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20 Mar 2018

Using bioinformatic databases (NCBI) about DNA sequence for the hen (Gallus gallus) egg-white (LYZ) lysozyme gene:

a. How many introns are in the LYZ (Gallus gallus) gene?

b. How many introns are in the LYZ (Gallus gallus) gene?

c. On which chromosome is the LYZ (Gallus gallus) gene located?

d. How many base pairs (b.p.) long is the LYZ (Gallus gallus) DNA gene sequence

e. What gene is located immediately upstream of the LYZ gene? (Select one: FRS2 or KEGG or CPM or CPSF6?)

f. How many bases long is the mRNA transcript generated by the LYZ gene?

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Elin HesselLv2

21 Mar 2018

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Section A â Edit distance (8 points total)

1. Find the edit distance between ACGAAGTTC and ACCAAGGTGTTC. How do you know it is at most that much? How do you know it is at least that much?

Section B â More on sequence alignment (52 points total)

2. (6 points) Which of the following would be the two most appropriate to assess whether there are regions of homology between two distantly related proteins? Select two.

A) Needleman-Wunsch Algorithm

B) edit distance

C) local sequence alignment

D) global sequence alignment

E) dot plot

3. Consider the following alignment: ACACCAGGTCCCC ACA-----TGACC

a) (3 points) With a match score of +3, and mismatch score of -1, and using a gap penalty of -2, what is the score of the above alignment?

b) (3 points) If we keep the same match score and mismatch score, but use a gap open penalty of -6 and a gap length penalty of -1 per additional residue, what is the score of the previous alignment?

c) (8 points) Using the scoring system used in part b (match +3; mismatch -1; gap open -6 ; gap extension -1), Which of the following alignments is best? Which is worst? How do you know?

A) ACACCAGGTCCC A---CATGA-CC

B) ACACCAGGTCCC ACA---TGACC

C) ACACCAGGTCCC ACATGA----CC

D) ACACCAGGTC-CC ACA-----TGACC

E) ACACCAGGTCCC ACA--TG-ACC

F) ACA---CCAGGTCCC ACATGACC-------

4. Look up the INS gene in Entrez Gene.

a) (2 points) What tag do you put inside square brackets after INS to search for INS as a gene symbol?

b) (2 points) Find the record for the human INS gene. Which chromosome is INS on?

c) (2 points) What is the accession number for the RefSeq record for the shortest mRNA for human INS?

d) (2 points) What is the accession number for the RefSeq record for the human geneâs genomic DNA?

d) (6 points) Using the Needleman-Wunsch program, how could you find the mRNA sequence within the genomic DNA version? Give the best strategy, including the scoring parameters.

e) (4 points) Find the next gene upstream of the INS transcription start site. Which neurotransmitter does the product of this next gene make? How many base pairs separate the two genes?

f) (2 points) Now look up ins-1 as a gene symbol in Entrez Gene. Choose the entry for the worm C. elegans. Which chromosome is it on?

g) (2 points) What is the URL for the Wormbase link on this Entrez Gene record? What is the gene accession number for ins-1 in the C. elegans genome database?

g) (10 points) Perform Needleman-Wunsch alignments between C. elegans INS- 1 protein and Homo sapiens INS preproprotein, using the default parameters, except changing the substitution matrix to PAM10 for one alignment, and PAM50 for the second alignment. Use the following online tool: https://www.ebi.ac.uk/Tools/psa/emboss_needle/ What are the number of identical residues, score, and number of gapped residues for each of the two alignments? What conclusions can you draw about which of the two matrices, PAM10 or PAM50, is more appropriate in this situation?

greengnu396

Cystic Fibrosis (CF) is an autosomal recessive genetic disease that is characterized by the secretion of thick, abnormal mucous in the lungs. The mutated gene that leads these symptoms is the CF transmembrane conductance regulator (CFTR gene). The encoded protein is a chloride channel that moves chloride ions out of epithelial cells. In a homozygous individual, the lack of this chloride channel function in a mutant slows the flow of water into extracellular spaces. This lack of water export leads to the heavy mucus in the lungs of CF patients. Although children with CF would die in childhood, current treatments provide life expectancies into the 30âs.

CF is the most frequently inherited genetic disorder among American children. It affects 1 of every 2,500 children; 30,000 currently have the disease. Although its frequency is higher in European populations, it affects all human populations. Heterozygous carrier frequencies in the US are estimated to be 1 out of 29 Caucasians, 1 out of 46 Hispanics, 1 out of 61 African Americans and 1 out of 90 Asians. There are genetic screens for carriers of CF but they are not routinely performed despite this high frequency of carriers. At least all states in the US proscribe testing of newborns to identify children with CF early so that treatment can be started. Newborn tests for CF: http://www.cff.org/AboutCF/Testing/NewbornScreening/ScreeningforCF/ . If CF is such a common genetic disease, and such a simple Mendelian trait, why is genetic screening of parents not done more frequently? Is it just economic, a pain to do, or is it more complex such that the results of genetic testing are not just positive or negative?

Answer the following questions:
1. If two parents are heterozygous carriers of CF, show a pedigree with four children showing the incidence of carriers and afflicted children. If each unafflicted child (carrier or not) mates with another person, who has a 1 out of 30 chance of being a carrier of CF, what is the expected incidence CF disease in the third generation (frequency of CF in any one of grandchildren of the original couple)?

