10/20-10/22/15 Notes 3500-1004
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This 8 page Class Notes was uploaded by Shannon Notetaker on Friday October 23, 2015. The Class Notes belongs to 3500-1004 at Bowling Green State University taught by Dr. Paul Morris in Summer 2015. Since its upload, it has received 36 views. For similar materials see Genetics in Biology at Bowling Green State University.
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BIOL3500 Genetics 102015 Chapter 23 Continued 0 P53 One of most important tumorsuppressor genes in cells Frequently mutated in tumor cells Is a transcription factor Is activated by DNA damage by means of phosphorylation Is a monitory protein Functions as a quottetramerquot 0 As a tetramer acts as a transcription factor in the nucleus Results in the synthesis of several genes 0 One being MDM2 0 Actually leads to p53 s degradation 0 The level of MDM2 controls the p53 in cell 0 When damage detected no control anymore I Because MDM2 amp p53 complex doesn t form When a cell has DNA damage role of cell is to prevent the cell from replicating its DNA until the DNA damage is repaired o If extensive damage to DNA cell is supposed to die I Programed cell death apoptosis In order for protein p53 to do all this p53 has different domains 0 These domains have different functions I See class handout I 4 domains of p53 1 Activation domain 2 Proline domain 3 DNA binding domain 4 Tetramerization domain allows to form a tetramer with itself I Domains can be activated or inactivated Why do mutations in p53 so frequently result in tumors 0 P53 initiates transcription of p21 I P21 binds to CDK which prevents DNA replication o If p53 mutated does not activate transcription of p21 so no control of preventing DNA replication I So cells divide accumulate more mutations tumors When Cells undergo apoptosis starts by 0 Stress causes p53 to produce a bunch of proteins 0 Puma protein blocks BdXL from binding to p53 0 Different protein complex then binds to mitochondria triggers apoptosis cell death 0 Figure 239 0 O 00 Most often cells divide in response to an exogenous signal Transmembrane receptor spans membrane and binds to growth factors I Like growth hormones This binding signals change in cell Then links to Ras I What is Ras o A protein 0 Stands for rat adinol sircoma probably spelled wrong here 0 Originally found in rat tumors 0 Ras normally found in the inactive state bound to the GDP 0 When adaptor molecular binds to transmembrane receptor GDP exchanged for GTP which turns Ras into the active state I Ras then binds to GTP and is activated I Activated Ras activates Raf which activates MEK I MEK activates MAP kinase I Activated MAP kinase moves into the nucleus and activates transcription factors Normally Ras has an onoff switch which controls if binds to GTP or not I Mutations often bind Ras to GTP and never lets go o If never lets go continuous cell division ensues I In a lot of cancers we see mutations in Ras and p53 because promotes cell division A mutation in any one gene won t immediately make the cell cancerous but a mutation in a selective set of genes increases the probability that mutations will accumulate and will turn cancerous P53 most common mutated gene in cancers I 2quot l most common Retinalblastoma I 3rd Ras I 4th a protein called telomerase o Gives cells quotimmunityquot divides forever 0 Until telomeres on ends of chromosomes get too short until can no longer divide I Unless ends are repaired in between divisions o Telomeres get shorter with every division 0 Figure 2311 0 Common mutation on chromosomes from drugs or Xrays chromosome breakage o Viruses amp Cancer 0 2 mark question will have 0 Cervical cancer results from a virus 0 HPV also can cause cancer 0 Viruses can cause cancer in multiple ways 1 Virus can enter into genome amp its position transcribes genes that promote cell division at inappropriate times 2 Viruses can produce proteins that inhibit the activity of other proteins 0 Such as p53 amp retinalblastoma 3 Via transduction o picking up extra DNA by the virus so when enters other cells infects it o Epigenetic changes a way of changing gene expression 0 Methylation suppresses gene expression 0 How else can you suppress gene expression I Acetylation of histones o How could Epigenetic changes accidently promote cancer I One way P53 doesn t get expressed so no cell division regulation 0 Going off TopHat question quotHow do Epigenetic changes quotcontribute to cancer 0 Gurstein paper will be talking about soon I I Find on Canvas read I Will want to make lots of lists I Important concept amp idea want to leave course with o How is the genetic information organized on a chromosome I The encyclopedia of DNAencoding elements project addresses this I Talked about in Gurstein paper Work on TopHat questions for practice 102115 BIOL3500 Genetics Chapter 