) dsRNA binds to RISC -RISC complex has a 21-23 bp strand which takes one of the strands http://www.youtube.com/watch?v=WJ_0afWCmhk | |
| 581623558 | Polycomb repression | -associated with chaingin Euchromatin to heterochromatin 1) PRC2 binds DNA and tri-methylates histone H3 lysinek27 (HH3K27) 2) After trimethylation PRC1 binds and leads to local turn of of transcription. *** this is a reversible process. -MLL protein takes of 3 methyl groups attached to lysine and thereafter turns on transcription ** similarities between methylation and polycomb repression |
