Final answer:
Individuals suffering from both xeroderma pigmentosum and Cockayne syndrome have a deficit in the nucleotide excision repair pathway, which is crucial for repairing thymine dimers caused by UV exposure. This inability to repair DNA leads to increased skin cancer risk for XP patients and also encompasses neurological issues in CS.
Step-by-step explanation:
The deficit that explains the combined symptoms of xeroderma pigmentosum (XP) and Cockayne syndrome (CS) points to a dysfunction in DNA repair mechanisms, particularly the nucleotide excision repair pathway. Xeroderma pigmentosum is characterized by a failure to repair thymine dimers that form when skin cells are exposed to UV light, resulting in skin lesions and an increased cancer risk. Individuals with both XP and CS suffer from the consequences of unrepaired DNA damage, which in the case of CS also includes neurological and developmental issues.
Patients with these disorders lack the ability to adequately repair thymine dimers due to a defect in the nucleotide excision repair enzymes, leading to a distortion in the DNA structure and an increased likelihood of errors during DNA replication. This impairment in DNA repair greatly increases the risk of developing skin cancer as cells accumulate genetic damage over time. The condition exemplifies the critical role of the DNA repair systems in maintaining genomic integrity and preventing disease.