Cryptococcus neoformans is a fungal pathogen that causes cryptococcosis, a disease that kills almost 200,000 people worldwide each year. A unique feature of this deadly yeast is its polysaccharide capsule, which is known to be associated with its virulence. Here, we systematically explore the effects of all possible combinations of 4 capsule-inducing signals on gene expression, cell size, and capsule size. These signals are medium (YPD, DMEM or RPMI), temperature (30°C or 37°C), CO2 (room air or 5%), cAMP (0 mM or 20 mM), and pH buffer (HEPES/no HEPES). We explore the effects of exogenous cAMP at a range of concentrations and of deletions of cAMP pathway genes PKR1, PDE1, and PDE2. We present a computational framework for identifying a set of genes that are putatively associated with capsule induction. In addition, we follow up with experiments to validate and corroborate the hypotheses from the computational analysis in search of new genes that may be involved in capsule growth.
","abstract_html":"<p><em>Cryptococcus neoformans</em> is a fungal pathogen that causes cryptococcosis, a disease that kills almost 200,000 people worldwide each year. A unique feature of this deadly yeast is its polysaccharide capsule, which is known to be associated with its virulence. Here, we systematically explore the effects of all possible combinations of 4 capsule-inducing signals on gene expression, cell size, and capsule size. These signals are medium (YPD, DMEM or RPMI), temperature (30°C or 37°C), CO<sub>2</sub> (room air or 5%), cAMP (0 mM or 20 mM), and pH buffer (HEPES/no HEPES). We explore the effects of exogenous cAMP at a range of concentrations and of deletions of cAMP pathway genes <em>PKR1</em>, <em>PDE1</em>, and <em>PDE2</em>. We present a computational framework for identifying a set of genes that are putatively associated with capsule induction. In addition, we follow up with experiments to validate and corroborate the hypotheses from the computational analysis in search of new genes that may be involved in capsule growth.</p>","abstract_has_math":false,"creators":["Jung, Yu Min"],"institution":null,"degree_name":"Master of Science (MS)","degree_level":"Thesis","degree_discipline":"Computer Science & Engineering","degree_department":null,"school":null,"contributors":["Michael Brent","Tamara Doering Jeremy Buhler"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2022,"date_issued":"2022-08-01T07:00:00Z","date_published":"2022-08-01T07:00:00Z","updated_at":"2026-07-24T06:13:31Z","subjects":["Bioinformatics","Engineering","Systems Biology"],"languages":["English (en)"],"rights":["I have not registered my thesis with the U.S. Copyright Office, and do not intend to."],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["https://openscholarship.wustl.edu/eng_etds/752"],"render_values":[{"text":"https://openscholarship.wustl.edu/eng_etds/752","href":"https://openscholarship.wustl.edu/eng_etds/752","code":true}]}]},"links":{"outbound_url":"https://doi.org/10.7936/0j5k-6e34","outbound_label":"DOI","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Michael Brent","Tamara Doering Jeremy Buhler"]},{"key":"dc:creator","label":"Author","values":["Jung, Yu Min"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2022-06-17T07:00:00Z"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Computer Science & Engineering","McKelvey School of Engineering"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Thesis"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Master of Science (MS)"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Bioinformatics","Engineering","Systems Biology"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["English (en)"]},{"key":"dc:rights","label":"Dc Rights","values":["I have not registered my thesis with the U.S. Copyright Office, and do not intend to."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://doi.org/10.7936/0j5k-6e34","https://openscholarship.wustl.edu/eng_etds/752"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Cryptococcus neoformans is a fungal pathogen that causes cryptococcosis, a disease that kills almost 200,000 people worldwide each year. A unique feature of this deadly yeast is its polysaccharide capsule, which is known to be associated with its virulence. Here, we systematically explore the effects of all possible combinations of 4 capsule-inducing signals on gene expression, cell size, and capsule size. These signals are medium (YPD, DMEM or RPMI), temperature (30°C or 37°C), CO2 (room air or 5%), cAMP (0 mM or 20 mM), and pH buffer (HEPES/no HEPES). We explore the effects of exogenous cAMP at a range of concentrations and of deletions of cAMP pathway genes PKR1, PDE1, and PDE2. We present a computational framework for identifying a set of genes that are putatively associated with capsule induction. In addition, we follow up with experiments to validate and corroborate the hypotheses from the computational analysis in search of new genes that may be involved in capsule growth.
"]},{"key":"dc:title","label":"Title","values":["The Effects of Host-like Environmental Signals and Gene Expression on Capsule Growth in Cryptococcus neoformans"]}]}],"canonical_facts":{"dc:contributor":["Michael Brent","Tamara Doering Jeremy Buhler"],"dc:creator":["Jung, Yu Min"],"dc:date.available":["2022-06-17T07:00:00Z"],"dc:description.abstract":["Cryptococcus neoformans is a fungal pathogen that causes cryptococcosis, a disease that kills almost 200,000 people worldwide each year. A unique feature of this deadly yeast is its polysaccharide capsule, which is known to be associated with its virulence. Here, we systematically explore the effects of all possible combinations of 4 capsule-inducing signals on gene expression, cell size, and capsule size. These signals are medium (YPD, DMEM or RPMI), temperature (30°C or 37°C), CO2 (room air or 5%), cAMP (0 mM or 20 mM), and pH buffer (HEPES/no HEPES). We explore the effects of exogenous cAMP at a range of concentrations and of deletions of cAMP pathway genes PKR1, PDE1, and PDE2. We present a computational framework for identifying a set of genes that are putatively associated with capsule induction. In addition, we follow up with experiments to validate and corroborate the hypotheses from the computational analysis in search of new genes that may be involved in capsule growth.
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