2. Pleiotropy of Cystic Fibrosis. Watch the two videos on the left at:

http://www.cftrscience.com/MOD-animation
or, if you can not view these, read the short NIH Genetics Home Reference for Cystic Fibrosis http://ghr.nlm.nih.gov/condition/cystic-fibrosis

Connect the description with one of the following videos, or related ones (there are many) you see:
video (10 minutes) of daily life of a child with Cystic Fibrosis http://www.youtube.com/watch?v=WUsuGKzdDg8
Lauraâs (20 year old) video diary of life with CF http://www.youtube.com/watch?v=Pgrf8qJXhpc&feature=related

In your own words, describe the range of CF phenotypes. List the other organs besides lungs that are affected and how does it affects those organs.

3.The DNA sequence of the CFTR gene is 170,000 base pairs in length and encodes the CFTR protein that is 1480 amino acids long. Open the accompanying text file (in Canvas/Files/Discussion folder) âCFTR gene DNA sequenceâ. You will see an alignment of the NIH human genome sequence of the CFTR gene â called âReferenceâ rather than âwild-typeâ- against a gene sequence containing a common mutation in CFTR. Look at the alignment and determine how the DNA sequence differs between them. What is the position number where they differ? How many and what nucleotides do they differ in? A â-â mark in one sequence in the alignment means that that base sequence is missing the corresponding bases in the other sequence. The sequence is a long one but the differences are in bolded bright red text. Matching sequence is marked with a | linking the two sequences. Look near the sequence AAATATCATC if you use FIND tool in Word.

In another file, you will an alignment of the reference translated into a protein sequence, compared to the mutant allele translated into protein sequence. The differences are again in red whereas the areas where the proteins match are in black. Look at the alignment. How do these two proteins differ? Again, find the position number and describe how they differ at that location. A â-â mark in the alignment means that amino acid is missing when compared to the other sequence.

4. Given that the CFTR gene can be analyzed for a mutation that causes CF, couples interested in being tested as carriers face several choices given the results.
What could be a consequence of a false positive result (couple is identified as carriers but they would not produce any children with symptoms)?

What could be a consequence of a false negative result (a test indicates the couple is not both carriers but they would produce some children with CF)?

5. The sensitivity of the test can vary with ethnic group. The following is a chart from the NCBI Genetic testing site. A sensitivity less than 100% would be likely to produce false negative results from an inability to determine that someone is carrier.

CF Carrier Test Sensitivity by Ethnic Group http://www.ncbi.nlm.nih.gov/projects/GeneTests/static/concepts/primer/ptscarr5.shtml
Ethnic Group ¹	Population Frequency of CF	Sensitivity of Carrier Detection ²
Caucasian	1 in 29	90%
Ashkenazi Jewish	1 in 29	97%
Native American	1 in 32	94%
Latino	1 in 46	57%
African-American	1 in 60	75%
Asian	1 in 90	30%

Why might different ethnic populations differ in the ability of the genetic test to identify carriers of CF?

Multiply questions here

Q2. What is the consequence of chromosome inversion on meiosis? (work on a zygote with one normal chromosome and one chromosome with an inversion)

Q3. Search the web or read the textbook. Find a disease that is caused by translocation. What kind of translocation causes the disease?

Q4. Briefly explain how downâs syndrome or other trisomy is generated (3 sentences should be enough for you to explain this clearly)

Q5. I mutated a culture of wild type E. coli cells and wanted to isolate mutants that are unable to synthesize uracil (a nitrogen base in RNA). How can I achieve my goal? (try to finish your answer in 2-3 sentences)

Q6. For the ura- mutant isolated in Q5, I want to convert it to URA+ by transformation. Please tell me how I can achive this transformation with 3 SIMPLE sentences

Q7. What is the difference and relationship between an Hfr cell and an F+ cell?

Q8. I want to set up a mating between an Hfr strain and an F- (ade- his- bio-) strain and detect bio+ recombinant. Please design the experiment for me. (What genotype for Hfr do you need to choose? How will you select your recombinant? etc).

Q9. I want to use phage T2 to transducer the wild type ADE2 gene from the wild type E. coli strain to an ade2- E. coli mutant. How can I do this experimentally? (please briefly describe the approach, not experimental details such as incubation for 10 min, etc).

Q10. We talked about recombination in both eukaryotes and prokaryotes. Are there any differences in these two recombination ? (what are they if there are?)

Q11. Whose (or what) experiment proves that DNA is the genetic material?

Q12. What knowledge did Watson and Crick use in constructing the DNA model?

Q13. How does the double helix model support the three major functions of genetic materials?

Q14. What is the major chemical force that holds DNA and histone together? Hydrogen bonds

Q15. If I label E. coli cells in an N15 medium overnight and chase cells in an N14 medium for 2 generations, what fraction of cells still carry the N15 label?

Q16. If a 1000 kilobase fragment of DNA has five evenly spaced replication origins and DNA polymerase moves at 1 kilobase per second, how many seconds will a cell take to produce two daughter molecules?

Q17. DNA polymerases catalyze the polymerization of nucleotides. Use the formula for enzyme catalyzed reaction (see the example) to describe DNA polymerases. Example: Enzyme Substrate A + substrate B -------------------ï product c + product D Q8. During DNA replication, what is the direction of the growing strand?

Q18. For DNA synthesis in cells, why are there a leading strand and a lagging strand?

Q19. The following is the DNA sequence of a template strand. If the primase begins to synthesize primers from the middle âgâ, what will the primer sequence be? (assuming the primer can be 8 nucleotides long) 5â GACTCTAgGACTCCT 3â

Q20. Both DNA polymerase I and DNA polymerase III synthesize DNA during DNA replication. Please state the different roles they played during DNA replication.