User:Puglisk1

My Annotations

Status	Page	Date/Time	GO Term (Aspect)	Reference	Evidence	Notes	Links
acceptable	BPPH2:NP	2017-04-05 10:13:51 CDT	GO:0017053 transcriptional repressor complex (C)	PMID:12426390	ECO:0000315 mutant phenotype evidence used in manual assertion	Figure 1 displays the mutations of protein p4 and their effects on forming the repression complex between proteins p4 and p6 that represses early transcription in Bacillus subtilis phage phi 29. These mutations disallow the formation of a stable complex, hence the repressor complex cannot be formed between proteins p4 and p6 to completely halt early transcription and switch to late transcription.	challenge
acceptable	BPPH2:NP	2017-04-05 10:33:09 CDT	GO:0006351 transcription, DNA-templated (P)	PMID:12426390	ECO:0000315 mutant phenotype evidence used in manual assertion	The wildtype gel in figure 1 supports transcriptional activity under normal conditions, and it is contrasted and supported by the change in transcription activity recorded in neighboring gels.	challenge
acceptable	LAMBD:G	2017-04-17 10:37:09 CDT	GO:0098003 viral tail assembly (P)	PMID:23851014	ECO:0000315 mutant phenotype evidence used in manual assertion	Figure 4 displays 3 plasmids and a control to be tested against 2 mutated phages missing either gpG and gpGT or just gpGT, and a wildtype phage. From protein expression, it was concluded that not only gpG is required for tail assembly, but also that the G of gpGT is also integral in successful tail assembly and phage growth.	challenge
updatedbyinstructor	BPPH2:NP	2017-04-23 15:59:40 CDT	GO:0001217 bacterial-type RNA polymerase transcriptional repressor activity, sequence-specific DNA binding (F)	PMID:12426390	ECO:0000315 mutant phenotype evidence used in manual assertion	In figure 4, RNAP binding to the promoters in phage phi 29 is monitored in the presence of proteins p4 and p6 with or without mutations at the C-end. The gel shows the inability of a stable p4-p6 complex to form in order to properly repress transcription (ie. blocking the binding of RNAP to the A2c promoter), due to a mutation at the C-end of the p4 protein.	challenge

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unacceptable:0
requires_changes:0
flagged:0

Annotations challenged by Puglisk1

Status	Author,Group	Page	GO Term (Aspect)	Reference	Evidence	Links	Page history

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