Difference between revisions of "Part:BBa K624033"

Revision as of 12:01, 9 October 2011

minC cell division inhibitor (revised)

This part, minC, is known as a cell division inhibitor. Its first record on iGEM was made by 2006 Chiba iGEM team(BBa_J29040), but there is not an available part. 2010 Warsaw iGEM team submitted another minC (BBa_K299806) with different sequence. However, there was a PstI site in the middle of the sequence.

We have cloned the minC gene from E. coli K-12 strain MG1655 by performing PCR, with a single nucleotide synonymous mutation to eliminate the PstI site.

Studies show that minC interacts directly with FtsZ and antagonizes FtsZ assembly. Overexpression of minC would lead to septation inhibition at all potential division sites.

Sequence and Features

Assembly Compatibility:

10
COMPATIBLE WITH RFC[10]
12
COMPATIBLE WITH RFC[12]
21
COMPATIBLE WITH RFC[21]
23
COMPATIBLE WITH RFC[23]
25
INCOMPATIBLE WITH RFC[25]
Illegal AgeI site found at 211
1000
COMPATIBLE WITH RFC[1000]

@@ Line 2: / Line 2: @@
 <partinfo>BBa_K624033 short</partinfo>
-This part, MinC, is known as a cell division inhibitor. Its first record on iGEM was made by 2006 Chiba iGEM team([https://parts.igem.org/partsdb/get_part.cgi?part=BBa_J29040 BBa_J29040]), but there is not an available part. 2010 Warsaw iGEM team submitted another minC ([https://parts.igem.org/wiki/index.php?title=Part:BBa_K299806 BBa_K299806]) with different sequence. However, there was a PstI site in the middle of the sequence.
+This part, minC, is known as a cell division inhibitor. Its first record on iGEM was made by 2006 Chiba iGEM team([https://parts.igem.org/partsdb/get_part.cgi?part=BBa_J29040 BBa_J29040]), but there is not an available part. 2010 Warsaw iGEM team submitted another minC ([https://parts.igem.org/wiki/index.php?title=Part:BBa_K299806 BBa_K299806]) with different sequence. However, there was a PstI site in the middle of the sequence.
 We have cloned the ''minC'' gene from E. coli K-12 strain MG1655 by performing PCR, with a single nucleotide synonymous mutation to eliminate the PstI site.
-Studies show that MinC interacts directly with FtsZ and antagonizes FtsZ assembly. Overexpression of MinC would lead to septation inhibition at all potential division sites.
+Studies show that minC interacts directly with FtsZ and antagonizes FtsZ assembly. Overexpression of minC would lead to septation inhibition at all potential division sites.
 <!-- Add more about the biology of this part here