Keith H. Turner: Difference between revisions

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*With [http://lorylab.med.harvard.edu/ Stephen Lory, Ph.D.]: Performed a transposon mutagenesis screen in ''Pseudomonas aeruginosa'' to look for novel transcriptional repressors of type III secretion exoenzymes in the RsmA/RsmZ regulatory pathway (September '06 - December '06)
*With [http://lorylab.med.harvard.edu/ Stephen Lory, Ph.D.]: Performed a transposon mutagenesis screen in ''Pseudomonas aeruginosa'' to look for novel transcriptional repressors of type III secretion exoenzymes in the RsmA/RsmZ regulatory pathway (September '06 - December '06)
===Undergraduate work with [http://www.medicine.uiowa.edu/microbiology/faculty/apicella.htm Michael A. Apicella, M.D.]===
===Undergraduate work with [http://www.medicine.uiowa.edu/microbiology/faculty/apicella.htm Michael A. Apicella, M.D.]===
In the Apicella lab, I worked briefly on cloning ''Francisella tularensis'' genes for cell division and LPS biogenesis, but the main bulk of my work there was on ''Haemophilus influenzae''.  ''H. influenzae'' is an obligate colonizer of the human upper respiratory tract, and is carried by about 80% of the population asymptomatically.  However, in patients with chronic obstructive pulmonary disorder or other immunocompromising conditions, it can cause acute episodes of bronchitis.  The basis for its high carriage rates and persistence in infection is in its use of ''N''-acetylneuraminic acid (Neu5Ac), or sialic acid, for decorating its LOS to evade the host innate immune response.  As the bacterium lacks a Neu5Ac synthase gene, it depends on scavenging free Neu5Ac from the human host, a process which is mediated by the SiaP/SiaT Neu5Ac TRAP transporter.  SiaP is a periplasmic protein that binds Neu5Ac and enables transport through the SiaT membrane transporter.  My work centered around characterizing the SiaP-Neu5Ac interaction quantitatively.  It was a great project that taught me a lot about microbiological and biochemical procedures, as well as research in general.  Unfortunately, we were scooped, but we have a paper in the works that builds on what we did by examining the active site more closely.
In the Apicella lab, I worked briefly on cloning ''Francisella tularensis'' genes for cell division and LPS biogenesis, but the main bulk of my work there was on ''Haemophilus influenzae''.  ''H. influenzae'' is an obligate colonizer of the human upper respiratory tract, and is carried by about 80% of the population asymptomatically.  However, in patients with chronic obstructive pulmonary disorder or other immunocompromising conditions, it can cause acute episodes of bronchitis.  The basis for its high carriage rates and persistence in infection is in its use of ''N''-acetylneuraminic acid (Neu5Ac), or sialic acid, for decorating its LOS to evade the host innate immune response.  As the bacterium lacks a Neu5Ac synthase gene, it depends on scavenging free Neu5Ac from the human host, a process which is mediated by the SiaP/SiaT Neu5Ac TRAP transporter <cite>Allen-IandI-2005</cite>.  SiaP is a periplasmic protein that binds Neu5Ac and enables transport through the SiaT membrane transporter.  My work centered around characterizing the SiaP-Neu5Ac interaction quantitatively.  It was a great project that taught me a lot about microbiological and biochemical procedures, as well as more general things about performing and communicating research.  Unfortunately, we were scooped on the initial work <cite>Severi-MolMicro-2005</cite>, but we have a paper in the works that builds on what we did by examining the active site more closely.
==References==
<biblio>
#Allen-IandI-2005 pmid=16113244
#Severi-MolMicro-2005 pmid=16262798
</biblio>

Revision as of 14:29, 6 December 2006

I am a Ph.D. student in the Department of Microbiology and Molecular Genetics at Harvard University, under the Biological and Biomedical Sciences (BBS) Program. I am interested in pathogenic bacteria, and have tried many times in many different ways to narrow that a bit, but it's tough! Luckily, my first year in the program here consists of lab rotations, so I can explore a bit before I declare a thesis topic. I hope to contribute much of what I learn in the coming years to OWW.

Education

Research

Rotations at Harvard

  • With Stephen Lory, Ph.D.: Performed a transposon mutagenesis screen in Pseudomonas aeruginosa to look for novel transcriptional repressors of type III secretion exoenzymes in the RsmA/RsmZ regulatory pathway (September '06 - December '06)

Undergraduate work with Michael A. Apicella, M.D.

In the Apicella lab, I worked briefly on cloning Francisella tularensis genes for cell division and LPS biogenesis, but the main bulk of my work there was on Haemophilus influenzae. H. influenzae is an obligate colonizer of the human upper respiratory tract, and is carried by about 80% of the population asymptomatically. However, in patients with chronic obstructive pulmonary disorder or other immunocompromising conditions, it can cause acute episodes of bronchitis. The basis for its high carriage rates and persistence in infection is in its use of N-acetylneuraminic acid (Neu5Ac), or sialic acid, for decorating its LOS to evade the host innate immune response. As the bacterium lacks a Neu5Ac synthase gene, it depends on scavenging free Neu5Ac from the human host, a process which is mediated by the SiaP/SiaT Neu5Ac TRAP transporter [1]. SiaP is a periplasmic protein that binds Neu5Ac and enables transport through the SiaT membrane transporter. My work centered around characterizing the SiaP-Neu5Ac interaction quantitatively. It was a great project that taught me a lot about microbiological and biochemical procedures, as well as more general things about performing and communicating research. Unfortunately, we were scooped on the initial work [2], but we have a paper in the works that builds on what we did by examining the active site more closely.

References

  1. Allen S, Zaleski A, Johnston JW, Gibson BW, and Apicella MA. Novel sialic acid transporter of Haemophilus influenzae. Infect Immun. 2005 Sep;73(9):5291-300. DOI:10.1128/IAI.73.9.5291-5300.2005 | PubMed ID:16113244 | HubMed [Allen-IandI-2005]
  2. Severi E, Randle G, Kivlin P, Whitfield K, Young R, Moxon R, Kelly D, Hood D, and Thomas GH. Sialic acid transport in Haemophilus influenzae is essential for lipopolysaccharide sialylation and serum resistance and is dependent on a novel tripartite ATP-independent periplasmic transporter. Mol Microbiol. 2005 Nov;58(4):1173-85. DOI:10.1111/j.1365-2958.2005.04901.x | PubMed ID:16262798 | HubMed [Severi-MolMicro-2005]

All Medline abstracts: PubMed | HubMed