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Chapter 161 Frederick Griffith a) discovered that the something inside dead cells could still be transformedinto live cells after work with pneumonia b) led to to many new research questions on the unit ofinheritance, later found out to be DNA

Avery, McCarty and MacLeod a) identified DNA as the driving factor behind transformationthrough injecting strains of bacteria into mice b) led to more emphasis on the view of protein vs.DNA inheritance, provided that DNA is the genetic material of lifeHershey and Chase a) discovered through radioative tagging that the DNA was the keytrasmitting substances for bacteriophages, taken as proof of the DNA molecules role in heredity

b) led to more research on the structure of DNA and the peculiarities. Disproved the proteintheory of inheritance, and proved the DNA inheritanceChargaff a) began to uncover the pairing of the bases in DNA when he noticed the same ratio of

Adendine to Thymine and Guanine to Cytosine b) led to new models of how DNA worked, withA bonding to T and C bonding to GRosalind Franklin a) used X-ray diffraction to find out the helical nature of DNA b) spurred

Watson and Crick to develop their model for DNAWatson and Crick, a) they discovered the double helix nature of DNA due to the data fromFranklin b) provided the double helix model of DNA we use today

Meselson and Stahl a) discovered that DNA of E Coli after 2 replications matched only thesemiconservative model of replication b) contributes to our understanding of DNA replication

2. The first density bands would look the same, except for the 15N would be equivalent to the14N of Meselson and Stahlx expirement in other words, the first generation would produce allmiddle-weight N, and then generation two would create a split between heavier and lighternitrogen atoms (around 50/50 split)

3. This is because the semi-conservative model of DNA replication states that DNA replicationhappens through the combination of a parent strand and one of the new strand. This is opposedto the conservative model, which indicates that every pair of strands that is replicated are madeof daughter strands, and the parent strands stay together. On the other hand, dispersive

replication suggests that sections of parent and daughter strands swap. DNA was shown to besemi-conservative by Meselson and Stahl after their expirement showed the results of DNAreplication through weights of isotopes.

4. Watson and Crick in their model suggested that new DNA strands were produced off ofmodel strands. They discovered that the nature of DNA was a double-helix, in which the twostrands seperated when replication occurs after modeling DNA with ball and stick models. Thismodel best matched the data that Rosalind Franklin had already discovered.

5.Enzyme Function

DNA polymerase III Catalyze elongation of new DNA at replication forks

Primase Makes an RNA chain in the order of DNA where the new DNA willoccur

DNA polymerase I Replaces RNA nucleotides with DNA nucleotides

Helicase Untwists the double helix at replication forks

topoisomerase Stabilization strain on the DNA ahead of the Helicase caused bytwisting

DNA ligase Joins the sugar-phosphate backbones of the Okazaki strand to form

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DNA

6. DNA replication on the leading strands and lagging strands are both produced by DNApolymerase III, but the leading strand replication occurs in one smooth flow. This is because thereplication fork moves toward the 5 end of the leading strand, so the polymerase III is able toreplicate toward the 3 end of the new strand. However, the replication on the lagging strandisnt continous, and occurs instead in little chunks joined togethr by Okazaki sections, since thefork is headed towards the new strands 5 end.

7. A chromosome telomere helps to keep the damage to chromosomes minimal. This is becauseevery time the chromosome replicates, some genes are lost at the end of the chromosome.Telomeres create useless genes at the end of each strand of crhomosome, so that way if they aredestroyed during the replication, it doesnt hinder succesful expression of the chromosomes.Normal lengths of telomeres allow for the cell to die at a natural time, preventing the infinitedivision evident in cancer.

8. This project can definitely be a a potential target for cancer therapy. Since abnormaltelomerase is connected to the prevalence of cancerous cells, it makes sense to target cells.

Specifically, if one found a drug that was able to recognize irregular telomerase enzymes andcorrect them, the cancerous cells would slowly wear down and die.

9. This would mean that the repair mechanism would be unable to fix DNA strands within theDNA replication. This would lead to uncorrected errors in the DNA sequence, which would passoff to all the future offspring of such a cell. The amount of errors in the DNA would graduallyincrase over time, leading to very mutated cells.

