Difference between revisions of "Part:BBa K143033"
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− | Transcriptional regulator proteins generally | + | Transcriptional regulator proteins generally regulate trancription by binding to specific operator sequences around the transcription start site. These proteins can affect transcription positively (activators) or negatively (repressors). In addition, many of these regulatory proteins can be regulated themselves by the presence of chemicals and compounds, such as the inducers IPTG. |
− | LacI is the regulator protein for the lactose operon in ''E.coli'' and the hyper-spank promoter of ''B. subtilis'' <cite>#1</cite> (<bbpart>BBaK143015</bbpart>) and is responsible for ensuring there is no expression through these promoters in the absence of lactose (or IPTG). LacI is not endogenous to ''B. subtilis'' so LacI will need to be expressed in the host in order for the hyper-spank promoter to be regulated. In the presence of IPTG or lactose, the LacI tetramer is unable to bind DNA and so transcription resumes. | + | LacI is the regulator protein for the lactose operon in ''E. coli'' and the hyper-spank promoter of ''B. subtilis'' <cite>#1</cite> (<bbpart>BBaK143015</bbpart>) and is responsible for ensuring there is no expression through these promoters in the absence of lactose (or IPTG). LacI is not endogenous to ''B. subtilis'' so LacI will need to be expressed in the host in order for the hyper-spank promoter to be regulated. In the presence of IPTG or lactose, the LacI tetramer is unable to bind DNA and so transcription resumes. |
− | This version of LacI lacks a Lva degradation tag and has a small (3 amino acid) N-terminal deletion relative to the current registry LacI (<bbpart>BBa_C0012</bbpart)> and its derivatives. The N-terminal deletion appears to be common to most of the LacI genes used in conjunction with ''B. subtilis'' though both forms are found in ''E.coli'' (in differing strains). | + | This version of LacI lacks a Lva degradation tag and has a small (3 amino acid) N-terminal deletion relative to the current registry LacI (<bbpart>BBa_C0012</bbpart)> and its derivatives. The N-terminal deletion appears to be common to most of the LacI genes used in conjunction with ''B. subtilis'' though both forms are found in ''E. coli'' (in differing strains). |
− | LacI can be used in conjunction with the '''lac operon promoter''' (<bbpart>BBa_K143015</bbpart>), where the LacI will act as a | + | LacI can be used in conjunction with the '''lac operon promoter''' (<bbpart>BBa_K143015</bbpart>), where the LacI will act as a receiver for an IPTG input to result in a '''polymerases per second''' (PoPS) output. |
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Revision as of 10:32, 19 September 2008
LacI (Lva-, N-terminal deletion) regulatory protein
Transcriptional regulator proteins generally regulate trancription by binding to specific operator sequences around the transcription start site. These proteins can affect transcription positively (activators) or negatively (repressors). In addition, many of these regulatory proteins can be regulated themselves by the presence of chemicals and compounds, such as the inducers IPTG.
LacI is the regulator protein for the lactose operon in E. coli and the hyper-spank promoter of B. subtilis #1 (BBaK143015) and is responsible for ensuring there is no expression through these promoters in the absence of lactose (or IPTG). LacI is not endogenous to B. subtilis so LacI will need to be expressed in the host in order for the hyper-spank promoter to be regulated. In the presence of IPTG or lactose, the LacI tetramer is unable to bind DNA and so transcription resumes.
This version of LacI lacks a Lva degradation tag and has a small (3 amino acid) N-terminal deletion relative to the current registry LacI (BBa_C0012), where the LacI will act as a receiver for an IPTG input to result in a polymerases per second (PoPS) output.
Sequence and Features
- 10COMPATIBLE WITH RFC[10]
- 12COMPATIBLE WITH RFC[12]
- 21COMPATIBLE WITH RFC[21]
- 23COMPATIBLE WITH RFC[23]
- 25COMPATIBLE WITH RFC[25]
- 1000COMPATIBLE WITH RFC[1000]
References
<biblio>
- 1 pmid=16166525
</biblio>