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Molecular Genetics - Final Exam Problems | BI 381, Exams of Molecular biology

Southeast Missouri State University (SEMO)Molecular biology
Prof. Allen C. Gathman

Material Type: Exam; Professor: Gathman; Class: Molecular Genetics; Subject: Biology; University: Southeast Missouri State University; Term: Spring 2009;

Typology: Exams

Pre 2010

Uploaded on 08/08/2009

koofers-user-z87
koofers-user-z87 🇺🇸

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BI 381 Final Spring
2009
Instructions: relax.
1. a. (15 points) Fill in the rest of this two base-pair DNA molecule. Show covalent bonds as
lines, hydrogen bonds as dotted lines, double bonds as double lines, carbons in a ring as
corners, and other atoms as their atomic symbols. You need not show hydrogens unless they
are part of hydrogen bonds or have some other functional significance.
MARK THE 5' and 3' ends of EACH STRAND.
pf3
pf4
pf5

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Download Molecular Genetics - Final Exam Problems | BI 381 and more Exams Molecular biology in PDF only on Docsity!

BI 381 Final Spring

Instructions: relax.

  1. a. (15 points) Fill in the rest of this two base-pair DNA molecule. Show covalent bonds as lines, hydrogen bonds as dotted lines, double bonds as double lines, carbons in a ring as corners, and other atoms as their atomic symbols. You need not show hydrogens unless they are part of hydrogen bonds or have some other functional significance. MARK THE 5' and 3' ends of EACH STRAND.
  1. de Boer et al. wanted to know what caused premature aging in XPD-^ mice (also known as TTD mice). In their experiment, they made crosses to produce XPA-/XPD-^ double mutants. XPA- mice completely lack nucleotide excision repair (NER); XPD-^ mice have partial defects in both NER and transcription. They were testing two hypotheses:  Premature aging in XPD-^ mice is caused by the defect in transcription alone.  Premature aging in XPD-^ mice is caused by the combination of defects in transcription and NER. (10 points) What did each of the hypotheses predict about aging in the double mutant mice, compared to aging in single mutant XPD-^ and wild type mice? Explain.
  2. (10 points) The diagram below shows a pre-mRNA, and two ways that it can be spliced. If a splicing repressor protein binds near the 3’ splice site of intron 1, what exons will be in the mature mRNA? Explain how this will occur, including where specific snRNPs will bind.
  1. (10 points) Godowski et al. proposed two hypotheses to explain the mechanism by which the glucocorticoid receptor (GR) is activated: induction and derepression. They transfected cell cultures with two plasmids (see last page of test) in order to test the hypotheses. Describe what they did in the experiment, and explain the role of each plasmid.
  2. a. (5 points) A baby is XYY. How did this condition arise, in what kind of cell division, in whom, when,? b. (5 points) Diagram the aberrant cell division described above.
  1. The classic enzyme imbalance hypothesis explaining phenotypic abnormalities in aneuploids starts with the assertion that the amount of an enzyme produced in a cell is proportional to the number of copies of the gene encoding that enzyme. To test this assertion, Guo and Birchler measured the amounts of mRNA transcribed from the Adh2 gene in corn embryos with various karyotypes. The Adh2 gene is located on the short arm of chromosome 4 (4S). a (10 points) Guo and Birchler measured the amount of Adh2 mRNA and the amount of rRNA extracted from corn embryos with various karyotypes, and calculated this ratio: mRNA ( t ested karyotype ) rRNA mRNA ( diploid ) rRNA to find the standardized amount of Adh2 mRNA expression for each of the embryos. For each embryo karyotype described below, give the relative amount (a number) of Adh2 mRNA expression predicted by the classic enzyme imbalance hypothesis. Karyotype PREDICTED Amount of Adh2 mRNA (Standardized using formula above) Diploid Monosomic-1L Trisomic - 1L Monosomic - 4S Trisomic - 4S

Plasmids for question 5.