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Abstract

A normal resident of healthy humans and warm-blooded animals, is a commensal fungus that is also among the most common opportunistic pathogens of humans. forms unique morphological structures called chlamydospores, which are large, spherical, thick-walled structures formed at the ends of hyphae that have unknown biological function. My goal is to discover the regulatory network controlling chlamydospore formation in . By determining this network, we can gain insight into the biological roles of chlamydospores in the lifestyle, better understand morphological transitions, and determine the selective advantage (if any) provided by chlamydospores to this pathogenic fungus. To determine this regulatory network, I have screened a library of 211 transcription factor (TF) homozygous deletion mutants to assay for their abilities to form chlamydospores under standard chlamydospore-inducing growth conditions. I have identified seven TF mutants that fail to produce any chlamydospores andthree TF mutants that produce high levels of chlamydospores relative to WT. To characterize the transcriptional changes occurring during chlamydospore formation, I have performed RNA sequencing (RNA-seq) on these identified regulator mutants to uncover the differentially regulated target genes of each chlamydospore regulator. I will use genome-wide chromatin immunoprecipitation followed by sequencing (ChIP-seq) on epitope-tagged versions of these regulators to determine which genes are directly under the control of each TF. RNA-seq coupled with ChIP-seq will allow me to determine the regulatory network controlling chlamydospore formation in .

  • This is an open-access article distributed under the terms of the Creative Commons Attribution License.
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/content/journal/acmi/10.1099/acmi.cc2021.po0013
2021-12-17
2025-02-07
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/content/journal/acmi/10.1099/acmi.cc2021.po0013
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