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Chapter 171. The genes inside the nucelar envelopes control the expression and code for strands of RNA.These starnds of RNA, in this case mRNA, then go to the ribosome, where they are read. Theribosomes brings in certain nucleic acides that correspond to the order of the bases in RNA, andassemble proteins based off of the order of these genes. These proteins control variousphenotypic factors, such as the pGLO gene we have observed that creates a green tint under a

blacklight.

2. They missed the fact that DNA codes for proteins thus, the two were already related.Proteins were a method of expressing the DNA, which means that you could observe genetic

variation from proteins. However, ultimately DNA controls behavior since it controls theproduction of protein.

3. Pre-mRNA is modfied in three ways. Two separate sequences of nucleotides are added to theend of the 5 and 3 of the RNA strand. The 5 is capped with a modified Guanine, while the 3 iscapped with a string of Adendine nucleotides, usually 50-250 As long. These help to allow themRNA to get out of the nucleus, help against degredation, and help with binding to ribosomes.The last modification that happens is RNA splicing, which splices the introns, or non-coding

regions, of the chromosome. Splicing helps chromosomes enter the cytoplasm, and somesusptect that introns play a regulatory role in the cell.

4. This drug is most likely to be bad for humans too, and thus kept off of the market, sinceanimal cells are very similar to human cels. The deletion of two base pairs at various intervalsmeans that after DNA transcription into RNA, the RNA will express entirely new codons becauseof the shift in base pairs to fill the positions that were deleted. This results in entirely differentamino acids, and thus vastly different proteins being produced. The frameshift may causenonsense or missense.

5. The damaged transcription factor molecule would likely be unable to function normally. Thiswould impair the ability of the cell to produce mRNA from DNA strands, since they wouldnt be

able to bind to the DNA and start proucing RNA. This would result in very little or ineffectiveproduction of protein, which would most certainly lead to the death of the cell.

6. The drug would definitely have effects on the growht of bacterial diseases. This drug wouldimpair the production of certain proteins which create negative reactions from our bodilysystems. Since the eukaryotic ribosome is much more complicated than the prokaryoticribosomes, there is less of a chance that the drug would impair the functioning of theprokaryotic ribosomes. Since prokaryotic cells use more different rRNA, the ribosomes wouldlikely be able to adapt better than the eukaryotic bacteria to the introduction of the drug.

7. The mRNA moves out of the nucleus directly to the ribosomes, where it is coded for a protein,which then moves along the cytoskeleton along the microtubules to the Golgi appareutus.

8. a)T-A-C-C-C-C-C-G-C-T-A-T-A-A-A-A-T-A-G-G-C-T-G-Cb) U-A-C-C-C-C-C-G-C-U-A-U-A-A-A-A-U-A-G-G-C-U-G-Cc)Try-Pro-Arg-Tyr-Asn-ile-Asn-Gly-Cys

9. Nonsense mutation results in a change to the codons to immediately produce a stop marker,and translation to stop Sense mutations result in no practical change, still codes for same codon,though base pair may have changed Missense mutation results in one wrong codon and one

wrong amino acid.

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10. This wouldnt directly affect me, since somatic cells that undergo mitosis will still be normal.However, my future children would be affected in whichever gene the mutagen mutated.

11. RNA is easily flexible, and thus corrects errors in replication with associated enzymes, muchlike DNA does. However, even if errors still appear on the mRNA, the tRNA reudces the chances

of error because translation includes redundancy for some amino acides, which means that oneletter changes sometimes have no effect on phenotype.

12. The TATA box would have mutated, which means that the promoter regions of the genesmay not be recognized. This results in transcription factors not binding to the right site, leadingto transcription of incomplete or wrong parts of the DNA, if at all.

13. Because genes have also been able to code for other things than protein molecules. They existindependantly of protein production- that is, DNA doesnt pressuppose protein production. Thismeans that a gene requires re-definition in terms of things other than proteins.