TLS Online TPP Program

#Id: 7062


In a phenomenon called codon bias, some codons for a particular amino acid are used more frequently (sometimes much more frequently) than others. A minimum of 32 tRNAs are required to translate all 61 codons (31 to encode the amino acids and 1 for initiation) due to wobble positioning

#Unit 3. Fundamental Processes #Prokaryotic Translation #Part B Pointers
More Pointers
TLS Online TPP Program

#Id: 3299

#Unit 3. Fundamental Processes

Another example of a fail-safe system is a glycosylase that removes a T opposite a G. Such a T:G mismatch can arise, as we have seen, by spontaneous deamination of 5-methylcytosine,which occurs frequently in the DNA of vertebrates. 

TLS Online TPP Program

#Id: 3301

#Unit 3. Fundamental Processes

DNA lesions that cause large distortions in the helical structure of DNA generally are repaired by the nucleotide-excision system, a repair pathway critical to the survival of all free-living organisms. 

TLS Online TPP Program

#Id: 3303

#Unit 3. Fundamental Processes

Nucleotide excision repair in E. coli is largely accomplished by four proteins: UvrA, UvrB, UvrC, and UvrD





TLS Online TPP Program

#Id: 3306

#Unit 3. Fundamental Processes

Unlike base excision repair, the nucleotide excision repair enzymes do not recognize any particular lesion. Rather, this system works by recognizing distortions to the shape of the double helix, such as those
caused by a thymine dimer or by the presence of a bulky chemical adduct on a base.

TLS Online TPP Program

#Id: 3309

#Unit 3. Fundamental Processes

Nucleotide excision repair in human cells. 
A DNA lesion that causes distortion of the double helix, such as a thymine-thymine dimer, is initially recognized by a complex of the XP-C (xeroderma pigmentosum C protein) and 23B proteins.




TLS Online TPP Program

#Id: 3311

#Unit 3. Fundamental Processes

Not only is nucleotide excision repair capable of mending damage throughout the genome, but it is also capable of rescuing RNA polymerase, the progression of which has been arrested by the presence of a lesion in the transcribed (template) strand of a gene, this phenomenon, known as transcription-coupled repair.