Difference between revisions of "Annotation Conf. Call, May 26, 2015"

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(April Mouse paper- http://www.ncbi.nlm.nih.gov/pubmed/?term=24349431)
(April Mouse paper- http://www.ncbi.nlm.nih.gov/pubmed/?term=24349431)
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===April Mouse paper- http://www.ncbi.nlm.nih.gov/pubmed/?term=24349431===
 
===April Mouse paper- http://www.ncbi.nlm.nih.gov/pubmed/?term=24349431===
  
* Link to Annotations from the April exercise-http://wiki.geneontology.org/index.php/Annotation_Conf._Call,_April_28,_2015
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* Link to Annotations from the April exercise- http://wiki.geneontology.org/index.php/Annotation_Conf._Call,_April_28,_2015
  
 
* Is cystin regulating necdin? There is no evidence to show that cystin is regulating necdin - What would constitute evidence for this? The paper does show physical interaction between the two proteins and an effect on activity when co-transfected. So we can't put necdin as the regulation target of cystin. How would you capture the fact that cystin has the antagonist effect when necdin is present but it has the opposite role when it is acting alone? Would you use the evidence code or Col-16?  
 
* Is cystin regulating necdin? There is no evidence to show that cystin is regulating necdin - What would constitute evidence for this? The paper does show physical interaction between the two proteins and an effect on activity when co-transfected. So we can't put necdin as the regulation target of cystin. How would you capture the fact that cystin has the antagonist effect when necdin is present but it has the opposite role when it is acting alone? Would you use the evidence code or Col-16?  

Revision as of 14:13, 19 May 2015


Agenda

Unresolved questions from Curation Consistency exercise

April Mouse paper- http://www.ncbi.nlm.nih.gov/pubmed/?term=24349431

  • Is cystin regulating necdin? There is no evidence to show that cystin is regulating necdin - What would constitute evidence for this? The paper does show physical interaction between the two proteins and an effect on activity when co-transfected. So we can't put necdin as the regulation target of cystin. How would you capture the fact that cystin has the antagonist effect when necdin is present but it has the opposite role when it is acting alone? Would you use the evidence code or Col-16?
  • Would you use IGI as the evidence for how cystin interacts with necdin? Is cotransfection considered IGI? Both Rama and Midori thought this was not IGI based on current definition. Ruth, Rebecca and Rachael felt this would be IGI. Kimberly - I had originally used the IDA evidence code for the co-transfection experiment, but it seems that what we are really trying to capture with annotating this experiment is a functional interaction between two gene products. Although the type of experiment differs from traditional genetic experiments using multiply mutant strains, the conclusion is similar: these gene products functionally interact, even if we don't know the exact mechanism. The IGI evidence code therefore seems more appropriate to me now.
    • Reason for use of IGI: 2 cDNA constructs (cystin and necdin) transfected into a cell line, the effect is only seen when both constructs are present, therefore the use of IGI code enables the cystin to be annotated to negative reg of transcription (child term), and the addition of the necdin protein ID in the WITH field (the reciprocal annotation would not be created).
    • Reason against use of IGI: When only one of these genes is transfected into the cells the annotations created (pos reg of transcription, child term) are supported by the IDA evidence code not the IMP evidence code. The GOC documentation on IGI states: Includes any combination of alterations in the sequence (mutation) or expression of more than one gene/gene product.
    • Reason for using Col-16: The evidence code for the single transfection is IDA, therefore the IGI code can’t be used. Using Col-16 enables this information to be captured.
    • Reasons against using Col-16: There is no suitable relationship available to capture this data. There would be a lack of consistency in the application of evidence codes, e.g. If mutant and wt double transfectants were used then the IGI evidence code would be applied, and there would be information in the WITH field. Where as double wt transfectants would have no information in the WITH field.
  • RNA pol II binding- this is redundant with RNA Pol II txn factor complex annotation. Is there a link between the two? This is not always true, so no. It is not clear why this is not always true from the minutes, is it because the definition for GO:0090575 RNA polymerase II transcription factor complex does not state RNA pol II binding is essential for these complexes: A transcription factor complex that acts at promoters of genes transcribed by RNA polymerase II?