21 0 Watched SciShow quotEpigeneticsquot YouTube video 0 Genome does the work 0 Epigenome tells it what to do 0 Chapter 21 0 Changes in chromatin structure alter gene expression 0 Leads to epigenetic changes 0 Large part of this is histone modification 0 Figure 213 0 DNA Methylation I 1 Before replication DNA fully methylated at CpG dinucleotides I 2 During replication new DNA strands are synthesized without methyl groups I After replication DNA is hemimthylated o Hemimethylation methylation on one strand od DNA but not the other I Methyl groups attract methyltransferase enzymes which add methyl groups to the unmethylated strand I Results in fully methylated DNA 0 Figure 214 0 Queen bee on left I Normal bee on the right 0 Queen is bigger because of methylation 0 Figure 215 0 Have a purple corn strain crossed with normal I All of offspring all different from parents looking I This is not Mendelian inheritance 0 Figure 216 0 Difference relates to tandem repeats o No transcription of tandem repeats o Tandem repeats encode RNAs 0 Figure 218 o If rats have more attentive mothers meaning lick amp groom rats more that pattern alters the stress response of the baby mice so they grow up to be less fearful 0 Another example is children growing up in staterun German orphanages 0 Also alcoholic pregnant women study done in England 0 Figure 219 o In women one of the Xchromosomes is inactivated I Inactivation regulated by a gene which is a long noncoding RNA I No genes on the silenced chromosome are expressed 0 An example of this Xchromosome inactivation is in orange amp white cats I Whether a patch is black or orange depends in that area of the developing embryo which chromosome was silenced 0 Figure 2111 0 Epigenetic changes can be associated with cell differentiation 0 Stem cells looked at for this 0 Epigenetics amp Cancer Chapter 233 o 90 of follicular lymphoma exhibit mutations in the MLL2 gene which encodes a histone methyltransferase enzyme I This enzyme adds methyl groups to DNA a type of epigenetic modification that alters chromatin structure and affects transcription 102215 BIOL3500 Genetics Notes 102215 Notes 0 RNASeg O Enables us to get a picture of what genes are being transcribed and in what amounts 0 An update of microarrays 0 Start with an RNA sample that s converted to cDNA 0 Make a RNA PolyA Library 0 Use technology called quotshort read assembly I Reads 200200bp shorter than a gene only a fragment of a total sequence I But in this experiment you get millions of reads I Then use programs to assemble the sequences from these reads I Assembly of a gene 1 2 3 AAA 0 RNASeq is more powerful than realtime PCR I Could test an effect of a drug on every single gene 0 Can see how gene expression changes with time 0 Can see what are called quotgenefusion events I In a cancer profile can have chromosome rearrangements o when a piece of chromosome breaks amp joins another chromosome 0 Can also see which genes are silenced 0 Can see what chromosomes are spliced 0 Can see which ones are highlyexpressed o In any sample will have 50006000 amount of genes I Some important some not 0 Cancer Essay 0 9 Questions have to answer 0 20 points 0 On the molecular biology of cancer I Whenever possible name specific genes involved amp what happens 0 How might estrogenlike ingested products be related to cancer I Hormones may stimulate cell division I If this is stimulated before the DNA had been checked to be sure it has no mutations can stimulate cancerous cell division due to muations 0 Notes on Cancer Essay Rubric O 1 Start looking in chapter 18 I Spontaneous mutation I Specific chemical mutations the kinds of mutations that take place I Examples to back up I Chemical mutagens o What genes are mutated in melanoma 0 Some chemicals cause chemical breakage 0 References in Cancer Paper 0 Reference comes at the end of the sentence in which the idea has been introduced Example Giuliano et al 2006 Genetics book Pierce 2014 I Don t need to add Pierce after every sentence if writing several sentences on an ideas from Pierce Add after first sentence then add after again if come back to it after switching to a new source On reference page need all the authors names complete title where from page numbers I Can copy and paste reference layoutformat from PubMed When using a website if it is a scientific website it will have a paper reference on the site usually at the bottom of the page cite that paper instead of the website directly 0 quotTurn it In Software 0 Software used to submit paper online 0 Has databases of papers amp internet sources o If copy amp paste something will get flagged 0 Not worried if have a few same words you will be talking about things which other people are talking about The problem arises when start copying whole sentences even whole paragraphs 0 Seems to be a problem every single semester don t do it 0