Transcription and Translation - Campbell Flashcards
(41 cards)
What is a mutation responsible for β-thalassemia that lies outside any globin gene?
mutation near the orgin of replication of beta-globin, which distrubes nucleosome location, which decreases the regulation of beta-globin, decreasing the amount of beta-globin, resulting in beta-thalassemia.
The part of a gene that transcription factors bind to is known as what? Keep straight that this is made of DNA and transcription factors are proteins.
bind to the DNA in sequence specific manner at a certain place called the promoter region
Which of the following is NOT necessarily a conserved sequence (only one correct
response this time)?
A. a nucleotide sequence (motif) that is the same or nearly the same in a promoter region from multiple species
B. a nucleotide sequence (motif) that is the same or nearly the same in a gene from multiple species
C. an amino acid sequence (motif) that is the same or nearly the same in a protein in multiple species
D. the TATA box
E. a nucleotide sequence (motif) in a promoter region that is actively transcribed in such a manner so as to allow an organism to conserve energy.
E. a nucleotide sequence (motif) in a promoter region that is actively transcribed in such a manner so as to allow an organism to conserve energy.
A consensus sequence (only one correct response this time)
A. is the sequence that best agrees with a collection of conserved sequences.
B. is the sequence that allows an organism to conserve energy.
C. is the sequence that is calculated by bioinformatics software.
D. is not derived from conserved sequences.
E. cannot be an amino acid sequence.
A. is the sequence that best agrees with a collection of conserved sequences.
Can a human disease (e.g. a β-thalassemia) result from a promoter region mutation in DNA sequence (hint- the promoter region is not part of the region of DNA that encodes a protein)? If so, what is the reason?
Yes. The promoter region is very important, so any mutation in the promoter by beta-globin can result in beta-thalassemia.
Name three ways DNA synthesis (replication) and RNA synthesis (transcription) are alike.
Alike:
- both occur due to a large complex
- both have similar chemistry (5’->3’)
- both use base complementary rules
Differences:
DNA has much more proofreading than RNA
DNA has AGCT bases; RNA has RGCU
Describe the transcriptional regulation of the LDL receptor gene by cholesterol.
Include in your description what occurs at the membrane that initiates the regulation, where in the cell this occurs, the name of the transcription factor that results, where the transcription factor goes to activate the gene, and the site to which the transcription factor binds.
When cholesterol is low, there will be low levels of cholesterol in the endoplasmic reticulum, SCAP and SREBP (sterol regulatory element binding protein) move from the ER to the Cis Golgi. Proteases will cleave SREBP, and a part of the SREBP (now a transcription factor) moves to the nucleus and binds to the DNA at SRE (sterol regulator element).
What DNA abnormality causes Fragile X syndrome, and what does that cause to happen too much or too little? What is thought to be a large part of the reason reproductive cloning is so fraught with difficulty?
a Triple Nucleotide Repeat causes Fragile X syndrome. There is too many repeats (of CGG) and therefore there is more methylation, which throws off the regultaion and decreases the amount of FMR1 produced causing metal retardation.
Methylation is thought to be a large part of why reproductive cloning is so difficult in mammals.
What does rifampicin do? What does α-amanitin do? Which is thought of as an antibiotic, and which a poison, and why?
rifampicin is an antibiotic translational inhibitor (works against bacteria).
alpha-amanitin is a poison that inhibits transcription that affects humans.
What is the first step of RNA processing known as?
capping (adds methyl group to 5’ end to prepare strand for translation)
How many diseases are the result of the long poly-dT stretches of DNA that encode the polyA tail of mRNAs (hint- this is a trick question)?
None. The tail is just used for mRNA stability that is a part of processing, so it does not come from DNA
What is the function of polyadenylation?
It’s an enzyme that adds polyA tail to the 3’ end for mRNA stability
How is it possible to make more than one different proteins having different properties from one gene?
alternative splicing allows for multiples proteins to be made that have different functions from one gene. (Ex. troponins)
Can a human disease (e.g. a β-thalassemia) result from a mutation in DNA sequence in the intron (hint- the intron is a region of DNA that is spliced away before synthesis of a protein)? If so, what is the reason?
