Final answer:
Thymine dimers can slow down or cause errors in transcription and replication by distorting the DNA structure, leading to frameshift or point mutations. Mechanisms like nucleotide excision repair exist to correct such damage, but conditions like xeroderma pigmentosum can impede this repair, increasing the risk of cancer.
Step-by-step explanation:
The impact of thymine dimers on transcription and replication is significant, as they can stall these critical cellular processes. Thymine dimers occur when two adjacent thymine bases covalently bond, usually due to UV light exposure. This dimerization distorts the DNA double helix structure, which can impede the DNA replication machinery. Specifically, DNA polymerase may replicate the dimer incorrectly, leading to frameshift or point mutations. If the dimers are not repaired, this can lead to errors during DNA replication and even during transcription, where RNA polymerase may fail to transcribe past the dimer.
Nonetheless, cells are equipped with repair mechanisms, such as nucleotide excision repair, where the damaged DNA strand with the dimer is recognized, excised, and replaced with the correct bases. However, in individuals with conditions like xeroderma pigmentosum, there is a deficiency in repairing such damage, which elevates the risk of skin cancer.
Therefore, the correct answer to the effects of thymine dimers is that they can slow down or cause errors in transcription and replication, covering choices B and C from the options presented. However, if left unrepaired, they can have a more severe impact, potentially leading to a halt in these processes depending on the cellular context and repair capabilities.