Team:Brown

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Brown University iGEM 2009

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The 2009 Brown iGEM Team consists of 9 undergraduates from diverse backgrounds in science and engineering. We are mentored by Brown graduate students, postdocs, iGEM alumni, and faculty. With support from Brown UTRA Scholarships, we are working on our project in the Multi Disciplinary Lab over the summer.

This year's team members are: Will Allen '12, Michael Chang '11, Stephanie Cheung '11, Ashley Kim '11, Flora Ko '12, Minoo Ramanathan '11, Ahmad Rana '11, Elias Scheer '12, Indu Voruganti '12

The 2009 Brown iGEM Team aims to treat allergic rhinitis by engineering Staphylococcus epidermidis to secrete a histamine binding protein in response to elevated histamine concentrations during an allergic attack. The histamine-binding protein, rEV131, has been cloned from a species of tick, Rhipicephalus appendiculatus. rEV131 binds histamine with an extremely high affinity, and normally functions to prevent the inflammatory response while the tick sucks blood. We are transforming the gene coding for rEV131 into an S. epidermidis, which is endogenous in the human nasal flora. rEV131 will have a secretion tag specific for S. epidermidis.

Additionally, to synchronize rEV131 production with elevation of histamine, we are engineering a novel histamine receptor by carrying out site-directed mutagenesis on Taz1, a fusion protein that contains a periplasmic receptor region and a transmembrane and cytoplasmic regions. The transmembrane and cytoplasmic regions are responsible for a signal transduction pathway that links to gene transcription. The eventual goal is to link this histamine-responsive receptor to activation of an operon that promotes transcription of rEV131.

Although S. epidermidis is a non-pathogenic specimen, additional safety precautions are being taken to control over-proliferation. When S. epidermidis reaches a certain population threshold, it begins to produce hazardous biofilms. We have cloned this population sensor, however, and placed its promoter over a DNA gyrase poison, cuing its "suicide" when populations have reached a dangerous level.

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-The 2009 Brown iGEM Team aims to treat allergic rhinitis by engineering "Staphylococcus epidermidis" to secrete a histamine binding protein in response to elevated histamine concentrations during an allergic attack. The histamine-binding protein, rEV131, has been cloned from a species of tick, "Rhipicephalus appendiculatus". rEV131 binds histamine with an extreme high affinity, and normally functions to prevent the inflammatory response while the tick sucks blood. We are transforming the gene for rEV131 into an endogenous nasal flora, "S. epidermidis". rEV131 will have a secretion tag specific for S. epidermidis.
+The 2009 Brown iGEM Team aims to treat allergic rhinitis by engineering Staphylococcus epidermidis to secrete a histamine binding protein in response to elevated histamine concentrations during an allergic attack. The histamine-binding protein, rEV131, has been cloned from a species of tick, Rhipicephalus appendiculatus. rEV131 binds histamine with an extremely high affinity, and normally functions to prevent the inflammatory response while the tick sucks blood. We are transforming the gene coding for rEV131 into an S. epidermidis, which is endogenous in the human nasal flora. rEV131 will have a secretion tag specific for S. epidermidis.
+Additionally, to synchronize rEV131 production with elevation of histamine, we are engineering a novel histamine receptor by carrying out site-directed mutagenesis on Taz1, a fusion protein that contains a periplasmic receptor region and a transmembrane and cytoplasmic regions. The transmembrane and cytoplasmic regions are responsible for a signal transduction pathway that links to gene transcription. The eventual goal is to link this histamine-responsive receptor to activation of an operon that promotes transcription of rEV131.
+Although S. epidermidis is a non-pathogenic specimen, additional safety precautions are being taken to control over-proliferation. When S. epidermidis reaches a certain population threshold, it begins to produce hazardous biofilms. We have cloned this population sensor, however, and placed its promoter over a DNA gyrase poison, cuing its "suicide" when populations have reached a dangerous level.
-Additionally, to synchronize rEV131 production with elevation of histamine, we are engineering a novel histamine receptor, via mutagenic PCR. We are mutating periplasmic receptors normally linked to gene transcription. The eventual goal is to link this histamine-responsive receptor to activation of an operon that promotes transcription of rEV131.
-Although "S. epidermidis" is a non-pathogenic specimen, additional safety precautions are being taken to control over-proliferation. When "S. epidermidis" reaches a certain population threshold, it begins to produce hazardous biofilms. We have cloned this population sensor, however, and placed its promoter over a DNA gyrase poison, cuing its "suicide" when populations have reached a dangerous level.
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