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Team:Brown
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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 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''. | ||
Revision as of 21:35, 7 August 2009
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.
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.
