| Summary: | Fungal infection is initiated by the adhesion of pathogens to biotic and abiotic surfaces, with various manifestations including biofilm formation and invasive growth, etc. A previous report, though devoid of functional data, speculated that the <i>Schizosaccharomyces pombe</i> glycoprotein SPBPJ4664.02 could be the homology of <i>Saccharomyces cerevisiae</i> Flo11. Here, our studies with <i>S. pombe</i> substantiated the previously proposed speculation by (1) the deletion of <i>SPBPJ4664.02</i> attenuated biofilm formation and invasive growth in <i>S. pombe</i>; (2) the <i>S. pombe</i>’s lack of <i>SPBPJ4664.02</i> could be complemented by expressing <i>S. cerevisiae flo11</i>. Furthermore, indole-3-acetic acid (IAA) and dodecanol were examined in <i>S. pombe</i> for their respective effects on biofilm formation. IAA and dodecanol at high concentrations could inhibit biofilm formation, whereas opposing effects were observed with low concentrations of these molecules. Mechanism studies with the <i>SPBPJ4664.02</i>Δ and <i>SPBPJ4664.02</i>Δ/<i>flo11</i><sup>OE</sup> versus the wild type have demonstrated that IAA or dodecanol might exert regulatory effects downstream of SPBPJ4664.02 in the signaling pathway for biofilm formation. Moreover, our research extrapolated to <i>Candida albicans</i> has pinpointed that IAA inhibited biofilm formation at high concentrations, consistent with the transcriptional downregulation of the biofilm-related genes. Dodecanol suppressed <i>C. albicans</i> biofilm formation at all the concentrations tested, in accord with the downregulation of biofilm-related transcripts.
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