Telomeres are composed of G-rich repeating DNA sequences that protect the ends of linear chromosomes from degradation and end-to-end fusions. Despite their protective function, telomeres undergo progressive shortening with each cell division due to the end-replication problem and eventually trigger cellular senescence. To counteract this shortening, most proliferating cells express telomerase, an enzyme that adds telomeric repeats at chromosome termini. However, 10-15% of cancer cells can maintain their telomeres even in the absence of telomerase by adopting a recombination-based mechanism, popularly known as Alternative Lengthening of Telomeres (ALT). ALT involves homologous recombination and the formation of extrachromosomal circles. The budding yeast Naumovozyma castellii is an attractive model for studying ALT, due to its ability to bypass the growth crisis following telomerase loss and rapidly switch to recombination-based telomere maintenance. This study investigated the roles of recombination genes RAD51 and RAD52 in the formation of extrachromosomal circles in N. castellii and assessed how their loss affects telomere length and structure in both ALT-positive and ALT-negative cells. N. castellii strains lacking both telomerase and the recombination genes demonstrated interclonal variation in telomere length, with lengths comparable to or below that of the ALT control (est2△). Surprisingly, the absence of these genes in the telomerase-proficient cells produced elongated telomeres, potentially due to unconstrained telomerase activity or the accumulation of aberrant telomeric structures. The C-circle abundance in the ALT control was not significant, and as a result, the role of RAD51 and RAD52 genes in extrachromosomal telomeric circle formation could not be fully established. No subtelomeric circle amplification was detected in any strain, suggesting that ALT in the N. castellii strains examined was restricted to telomeric sequences. Future studies analyzing cells across multiple streaks will be required to fully characterize the mechanism of circle-based telomere maintenance in this organism.