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Cryptococcus neoformans transcriptio...

O'Meara, Teresa Rodgers.

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Cryptococcus neoformans transcriptional regulation of the host-pathogen interface.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Cryptococcus neoformans transcriptional regulation of the host-pathogen interface./
作者:	O'Meara, Teresa Rodgers.
面頁冊數:	243 p.
附註:	Source: Dissertation Abstracts International, Volume: 74-08(E), Section: B.
Contained By:	Dissertation Abstracts International74-08B(E).
標題:	Biology, Genetics. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3558571
ISBN:	9781303030079

Cryptococcus neoformans transcriptional regulation of the host-pathogen interface.
O'Meara, Teresa Rodgers.

Cryptococcus neoformans transcriptional regulation of the host-pathogen interface. - 243 p.

Source: Dissertation Abstracts International, Volume: 74-08(E), Section: B.

Thesis (Ph.D.)--Duke University, 2013.

Cryptococcus neoformans is a human fungal pathogen that is also ubiquitous in the environment. To cause disease inside a human host, C. neoformans must be able to sense and respond to a multitude of stresses. One of the major responses to the host is the induction of a polysaccharide capsule, which allows the fungus to resist damage and evade the host immune response. This capsule is regulated by a number of signal transduction cascades, but a major contributor is the conserved cAMP/PKA pathway.

ISBN: 9781303030079Subjects--Topical Terms:

1017730
Biology, Genetics.

Cryptococcus neoformans transcriptional regulation of the host-pathogen interface.
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500 $a Adviser: Andrew Alspaugh.
502 $a Thesis (Ph.D.)--Duke University, 2013.
520 $a Cryptococcus neoformans is a human fungal pathogen that is also ubiquitous in the environment. To cause disease inside a human host, C. neoformans must be able to sense and respond to a multitude of stresses. One of the major responses to the host is the induction of a polysaccharide capsule, which allows the fungus to resist damage and evade the host immune response. This capsule is regulated by a number of signal transduction cascades, but a major contributor is the conserved cAMP/PKA pathway.
520 $a Using genetic and molecular biology techniques, I identified Gcn5 and Rim101 as key transcriptional regulators of capsule within the host. I determined that C. neoformans Rim101 is activated by a combination of the canonical pH sensing pathway and the cAMP/PKA pathway. This novel connection potentially gives the pathogen greater flexibility in responding to environmental stimuli, thus allowing for a greater capacity for disease.
520 $a I determined that the Rim101 transcription factor regulates cell wall remodeling in the context of the host by deep mRNA sequencing, electron microscopy, and biochemical assays. Using chromatin immunoprecipitation, I confirmed that these cell wall changes are under direct control of Rim101. I then confirmed the importance of cell wall changes in the host by nanoString profiling of fungal RNA in the context of a murine lung infection. I also examined the lungs of infected mice for cytokine and immune cell infiltrate and determined that C. neoformans cell wall changes are important in avoiding triggering an aberrant host response. I hypothesize that this cell wall remodeling via Rim101 activation is required for full capsule attachment and for masking immunogenic molecules from the host immune system.
590 $a School code: 0066.
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