Final answer:
The false statement is C, as uvr-/recA- double mutants cannot tolerate up to 50 thymine dimers because they lack the necessary repair capabilities due to defects in nucleotide excision repair and recombination pathways.
Step-by-step explanation:
The question presents a collection of statements related to the ability of cells to repair damage caused by UV light, specifically the formation of thymine dimers in DNA.
These statements involve the nucleotide excision repair mechanism, which is capable of excising and replacing damaged DNA such as thymine dimers. The incorrect statement among the options provided is C.
The uvr-/recA- double mutants can tolerate up to 50 thymine dimers. This is false because uvr mutants lack nucleotide excision repair capability, and when combined with a recA mutation, the cell loses essentially all repair capabilities, including the ability to tolerate a significant number of thymine dimers.
People with xeroderma pigmentosa, who are deficient in nucleotide excision repair enzymes, demonstrate the importance of this mechanism as they have an increased risk of developing skin cancer due to DNA damage that is not repaired.
The interconnected nature of the uvr (excision repair) and rec (recombination) pathways is highlighted in how cells normally handle this kind of damage.