Difference between revisions of "Team:RHIT"

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<p> Our project focuses on controlling the expression of a mitochondrial ribosomal protein gene (<i>MRPS12</i>). By creating a genetic switch that can repress or derepress <i>MRPS12</i>, we can affect whether yeast (<i>S. cerevisiae</i>) undergoes aerobic respiration or fermentation. MRPS12 is vital to mitochondrial ribosomal function, therefore when it is not expressed, the mitochondrial ribosomes cannot translate the proteins required for the electron transport chain. Following this line of progression, when <i>MRPS12</i> is repressed, aerobic respiration does not occur and the cells are forced to ferment. </p>  
 
<p> Our project focuses on controlling the expression of a mitochondrial ribosomal protein gene (<i>MRPS12</i>). By creating a genetic switch that can repress or derepress <i>MRPS12</i>, we can affect whether yeast (<i>S. cerevisiae</i>) undergoes aerobic respiration or fermentation. MRPS12 is vital to mitochondrial ribosomal function, therefore when it is not expressed, the mitochondrial ribosomes cannot translate the proteins required for the electron transport chain. Following this line of progression, when <i>MRPS12</i> is repressed, aerobic respiration does not occur and the cells are forced to ferment. </p>  
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<img src="https://static.igem.org/mediawiki/2015/5/57/RHIT_HOMEPAGE.png">
  
  

Revision as of 16:09, 13 September 2015

Welcome to Rose-Hulman's MitochONdriOFF project!

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Our project focuses on controlling the expression of a mitochondrial ribosomal protein gene (MRPS12). By creating a genetic switch that can repress or derepress MRPS12, we can affect whether yeast (S. cerevisiae) undergoes aerobic respiration or fermentation. MRPS12 is vital to mitochondrial ribosomal function, therefore when it is not expressed, the mitochondrial ribosomes cannot translate the proteins required for the electron transport chain. Following this line of progression, when MRPS12 is repressed, aerobic respiration does not occur and the cells are forced to ferment.

Our project used yeast strains that had their endogenous MRPS12 gene disrupted with a kanamycin gene. We showed that when the MRPS12 gene was reintroduced to this strain on a plasmid, ETC function was restored.

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