AI Article Synopsis

  • Candida albicans, a fungal pathogen, can switch between white and opaque cell types, with this switching typically regulated by the a1/α2 heterodimer in MTLa/α cells.
  • Recent research showed that some natural MTLa/α strains can switch under specific environmental conditions, but the regulatory mechanisms behind this are still unclear.
  • The study identified the transcription factor Ofi1 as a key regulator that enhances this white-to-opaque switching in clinical isolates, as deleting OFI1 decreased switching frequency and its stability.

Article Abstract

Candida albicans, an opportunistic fungal pathogen, is able to switch between two distinct cell types: white and opaque. While white-to-opaque switching is typically repressed by the a1/α2 heterodimer in MTLa/α cells, it was recently reported that switching can also occur in some natural MTLa/α strains under certain environmental conditions. However, the regulatory program governing white-opaque switching in MTLa/α cells is not fully understood. Here, we collected 90 clinical isolates of C. albicans, 16 of which possess the ability to form opaque colonies. Among the known regulators implicated in white-opaque switching, only OFI1 exhibited significantly higher expression in these 16 strains compared to the reference strain SC5314. Importantly, ectopic expression of OFI1 in both clinical isolates and laboratory strains promoted switching frequency even in the absence of N-acetylglucosamine and high CO , the optimal condition for white-to-opaque switching in MTLa/α strains. Deleting OFI1 resulted in a reduction in opaque-formation frequency and the stability of the opaque cell in MTLa/α cells. Ofi1 binds to the promoters of WOR1 and WOR3 to induce their expression, which facilitates white-to-opaque switching. Ofi1 is conserved across the CTG species. Altogether, our study reported the identification of a transcription factor Ofi1 as the critical regulator that promotes white-to-opaque switching in natural MTLa/α isolates of C. albicans.

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Source
http://dx.doi.org/10.1111/mmi.15222DOI Listing

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