Fancc, a gene within the Fanconi anemia (FA) gene family, plays crucial roles in DNA damage signaling, oxygen radical metabolism, signal transduction, transcriptional regulation, and apoptosis [3]. It is part of the FA/BRCA repair pathway, which is vital for maintaining genomic stability [4]. Genetic models, such as gene knockout (KO) mouse models, are valuable tools for studying Fancc's functions.

In meiotic studies, Fancc was identified as a new anti-crossover (anti-CO) gene in Arabidopsis thaliana, and its physical interaction with Fance-Fancf is conserved from vertebrates to plants. Mutations in Fancc, along with Fance or Fancf, can partially rescue CO-defective mutants, especially in female meiosis. Loss of function of these genes leads to synthetic meiotic catastrophe with the pro-CO factor MUS81, suggesting that Fancc, together with Fance and Fancf, regulates meiotic recombination [1].

In traumatic spinal cord injury (SCI) mouse models, FANCC deficiency was found to mediate microglial pyroptosis, secondary neuronal apoptosis, and neurological damage. Overexpression of FANCC suppressed microglial pyroptosis via inhibiting p38/NLRP3 expression, reducing neuronal apoptosis, while knockdown of FANCC had the opposite effect [2].

In conclusion, Fancc is essential for regulating meiotic recombination and has a significant impact on processes related to SCI. Studies using KO mouse models have revealed its role in maintaining genomic stability during meiosis and in modulating neuroinflammatory responses after SCI, providing insights into potential therapeutic targets for related diseases.