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Slipped strand mispairing (SSM, also known as replication slippage) is a mutation process which occurs during DNA replication. It involves denaturation and displacement of the DNA strands, resulting in mispairing of the complementary bases. Slipped strand mispairing is one explanation for the origin and evolution of repetitive DNA sequences. [1]
For example, denaturation of DNA due to high temperatures results in the disruption of base pairs and the separation of the double stranded helix into two single strands. Nucleic acid strands are capable of re-annealling when " normal " conditions are restored, but if restoration occurs too quickly, the nucleic acid strands may re-anneal ...
Spontaneous deamination of 5-methylcytosine results in thymine and ammonia. This is the most common single nucleotide mutation. This is the most common single nucleotide mutation. In DNA, this reaction, if detected prior to passage of the replication fork, can be corrected by the enzyme thymine-DNA glycosylase , which removes the thymine base ...
The most famous example is the hyperchromicity of DNA that occurs when the DNA duplex is denatured. [1] The UV absorption is increased when the two single DNA strands are being separated, either by heat or by addition of denaturant or by increasing the pH level. The opposite, a decrease of absorbance is called hypochromicity.
Translation can be downregulated by miRNAs (microRNAs). These RNA strands can cleave mRNA strands they are complementary to and will thus stop translation. [15] Translation can also be regulated via helper proteins. For example, a protein called eukaryotic initiation factor-2 can bind to the smaller subunit of the ribosome, starting translation.
Limited proteolysis of a polypeptide during or after translation in protein synthesis often occurs for many proteins. This may involve removal of the N-terminal methionine, signal peptide, and/or the conversion of an inactive or non-functional protein to an active one.
Initiation of translation is regulated by the accessibility of ribosomes to the Shine-Dalgarno sequence. This stretch of four to nine purine residues are located upstream the initiation codon and hybridize to a pyrimidine-rich sequence near the 3' end of the 16S RNA within the 30S bacterial ribosomal subunit . [ 1 ]
DNA end resection is key in determining the correct pathway in NHEJ. For NHEJ pathway to occur, positive regulators such as the Ku and MRX complex mediate recruitment of other NHEJ-associated proteins such as Tel1, Lif1, Dnl4, and Nej1. [3] Since NHEJ does not rely on end resection, NHEJ could only happen in the G1 phase of the cell cycle.