Difference between revisions of "Team:Reading/Parts"

 
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<title1> Our Proposed Parts </title1> </br>
  
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<h2> Part Documentation</h2>
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<title2> PilA1 (Part: BBa_K1476001):</title2>
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<p>The proposed function of this part is the production prepilin<sup>1</sup>, a pilus subunit, the theory of transforming in this part is that it will promote hyperpilation and increase the surface area in which electrons can be transferred from the plastoquinone pool to the anode. Making the cell ‘leak’ more electrons.
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This part also contains the pilA1 gene and the upstream Pcpc560 super-strong promoter, this will ensure the overproduction of the proteins necessary for hyperpilation. This biobrick part does have some complications however, see the safety section for more details. </p>
  
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<p>Each team will make new parts during iGEM and will submit them to the Registry of Standard Biological Parts. The iGEM software provides an easy way to present the parts your team has created. The <code>&lt;groupparts&gt;</code> tag (see below) will generate a table with all of the parts that your team adds to your team sandbox.</p>
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<title2> PetF (Part: BBa_K1476004):</title2>
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<p>Remember that the goal of proper part documentation is to describe and define a part, so that it can be used without needing to refer to the primary literature. Registry users in future years should be able to read your documentation and be able to use the part successfully. Also, you should provide proper references to acknowledge previous authors and to provide for users who wish to know more.</p>
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<p>PetF codes for ferredoxin, which is an iron-sulphur protein found in photosystem I. Ferredoxin transfers electrons to the ferredoxin reductase protein, which reduces the cofactor NADP to NADPH.
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This insertion is controversial, increasing the production of a protein which actively takes up electrons into a metabolic pathway will decrease electron leakiness, and therefore decrease the voltage given of by the fuel cell.</p>
  
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<title2> PsaD (Part: BBa_K1476003):</title2>
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<p>The PsaD subunit is a peripheral protein which helps to dock ferredoxin onto photosystem I<sup>2</sup>. Deletion of this gene will decrease the amount of ferredoxin in photosystem I decreasing the amount of electrons entering the electron pathway.
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However, deletion of this gene will have implications for the cell’s hardiness and survivability. Deletion of the PsaD protein could cause cell death and/or greatly impair growth. </p>
  
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<h4>Note</h4>
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<title2> PilT1 (Part: BBa_K1476000): </title2>
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<p>Note that parts must be documented on the <a href="http://parts.igem.org/Main_Page"> Registry</a>. This page serves to <i>showcase</i> the parts you have made. Future teams and other users and are much more likely to find parts by looking in the Registry than by looking at your team wiki.</p>
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<p> Deletion of the PilT1 subunit will suppress pilus retraction, by reducing the activity of the ATPase responsible, again focusing on the hyperpilation of the <i>Synechocystis</i>. This will not lead to added growth of pili, but more the decreased subtraction of them once they are formed. This increases the surface area for which electron transfer can take place.
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However,<i> Synechocystis</i> is reliant on the PilT1 subunit for it’s motility and transformation competency. This will have direct consequences on the cell’s ability to reach nutrients and therefore grow, possibly meaning an even more exaggerated stumped growth and replication when nutrients start to become more scarce. </p>
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<title2> How our knockouts and insertions will work: </title2>
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<p> <i>Synechocystis</i> have an interesting characteristic in that it will undergo homologous recombination between its’ chromosome and plasmid in the homologous region. This is because <i> Synechocystis</i> is naturally transformable.
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Our gene deletions and insertions work by undergoing recombination in regions that they share homology with. The gene deletions will replace the gene with kanamycin resistance and the insertions simply place another copy of the desired gene into the <i>Synechocystis</i> genome. </p>
  
  
  
