Overexpression of Quorum Sensing Transcription Factors NRG1 and CQS2 Affects Filamentation in Cryptococcus neoformans

Emma Blackburn ’22

Student: Emma Blackburn ’22
Research Mentor: Xiaorong Lin (University of Georgia Department of Microbiology)

Quorum sensing a major mechanism of cellular communication regulates the expression of genes in response to cell density. This communication is facilitated by various proteins that act as signals. We hypothesized two potential quorum sensing proteins, specifically transcription factors to be responsible for this communication. We found that artificially producing these proteins caused the cell morphology of Cryptococcus neoformans to change.

Cryptococcus neoformans is an opportunistic fungal pathogen responsible for cryptococcal meningitis, a lethal infection most prominent in immunocompromised individuals. The disease kills over 180,000 people annually. C. neoformans utilizes quorum sensing, an essential form of communication that enables the organism to regulate gene expression in response to changes in cell density. Quorum sensing is involved in cryptococcal progression within the host. Quorum sensing relies on autoinducers, which are chemical signals released that increase proportionally with cell density. QSP1, a quorum sensing peptide, of C. Neoformans, activates the transcription factors NRG1 and CQS2. I discovered that overexpression of these transcription factors results in phenotypic changes in filamentation and the growth rate, both essential components of virulence.