Annotation Conf. Call 2015-10-27: Difference between revisions
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It is possible that the eye/head phenotype is a secondary phenotype. | It is possible that the eye/head phenotype is a secondary phenotype. | ||
What is the timing of the different organs' development during zebrafish embryogenesis? Would this help to determine the likelihood of a secondary phenotype? Are there other mutations that affect the heart but not these other tissues? (Kimberly) | |||
- The terms including “development”, “morphogenesis”, “formation” are confusing. What is the difference? Which one should we use in this context? | - The terms including “development”, “morphogenesis”, “formation” are confusing. What is the difference? Which one should we use in this context? |
Revision as of 10:51, 27 October 2015
Meeting URL: https://bluejeans.com/993661940
Agenda
Annotation Consistency Exercise
Annotation consistency paper picked by ZFIN- PMID:24430697
Choice of paper-motivation: discussing the use of IGI as evidence code. When should we use IGI?
- - mutation in gene A is rescued by a mutation in gene B
- - mutation in gene A is rescued by over-expression of gene B
In this paper, how do we capture
- - the repression of transcriptional activation activity of tbx5a by kctd10?
- - the information about has2
Summary of the paper (PMID:24430697)
- mutants in kctd10 show heart defects (heart looping, atrioventricular canal development)
Note: phenotypes determined by
- - analysis of heart morphology
- - gene expression analysis of genes known to be expressed in specific part of the heart).
[Fig 1, 2, 3]
- downregulation of tbx5a or has 2 (using MO) rescue kctd10 mutant heart phenotypes. [Fig 4]
- in vitro experiments [Fig5]:
- - luciferase reporter assay
- kctd10 inhibits tbx5 transcriptional activity
- - Co-IP ; Pull down assay:
- tbx5a and kctd10 physically interact with each other.
Annotations: 9 sets of annotations received.
Analysis and points of discussion: (in no particular order)
- Most of us annotated kct10 to heart looping/atrioventricular canal development with IMP
- Use of IEP: One annotation used IEP (Inferred from Expression Pattern) as evidence code because the annotation based on altered expression of AVC marker genes (Fig 2)
kctd10 | atrioventricular canal development | GO:0036302 | IEP |
- “negative regulation of transcription from RNA polymerase II promoter” (GO:0000122) based on the change in gene expression assessed by in situ hybridization (Fig2). examples:
kctd10 | negative regulation of transcription from RNA polymerase II promoter | GO:0000122 | IMP | regulates_transcription_of(anf)|regulates_transcripition_of(amhc)|regulates_transcripion_of(Bmp4)|regulates_transcription_of(Notch1b) | |
kctd10 | negative regulation of transcription from RNA polymerase II promoter | GO:0000122 | IMP | regulates_transcription_of: tbx2b, occurs_in myocardium, happens_during cardiac chamber morphogenesis |
- Is there enough evidence for the following annotations?
kctd10 | eye development | GO:0001654 | IMP |
kctd10 | head development | GO:0060322 | IMP |
It is possible that the eye/head phenotype is a secondary phenotype.
What is the timing of the different organs' development during zebrafish embryogenesis? Would this help to determine the likelihood of a secondary phenotype? Are there other mutations that affect the heart but not these other tissues? (Kimberly)
- The terms including “development”, “morphogenesis”, “formation” are confusing. What is the difference? Which one should we use in this context?
- Statements from paper:
Figure 1. (i-k) Both the myocardium (green) and the endocardium (red) are substantially smaller in the mutant and the morphant, and no cavity is visible inside the heart lumen.
Figure 4. (a,f) The endocardium of the mutant was extremely shrunken and the space between the myocardium and endocardium was much wider than that of the wild-type.
Example:
kctd10 | endocardium development | GO:0003157 | IMP |
kctd10 | endocardium morphogenesis | GO:0003160 | IMP |
kctd10 | endocardium formation | GO:0060214 | IMP |
- in Figure 3: hyaluronic acid staining was performed to visualize the cardiac jelly. Annotation:
kctd10 | negative regulation of hyaluronan biosynthetic process | GO:1900126 | IMP |
Is there enough evidence that kctd10 is involved in hyaluronan biosynthesis? Could it be possible that the increase in staining is a secondary effect?
- Fig4: injection of tbx5MO and has2MO rescue kctd10 mutant phenotype: Most of us annotated using IGI between tbx5 and kctd10, and between has2 and kctd10 heart looping/atrioventricular canal development
- Should kct10 be annotated as “positive/negative regulation” of heart looping / atrioventricular canal development?
- Annotation:
has2 | negative regulation of heart looping | GO:1901208 | IGI | kctd10 |
- Fig 5: regulation of transcription : which evidence code should be used?
kct10 | negative regulation of sequence-specific DNA binding transcription factor activity | GO:0043433 | IDA | ||
kct10 | negative regulation of sequence-specific DNA binding transcription factor activity | GO:0043433 | IDA | has_regulation_target(Tbx5a) | |
kct10 | negative regulation of sequence-specific DNA binding transcription factor activity | GO:0043433 | IDA | tbx5a | has_regulation _target(Tbx5a) |
kct10 | negative regulation of sequence-specific DNA binding transcription factor activity | GO:0043433 | IGI | tbx5a | has_regulation _target(Tbx5a) |
kct10 | negative regulation of sequence-specific DNA binding transcription factor activity | GO:0043433 | IMP | has_regulation_target: tbx5b |
- protein binding: which evidence code should be used? examples:
kct10 | protein binding | GO:0005515 | IPI | tbx5a | |
kct10 | transcription factor binding | GO:0008134 | IPI | tbx5a | |
kct10 | activating transcription factor binding | GO:0033613 | IPI | ||
kct10 | RNA polymerase II activating transcription factor bindin | GO:0001102 | IDA | has_direct_input Tbx5 | |
kct10 | transcriptional repressor activity, RNA polymerase II transcription factor binding | GO:0001191 | IPI | tbx5a |