Aspergillus nidulans snxA, an ortholog Saccharomyces cerevisiae Hrb1/Gbp2 messenger RNA shuttle proteins, is in contrast to budding yeast, involved in cell cycle regulation, in which snxA1 and snxA2 mutations as well as a snxA deletion specifically suppress the heat-sensitivity of mutations in regulators of the CDK1 mitotic induction pathway. All three alleles exhibit strong cold-sensitive lethality, and at the permissive temperature for growth, snxA mRNA and protein expression are strongly repressed. Initial attempts to identify the causative snxA mutations revealed no defects in the SNXA protein. However, in further genetic analyses, snxA1/A2 cold-sensitivity displayed strong linkage to markers on different chromosomes, suggesting the possibility of a chromosomal rearrangement. Whole-genome sequencing followed by Southern blot revealed a chromosome I - II reciprocal translocation with breakpoints in the snxA first intron and the fourth exon of a GYF-domain gene that we have named gyfA. Surprisingly, a gyfA deletion and a reconstructed gyfA translocation allele both suppressed the heat-sensitivity of CDK1 pathway mutants in a snxA+ background, demonstrating that the reciprocal translocation simultaneously interrupted two unrelated genes, both of which act through the CDK1-CyclinB axis to restrain the G2-M transition, and for the first time identifying a role in G2-M regulation for a GYF-domain protein. To better understand snxA1/A2 reduced expression, we generated suppressors of snxA cold-sensitivity, and discovered two suppressor genes: (1) loss of the abundant nucleolar protein nsr1/nucleolin bypassed the requirement for snxA and (2) loss of the set2 histone H3 lysine36 (H3K36) methyltransferase rescued hypomorphic snxA mutants by restoring full transcriptional proficiency. These phenotypes were largely mirrored by a non-methylatable histone H3K36L mutant, indicating that methylation of H3K36 acts normally to repress transcription at the snxA locus. These observations are in line with known set2 functions in preventing excessive and cryptic transcription of active genes.