WorksheetsBIO 121 EXAM 2 REVIEW
Total questions: 26
Worksheet time: 20mins
These proteins are required for transcription of all genes expressed in all cells, regardless of cell-type.
Promoters
TFII Transcription Factors
Tissue Specific Transcription Factors
RNA Pol II
B and D
This is the regulatory region of DNA that can be found upstream, downstream, or within introns of genes.
Exons
Promoters
TFIIs
Enhancers
Fzd5 is a gene that is normally expressed in intestinal Paneth cells, but not in absorptive cells. How is Fzd5 normally expressed in Paneth cells, but not absorptive cells?
The Fzd5 enhancer is present in the genome of Paneth cells, but not absorptive cells
There is a Tissue Specific (TS) transcription factor expressed in Paneth cells that promotes Fzd5 transcription, but there is no such TS transcription factor in absorptive cells
The Fzd5 gene is not present in the genome of absorptive cells
You are a molecular biologist working in a lab. You want to induce (i.e. force) the expression of Fzd5 in absorptive cells. How could you do this?
Introduce the TS transcription factor from Paneth cells (that binds to the Fzd5 enhancer) in absorptive cells
Introduce RNA Pol II in absorptive cells
Remove Fzd5 promoter sites from Paneth cells
Add the Fzd5 enhancer (present in Paneth cells) to the absorptive cells
Which of the following statements about TF II transcription factors is false?
TFII transcription factors bind promoters
TFII transcription factors transcribe genes
TFII transcription factors are found in all eukaryotic cells and are required for transcription
TFII transcription factors help recruit RNA Pol II to the promoter
Which of the following is required for Nonsense Mediated Decay to occur?
A frameshift mutation in the open reading frame
A shortened Poly A tail
Detection of a premature termination codon upstream of an EJC (Exon Junction Complex)
Protein misfolding resulting from failed attempts by chaperone proteins
C and D are both correct
You are examining the expression of a gene called DISC1 in a neuron. You notice that the cell transcribes the DISC1 gene and produces nRNA, but there is no DISC1 protein present. Which of the following NOT a possible explanation?
A nonsense mutation in the coding sequence caused the mRNA to be degraded
A miRNA prevented association of the mRNA with translation machinery
A miRNA recruited a protein-digesting enzyme (protease) to the mRNA.
eIFs did not get recruited to the mRNA
None of the above (all could explain the lack of DISC1 protein)
You are examining a cell that has a very high amount of casein. What is the most likely cause of the increase in casein?
Exposure to prolactin prevented the 5’ cap from forming on the casein nRNA
The casein nRNA was differentially spliced to produce various isoforms
Exposure to prolactin prevented the formation of the casein mRNA poly-A tail
Prolactin increased expression of an miRNA that binds the casein mRNA transcript
Exposure to prolactin increased the length of the casein mRNA poly-A tail
A protein is being synthesized in the cytosol. It begins to misfold during translation because all of the hydrophobic residues are inappropriately interacting with other residues. Which of the following proteins is not functioning properly?
Calnexin
Calreticulin
Hsp70
Hsp60
C and D are correct
You are examining a group of cells that has very high amounts of protein aggregates. You are making a list of proteins that could be improperly functioning, and thereby causing this defect. Which of the following proteins should NOT be on your list?
Calnexin
Hsp60
Hsp70
Proteasome
None of the above (all of these should be on the list)
A multi-pass transmembrane protein is found in the ER membrane. Which of the following is NOT true?
It was inserted by a protein translocator
It was inserted post-translationally
Start-stop transfer sequences determined how many times the protein passed through the membrane
None of the above (all are true)
All of the above (all are false)
Which of the following is NOT a true statement about proteolysis and phosphorylation?
Both can change the function of proteins
Both are irreversible
Both can activate proteins
Both can can inactivate proteins
A and B are both untrue statements
Which of the following would not change the function of a protein?
Glycosylation of the protein
Change in the length of the Poly A tail of the mRNA transcript encoding the protein
Phosphorylation of a protein
Lipid modification of the protein
None of the above (all would change the function of a protein)
You are analyzing the activity of the protein ps53 in two different cell types. You notice that ps53 has the same primary structure in both cells, but has a different function in each cell. What could be the reason for the functional difference in this case?
Two different splicing isoforms of ps53
Ps53 may have a different set of covalent modifications in each cell
One ps53 is the result of leaky scanning and the other is not
All of the above
A and B are both correct
Which of the following describes allostery?