Yes. Sequences are important, even in intron information. In this case, splicing can be effected by the sequence of the intron, that can result in beta-thalassemia.
How are tRNAs involved in “breaking” the genetic code? What is at one end of a tRNA and what is at the other end?
tRNA segments the genetic code into groups of three (codons) that code for different amino acids. Each tRNA is specific for a certain amino acid.
What do we mean by “activation” of a tRNA? What is the enzyme that links the amino acid to the tRNA? What antibiotic has this step as a drug target?
Specific enzymes add amino acids (aminoacyl tRNA synthetases) to activate the tRNA
Mupirocin is an antibiotic that has this step as a drug target. (Isoleucyl aminoacyl tRNA synthetase)
Does the entire mRNA encode a protein? What is the role of the 5’ UTR? What is the role of the 3’ UTR?
No, only the portion from the start codon to the stop codon is translated. 5’ UTR regulates transcription. 3’ UTR regulates stability (lifetime)
Describe silent, missense, nonsense, and frameshift mutations. Which of these when mutated are likely to give rise to a genetic disease, and describe how the protein is changed? You may use globin proteins for your examples.
Silent mutation – point mutation resulting in the same A.A. being coded
Missense – point mutation resulting in a different A.A. being coded. (disease)
Nonsense – point mutation resulting in a stop codon. (disease)
Frameshift – insertion/deletion of one nucleotide that shifts the reading frame. (disease)
The start codon of a gene related to MAP kinase kinase kinase is located in exon 2. If the DNA sequence in exon 3 of the MAP kinase kinase kinase-related gene is mutated from ATG (which normally codes for methionine in the amino acid sequence) to ACG, how does that alter the amino acid sequence (consult the genetic code in Table 37-1 on p396 of Murray et al. IF you need to)?
Would that be a silent, missense, or nonsense
mutation, or would there be the possibility of another kind of amino acid sequence
change? How about if the mutation inverted the AT to TA (ATG to TAG)?
ATC to ACG = missense
ATG to TAG = nonsense
If a gene sequence in an INTRON is inverted from TGG to GGT, how does that alter the amino acid sequence (consult the genetic code in Table 37-1 on p396 of Murray et al. IF you need to)? Would that be a silent, missense, or nonsense mutation, or would there be the possibility of another kind of amino acid sequence change?
missense
How many subunits are in a ribosome, and what are their names? There are ribosomes in eukaryotes, prokaryotes, and mitochondria. Which of these are more similar, and what is the medical relevance of this?
2 subunits (1 small subunit and 1 large subunit).
Prokaryotic ribosomes are similar to Mitochondria ribosomes. These two are pretty different than eukaryotic ribosomes. The medical relevance is that antibiotics rely on the difference between prokaryotic and eukaryotic ribosomes to work, but because of their similarity to mitochondria ribosomes, the will slightly affect eukaryotes.
What are the three repeated steps of translation, repeated each time an amino acid is added to the growing polypeptide chain? What is the step that precedes these repeated steps, and what is the step that follows these repeated steps?
The repeated steps are:
1) binding of next tRNA
2) new tRNA is bound to the first tRNA and a peptide bond is formed.
3) mRNA and ribosome moves along, causing the first tRNA to leave and opening up the spot of binding at the new spot. (translocation)
Initiation phase begins translation and preceeds the repeated steps..
The step that follows these repeated step is called termination.
Accessory proteins IEF4E, EIF4G aid in termination
Accessory protein eEF2 aid in translocation.
Which step of translation is affected by macrolides? Aminoglycosides? Tetracyclines? Chloramphenicol?
These are all antibiotics:
Aminoglycosides: blocks initiation of translation
Tetracyclines: affects binding of tRNA
Chloramphenical: affects bonding step
Macrolides: affects translocation
What is the most serious adverse effect of chloramphenicol use?
fatal aplastic anemia
