Raw sequence reads of Candida albicans Hap31 and Hap32, two subunits of the CCAAT binding complex

The opportunistic fungal pathogen Candida albicans has recently impacted a substantial portion of the population. The highly conserved CCAAT-binding complex (CBC), also known as the Hap complex in yeast, plays a critical role in multiple cellular functions. Additionally, the cell wall of this pathogen serves as an effective barrier against environmental stresses and undergoes continuous renewal through a complex regulatory network. This network is tightly controlled by numerous cell signaling pathways and transcription factors. Mutants with individual deletions of components of the Hap complex were generated and compared to the wild-type strain to investigate the regulatory role of the CBC in cell wall maintenance and biofilm formation. Additionally, RNA sequencing was performed to uncover novel insights into the regulatory pathways associated with the CBC. Deletion of CBC components significantly impacts the cell wall structure and composition, leading to an imbalance in the cell wall carbohydrate profile, as well as cell wall unmasking, which triggers the activation of the Cell Wall Integrity (CWI) signaling pathway. These alterations subsequently affect the ability to form biofilms on polystyrene surfaces. Notably, the small GTPase Rhb1 is implicated in CBC-mediated CWI maintenance. Moreover, RNA sequencing of the expression profiles of the two Hap3 paralogs suggests their involvement in rRNA processing, ribosomal biogenesis, carbohydrate transport and metabolism, and amino acid biosynthesis, all contributing to cell wall maintenance. Our findings provide novel insights into the molecular pathways that govern cell wall biogenesis. The discovery of this regulatory mechanism is crucial for understanding the relationship between the highly conserved CBC and cell wall maintenance in C. albicans. Candida albicans SC5314 was used as the parent strain. From the the SC5314, deleted mutants of the HAP31, HAP32 genes, and the double-deleted mutants of the HAP31-HAP32 were constructed. Then, RNA sequencing was performed to explore the transcription profile of these mutants. Raw FASTA files were provides in this submission, which are three biology replicated samples from each of the strains, including the SC5314 for the control.