Final answer:
The DNA repair system most likely to detect and correct the defect when a cytosine becomes uracil in a mouse cell is the Base Excision Repair (BER) mechanism. This system involves specific enzymes that remove the incorrect uracil and replace it with the correct cytosine, thus preventing a possible G-C to A-T mutation.
Step-by-step explanation:
DNA Repair Mechanisms
When a cytosine in a mouse cell spontaneously deaminates and becomes uracil, the most likely DNA repair system to detect and correct this defect is the Base Excision Repair (BER) mechanism. This repair process involves the detection of uracil, which is not normally found in DNA, by specific DNA glycosylases. These enzymes catalyze the hydrolysis and removal of the uracil from the DNA backbone. Following removal, an enzyme complex fills in the gap with the correct deoxycytidine phosphate residue, thus returning the DNA to its proper structure.
Spontaneous deamination is a common form of DNA damage that can lead to mutations if not repaired. Deamination of cytosine to uracil, if left uncorrected, could result in the substitution of a G-C base pair with an A-T pair during DNA replication. Therefore, the repair by the Base Excision Repair system is crucial to maintain the integrity of the genetic material and prevent mutations that could have deleterious effects on the organism.
There are other DNA repair pathways—including Nucleotide Excision Repair, Transcription Coupled Repair, Non-homologous End-Joining, and Homologous Recombination—that fix various forms of DNA damage to ensure the stability and proper functioning of the cell's genome.