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<h4>Adding parts to the registry</h4>
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<title2>Part Table </title2>
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<p>You can add parts to the Registry at our <a href="http://parts.igem.org/Add_a_Part_to_the_Registry">Add a Part to the Registry</a> link.</p>
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<groupparts>PilA1 (Part: BBa_K1476001)</groupparts>
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<p>We encourage teams to start completing documentation for their parts on the Registry as soon as you have it available. The sooner you put up your parts, the better you will remember all the details about your parts. Remember, you don't need to send us the DNA sample before you create an entry for a part on the Registry. (However, you <b>do</b> need to send us the DNA sample before the Jamboree. If you don't send us a DNA sample of a part, that part will not be eligible for awards and medal criteria.)</p>
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<title2> References </title2>
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<h4>What information do I need to start putting my parts on the Registry?</h4>
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<li>Yoshihara, S., Geng, X. X., Okamoto, S., Yura, K., Murata, T., Go, M., Ohmori, M., and Ikeuchi, M., (2001). Mutational Analysis of Genes Involved in Pilus Structure, Motility and Transformation Competency in the Unicellular Motile Cyanobacterium Synechocystis sp. PCC 6803. Oxford journals 63-73. </li>
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<p>The information needed to initially create a part on the Registry is:</p>
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<li>Chitnis, V. P., Ke, A., and Chitnis P. R., (1997). The PsaD subunit of photosystem I. Mutations in the basic domain reduce the level of PsaD in the membranes. Plant physiology 1699-1705.</li>
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</ol>
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<li>Part Name</li>
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<li>Part type</li>
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<li>Creator</li>
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<li>Sequence</li>
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<li>Short Description (60 characters on what the DNA does)</li>
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<li>Long Description (Longer description of what the DNA does)</li>
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<li>Design considerations</li>
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<p>
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We encourage you to put up <em>much more</em> information as you gather it over the summer. If you have images, plots, characterization data and other information, please also put it up on the part page. </p>
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<h4>Inspiration</h4>
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<p>We have a created  a <a href="http://parts.igem.org/Well_Documented_Parts">collection of well documented parts</a> that can help you get started.</p>
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<p> You can also take a look at how other teams have documented their parts in their wiki:</p>
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<li><a href="https://2014.igem.org/Team:MIT/Parts"> 2014 MIT </a></li>
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<li><a href="https://2014.igem.org/Team:Heidelberg/Parts"> 2014 Heidelberg</a></li>
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<li><a href="https://2014.igem.org/Team:Tokyo_Tech/Parts">2014 Tokyo Tech</a></li>
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<h4>Part Table </h4>
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</html>
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<groupparts>iGEM015 Example</groupparts>
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Latest revision as of 14:12, 17 September 2015

Our Proposed Parts
PilA1 (Part: BBa_K1476001):

The proposed function of this part is the production prepilin1, a pilus subunit, the theory of transforming in this part is that it will promote hyperpilation and increase the surface area in which electrons can be transferred from the plastoquinone pool to the anode. Making the cell ‘leak’ more electrons. This part also contains the pilA1 gene and the upstream Pcpc560 super-strong promoter, this will ensure the overproduction of the proteins necessary for hyperpilation. This biobrick part does have some complications however, see the safety section for more details.

PetF (Part: BBa_K1476004):

PetF codes for ferredoxin, which is an iron-sulphur protein found in photosystem I. Ferredoxin transfers electrons to the ferredoxin reductase protein, which reduces the cofactor NADP to NADPH. This insertion is controversial, increasing the production of a protein which actively takes up electrons into a metabolic pathway will decrease electron leakiness, and therefore decrease the voltage given of by the fuel cell.

PsaD (Part: BBa_K1476003):

The PsaD subunit is a peripheral protein which helps to dock ferredoxin onto photosystem I2. Deletion of this gene will decrease the amount of ferredoxin in photosystem I decreasing the amount of electrons entering the electron pathway. However, deletion of this gene will have implications for the cell’s hardiness and survivability. Deletion of the PsaD protein could cause cell death and/or greatly impair growth.

PilT1 (Part: BBa_K1476000):

Deletion of the PilT1 subunit will suppress pilus retraction, by reducing the activity of the ATPase responsible, again focusing on the hyperpilation of the Synechocystis. This will not lead to added growth of pili, but more the decreased subtraction of them once they are formed. This increases the surface area for which electron transfer can take place. However, Synechocystis is reliant on the PilT1 subunit for it’s motility and transformation competency. This will have direct consequences on the cell’s ability to reach nutrients and therefore grow, possibly meaning an even more exaggerated stumped growth and replication when nutrients start to become more scarce.

How our knockouts and insertions will work:

Synechocystis have an interesting characteristic in that it will undergo homologous recombination between its’ chromosome and plasmid in the homologous region. This is because Synechocystis is naturally transformable. Our gene deletions and insertions work by undergoing recombination in regions that they share homology with. The gene deletions will replace the gene with kanamycin resistance and the insertions simply place another copy of the desired gene into the Synechocystis genome.

Part Table PilA1 (Part: BBa_K1476001)
References
  1. Yoshihara, S., Geng, X. X., Okamoto, S., Yura, K., Murata, T., Go, M., Ohmori, M., and Ikeuchi, M., (2001). Mutational Analysis of Genes Involved in Pilus Structure, Motility and Transformation Competency in the Unicellular Motile Cyanobacterium Synechocystis sp. PCC 6803. Oxford journals 63-73.
  2. Chitnis, V. P., Ke, A., and Chitnis P. R., (1997). The PsaD subunit of photosystem I. Mutations in the basic domain reduce the level of PsaD in the membranes. Plant physiology 1699-1705.
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