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User:Michael B Chun

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My Annotations

StatusPageDate/TimeGO Term (Aspect)ReferenceEvidenceNotesLinks
acceptableARATH:RPM12013-04-13 22:53:37 CDTGO:0031234 extrinsic component of cytoplasmic side of plasma membrane (C)PMID:9861059ECO:0000314 direct assay evidence used in manual assertion

Fig. 2A shows the protein is present in the total and microsomal membrane fractions, but not in the soluble fraction; the protein is likely associated with the membrane.

Fig. 2B shows that treatments with detergent (to solubilize the microsomal membrane), sodium carbonate or urea (which do little damage to the lipid bilayer), and even extraction buffer (due to the physical force of resuspension) can release the protein from the membrane; the protein is likely not transmembrane.

Fig. 2D shows that RPM1∷MYC, like RD28, is enriched in the plasma membrane vesicles; the protein is likely associated with the plasma membrane.

challenge
updatedbyinstructorARATH:RAR12013-04-13 23:44:34 CDTGO:0051879 Hsp90 protein binding (F)PMID:14504384ECO:0000021 physical interaction evidence

Fig. 1B shows that both HvRAR1 (RAR1 from barley) and AtRAR1 (RAR1 from Arabidopsis) interact with HvHSP90 (HSP90 from barley); the HSP90-binding function is likely conserved between monocots and dicots.

The first paragraph of the Results section ("RAR1 Interacts with HSP90") mentions how the authors found using a yeast two-hybrid screen of Arabidopsis that Arabidopsis HSP90.1 (AtHSP90.1) also interacts with RAR1 (data not shown).

challenge
requireschanges?2013-04-13 23:57:26 CDTGO:0051879 Hsp90 protein binding (Fig. 1E shows that both HvSGT1 (SGT1 from barley) and AtSGT1b (SGT1b from Arabidopsis) interact with full-length HvHSP90 (HSP90 from barley); the HSP90-binding function is likely conserved between monocots and dicots.)PMID:14504384IDA: Inferred from Direct Assay
challenge
unacceptableARATH:RAR12013-04-14 00:09:17 CDTGO:0005515 protein binding (F)PMID:11847307ECO:0000021 physical interaction evidence

Fig. 1C shows that AtRAR1 (RAR1 from Arabidopsis) interacts with AtSGT1a and AtSGT1b (SGT1a and SGT1b from Arabidopsis, respectively) using a yeast two-hybrid screen of Arabidopsis.

challenge
requireschangesARATH:DCL42013-04-28 15:06:35 CDTGO:0009616 virus induced gene silencing (P)PMID:20190077ECO:0000315 mutant phenotype evidence used in manual assertion

Figure 5.A. (right) shows that only mutants lacking DCL4 (dcl4, dcl2/dcl4, dcl3/dcl4, and dcl2/dcl3/dcl4), when infected with TuMV-AS9-GFP (which lacks a silencing suppressor), have infection levels comparable to when infected with TuMV-GFP.

challenge
updatedbyinstructorARATH:AGO12013-04-28 17:36:21 CDTGO:0060145 viral gene silencing in virus induced gene silencing (P)PMID:18799732ECO:0000315 mutant phenotype evidence used in manual assertion

Supplemental Figure S5. shows that ago1-11 mutants (which have partial loss of AGO1 function) have higher levels of ΔCP RNA accumulation than wild-type when infected with a turnip crinkle virus (TCV) mutant without a silencing suppressor.

challenge
updatedbyinstructorARATH:DRB42013-04-28 17:51:39 CDTGO:0051607 defense response to virus (P)PMID:21883552ECO:0000315 mutant phenotype evidence used in manual assertion

Fig. 1.B. and 1.C. show that drb4 mutants lacking DRB4 have enhanced severity of virus infection symptoms. Viral coat protein levels are higher in drb4 mutants and dcl4 mutants compared to wildtype.

However, Fig. 3. shows that viral RNA levels are not elevated (unlike in dcl4 mutants), suggesting that DRB4 does not act in viral gene silencing.

challenge
updatedbyinstructorARATH:AGO72013-04-28 17:55:42 CDTGO:0060145 viral gene silencing in virus induced gene silencing (P)PMID:18799732ECO:0000315 mutant phenotype evidence used in manual assertion

Supplemental Fig. 5.B. shows that ago7 mutants lacking AGO7 have a modest increase in ΔCP and TCV-GFP RNA accumulation. This suggests that AGO7 may not be the most efficient slicer of RNA, but serves as a surrogate slicer in the absence of AGO1.

challenge
acceptableARATH:RDR12013-05-12 14:43:11 CDTGO:0030422 production of siRNA involved in RNA interference (P)PMID:20190077ECO:0000315 mutant phenotype evidence used in manual assertion

Notes: Fig. 8 shows significant differences in TuMV-GFP–derived siRNA accumulation among the mutants; accumulation of siRNAs derived from the cylindrical inclusion (CI) or from the 5′ UTR of TuMV was significantly reduced in each single, double, and triple mutants with the rdr1-1 allele. This suggests that RDR1 is a major contributor to biogenesis of TuMV-derived siRNAs.

challenge
acceptableARATH:RDR22013-05-12 14:45:42 CDTGO:0070919 production of siRNA involved in chromatin silencing by small RNA (P)PMID:15024409ECO:0000315 mutant phenotype evidence used in manual assertion

Notes: Fig. 1.B. shows that rdr2-1 mutants lacking RDR2 do not accumulate any of the endogenous siRNA tested (siRNA02, AtSN1 siRNA, Cluster2 siRNA, or siRNA1003).

challenge

acceptable:3
unacceptable:1
requires_changes:2
flagged:0

Annotations challenged by Michael B Chun

StatusAuthor,GroupPageGO Term (Aspect)ReferenceEvidenceLinksPage history
requireschangesBewu,
Team Database Backend
RALME:Q1LFV2GO:0018710 - acetone carboxylase activity (F)PMID:22492439ECO:0000314 direct assay evidence used in manual assertionchallengeC: 1
updatedbyinstructorEuglurie,
Team quaternary structure
ORYSJ:MAD29GO:0043068 - positive regulation of programmed cell death (P)PMID:22408076ECO:0000315 mutant phenotype evidence used in manual assertionchallengeC: 1

fixed by Michael B Chun
correctedthroughchallengesWpnicolay,
Team G'nUnit
TGMVY:TRAPGO:2000144 - positive regulation of DNA-templated transcription initiation (P)PMID:1984661ECO:0000315 mutant phenotype evidence used in manual assertionchallengeC: 1

fixed by Michael B Chun

2 annotations fixed by Michael B Chun

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