Is the decision here to annotate to both if this is shown? Does this paper support the annotation to GO:0090575 RNA polymerase II transcription factor complex?

  • I don’t understand what is meant in the minutes by: annotating to chromtin binding and putting Myc1 in col-16 is not right. It is upstream. David pointed out that we can include C16 information to show the region of either chromatin binding or if nuclear chromatin is used then C16 info can be included here. How can this be done? From the table annotations is the correct option: chromatin binding: has_input (Myc,promoter ; SO:0000167; 1 annotation) in which case what ID should be used for Myc1? nuclear chromatin (coincident_with('GN box' or Myc P1 promoter' SO:new). It would be good to have this clearly stated. coincident_with does not have any C16 usage examples (nor is it listed) on the C16 relationship wiki.
  • Chromatin- is not just histones and DNA. Should Txn factors be annotated to chromatin? Would you make a CC annotation to chromatin over a MF annotation to chromatin binding when you have ChiP evidence? Karen mentioned that in the paper she worked on with the Norway folks they decided all ChiP experiments should be CC. David mentioned that the way he decides between the two is : When you are binding chromatin you are not part of the chromatin. Is txn factor part of chromatin? We need to resolve this issue at the next GOC meeting (Midori has some rules, so does David). We will collect some use cases and present it at the GOC meeting. What should be included in the definition of chromatin? Note that we also have terms like 'transcriptionally active chromatin' and 'transcriptionally silent chromatin'.
    • DNA
    • RNA
    • histones
    • histone modifying complexes? - these are not children of chromatin in the CC
    • chromtin re-modeling complexes? - these are also not children of chromatin in the CC
    • transcription factors?
  • cystin binds to necdin, and also this binding is required in order for cystin to repress necdin positive regulation of transcription. I would like to use the GO term (or child) GO:0016564 transcription repressor activity. However this is obsolete. The GOC has introduced a rule that in order to annotate to an inhibitor or activator activity the inhibited/activated protein has to be bound by the inhibitor/activator. Why not have this rule for new child terms to the GO:0016564 transcription repressor activity term, eg: new term: transcription factor binding transcription repressor activity; new term: DNA binding transcription repressor activity. Note that GO:0003714 transcription corepressor activity describes repressing transcription factor in the definition: Interacting selectively and non-covalently with a repressing transcription factor and also with the basal transcription machinery in order to stop, prevent, or reduce the frequency, rate or extent of transcription. Cofactors generally do not bind the template nucleic acid, but rather mediate protein-protein interactions between repressive transcription factors and the basal transcription machinery.
  • Should transfected experiments ever be annotated to the cell type that the constructs are transfected into? In this case, the authors had demonstrated that cystin and necdin are expressed in these cell types therefore their intention was to elucidate the role of these proteins in these cells. UCL team have not added cell type information in C16, however there was some discussion about whether or not to do this as the protein data was not based on the endogenous protein, and we did not reach an agreement.

March Yeast paper- http://www.ncbi.nlm.nih.gov/pubmed/12048186

  • Use of in_the_presence_of and in_the_absence_of relationships in col-16.
    • these relationships are slated for obsoletion. We could capture the data using different relationships
    • BFA1 has inhibitory role on the Tem1 GTPase when it is acting alone. It is okay to say that it is acting alone and no need to use in_the_absence_of: Bub2.
    • Bub2 gets GAP activity that can activate Tem1 GTPase (when present together as a complex with Bfa1) . part_of: BFA1-BUB2 complex, has_regulation_target:Tem1p
    • Would you annotate Bfa1 to GAP activity or contributes to GAP activity? Data in the paper points to BFA1 being an inhibitor by itself. So may it shouldn't get this term. May be its role is to bridge Tem1 and Bub2 but there is not enough data in the paper to give it a protein binding, bridging annotation