Binding of a molecule at one site of a protein reduces binding of a molecule at a different site on the same protein
Removal of a molecule that is physically blocking the binding site of a protein allows the protein to bind its substrate
A molecule binding at one site of a protein increases binding of a molecule at a different site of the same protein
All of the above
A and C only
What modification allows differentiating cells to maintain the repression state of specific genes with all of its mitotic descendants?
Histone acetylation
DNA acetylation
DNA methylation
Histone demethylation
None of the above
You are studying a disease caused when the gene TGFb is not transcribed in fibroblasts. All other genes are transcribed normally. To investigate why TGFb is not transcribed, you create a reporter transgene by putting GFP under the control of the TGFb enhancer found in the diseased fibroblasts. You put this reporter transgene into a normal fibroblast. The normal fibroblast with your reporter transgene turns green (GFP is expressed). What does this result indicate?
The diseased form of the TGFb enhancer must be mutated in a way that prevents binding to the enhancer
The enhancer is not the problem — the disease could be the result of a mutated TSTF in the diseased fibroblast that cannot bind the TGFb enhancer.
The enhancer is not the problem — the disease could be the result of a mutated RNA Pol II in the diseased fibroblast that cannot bind any promoters.
None of the above
B and C are both correct
What is the significance of DNA being methylated on cytosines at CpG islands?
It enables methylation of the complementary DNA strand by Dnmt1 (perpetuating methyltransferase)
IT cases the propagation of methylation to nearby genes on the chromosome
CpG islands are only present in intronic sequences
All of the above
A and B only are correct
The gene encoding Dnmt3 (de novo methyltransferase) has a premature termination (stop) codon in its very first exon. Which of the following would likely result because of this mutation?
Nonsense Mediated Decay of the Dnmt3 mRNA in the nucleus
DNA would not be methylated in a cell with this mutation
DNA would be methylated on one strand, but the opposing strands would not be methylated
A and B are both correct
B and C are both correct
An nRNA (pre-mRNA) is transcribed, but not transported out of the nucleus into the cytosol. Which of the following explanations does NOT make sense?
Splicing did not occur properly; introns are still present and there are no detectable EJCs on the transcript
PolyA binding proteins did not bind the PolyA tail
The Cap Binding Complex did not bind to the 5’ cap
The capping enzymes that add the 5’ cap could not associate with the C-terminal Domain (CTD) of RNA Pol II
eIFs could not promote the formation of the circular conformation of the mRNA
A macrophage is exposed to LPS from a bacterial cell, which causes a change in the site of Poly-A tail addition in the nRNA encoded by the defensin gene (defensin encodes a protein that helps macrophages in their defense against bacteria). What is the most likely consequence of this change?
It changes the translational regulation performed by the 3’UTR of defensin mRNA
It changes the amount of defensin nRN9A that is transcribed
It changes the translational regulation performed by the 5’UTR of defensin mRNA
Degradation of the 5’cap, which leads to degradation of the mRNA transcript
It causes alternative splicing of the defensin mRNA
A gene is transcribed, but the mRNA it encodes is not exported from the nucleus into the cytosol. Which of the following are possible reasons why?
No exon junction complexes were added
No cap binding complex was added
A and B are both correct
All of the above are correct
Which of the following could increase the amount of peptide translated from an mRNA transcript?
Increase in poly a tail
Remove the five cap tail
Express different splicing recognition factors
Shorten the poly a Tail
Both A and C are correct
You are analyzing two proteins that are identical except that one is missing 20 amino acids at the carboxy terminus. What likely happened? (Note: the carboxy terminus corresponds to the 3’ end of the mRNA).
Leaky scanning
Poly A tail was shorter on the shorter protein
Alternative Poly A site was used
There was no poly A site
All of the above
An osteocyte and a chondrocyte express splicing isoforms of a protein called BMP4. Which of the following explain the differential splicing of BMP4 in these two cell types?
Nonsense mediated decay of bmp4 is occurring in one of the cells.
A frame shift mutation in the bmp4 open reading frame
Different splicing recognition factors expressed in different cells
A different poly A site was used
Which of the following would NOT cause RNA degradation in the nucleus?
RNA processing enzymes were unable to associate with the CTD or RNA pol II
The 5’ cap was not added
Splicing didn’t occur normally
polyA binding proteins did not bind the poly A tail
A nonsense mutation/ premature termination codon was detected upstream prior to an EJC
