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Category:Team Its Miller Time
|Status||Page||User||Date/Time||GO Term (Aspect)||Reference||Evidence||Notes||Links|
|FRATU:K0E856||Mill1856, Team Its Miller Time||2013-04-14 17:16:25 CDT||GO:0009297 pilus assembly (Figure 3 shows that pilF mutants do not produce pili like the wild-type. When complemented with a plasmid containing the functional pilF gene, the mutant regains the ability to produce pili.)||PMID:18426883||IMP: Inferred from Mutant Phenotype||challenge|
|GEOSL:Q747G2||Mill1856, Team Its Miller Time||2013-04-14 17:12:43 CDT||GO:0033215 iron assimilation by reduction and transport (P)||PMID:16000176||ECO:0000315 mutant phenotype evidence used in manual assertion|
Figure 4 shows that the OmpJ mutant is unable to reduce Fe(III) like the wild-type.
|CHLTE:Q8KAB9||Mill1856, Team Its Miller Time||2013-04-14 14:54:29 CDT||GO:0019418 sulfide oxidation (P)||PMID:21233162||ECO:0000315 mutant phenotype evidence used in manual assertion|
Figure 4 shows that the dsrM mutant is unable to oxidize sulfur globules to sulfate like the wild-type. When a complementation is done with the wild-type dsrM gene, ability to oxidize sulfur globules to sulfate is restored.
|ARATH:TCP18||Mill2034, Team Its Miller Time||2013-04-14 14:45:16 CDT||GO:0010223 secondary shoot formation (P)||PMID:23524661||ECO:0000315 mutant phenotype evidence used in manual assertion|
Fig 1 & 3.
|ALLVD:DSRE||Mill1856, Team Its Miller Time||2013-04-14 14:39:53 CDT||GO:0019417 sulfur oxidation (P)||PMID:18952098||ECO:0000315 mutant phenotype evidence used in manual assertion|
Figure 2 shows that dsrE mutant is unable to oxidize sulfur to sulfate. A complementation with the wild-type dsrE gene restores the ability of A. vinosum to oxidize sulfur to sulfate.
|HUMAN:Q6NVY4||Mill2034, Team Its Miller Time||2013-04-14 14:27:45 CDT||GO:0000975 regulatory region DNA binding (F)||PMID:23579274||ECO:0000314 direct assay evidence used in manual assertion|
Figure 3 shows how the protein binds to DNA at a specific region in the DR5 promoter, through oligo binding and Western blots
|PSEAE:FUR||Mill1856, Team Its Miller Time||2013-04-14 12:56:39 CDT||GO:0019290 siderophore biosynthetic process (P)||PMID:8478325||ECO:0000315 mutant phenotype evidence used in manual assertion|
Table 3 shows that the fur mutant constitutively produces pyoverdin. When the mutant is complemented with the wild-type gene it no longer constitutively produces pyoverdin.
|?||Mill2034, Team Its Miller Time||2013-04-13 14:02:27 CDT||GO:0010629 negative regulation of gene expression (Figure 8 shows that when a mutant for the gene is made, there is an increase in expression of the gene regulated by HDA6)||PMID:22102827||IMP: Inferred from Mutant Phenotype||challenge|
|ARATH:MSI5||Mill2034, Team Its Miller Time||2013-04-13 13:53:29 CDT||GO:0010629 negative regulation of gene expression (P)||PMID:22102827||ECO:0000315 mutant phenotype evidence used in manual assertion|
Figure 2 and 3 both show how the gene negatively regulates the expression of other genes by looking at the expression of those genes in wild type and mutant plants.
|NOSS1:Q8Z0A3||Mill1856, Team Its Miller Time||2013-04-12 13:44:59 CDT||GO:0030611 arsenate reductase activity (F)||PMID:23086594||ECO:0000316 genetic interaction evidence used in manual assertion|
Figure 6 shows a complementation assay of arsenate reductase activity in ΔarsC E. coli WC3110. When all0195, an arsenate reductase from Anabaena sp. PCC7120, is transformed into E. coli that has its arsenate reducatase gene (arsC) deleted, it regains function and it able to perform similar to the wild-type strain.
|GEOSL:Q74D23||Mill1856, Team Its Miller Time||2013-04-10 23:38:02 CDT||GO:0009297 pilus assembly (P)||PMID:15973408||ECO:0000315 mutant phenotype evidence used in manual assertion|
Figure 2 shows that pilA deficient mutants are unable to produce pili compared to the wild-type, and that complementation of the mutant strain with a functional copy of pilA restores function.
|ARATH:AB1D||Mill2034, Team Its Miller Time||2013-04-10 16:42:22 CDT||GO:0016042 lipid catabolic process (P)||PMID:12065405||ECO:0000315 mutant phenotype evidence used in manual assertion|
Figure 3 shows failure of lipid breakdown in germinated cotyledons in cts-1 mutants. Figure 5 shows TAG-derived fatty acids and acyl CoA levels in wild type and cts-1 and cts-2 mutants. There was much less breakdown of fatty acids in the mutants
|ECOLI:CPXR||Mill2034, Team Its Miller Time||2013-04-09 21:30:27 CDT||GO:0045893 positive regulation of transcription, DNA-dependent (P)||PMID:15743952||ECO:0000314 direct assay evidence used in manual assertion|
|ECO57:HHA||Mill2034, Team Its Miller Time||2013-04-09 20:56:09 CDT||GO:1900191 negative regulation of single-species biofilm formation (P)||PMID:23377937||ECO:0000315 mutant phenotype evidence used in manual assertion|
Figure 2 shows when you have a hha mutant, biofilm formation increases but when you complement the mutant with hha+, biofilm formation goes down, as hha is a negative regulator of biofilm production
|ARATH:DSP4||Mill2034, Team Its Miller Time||2013-03-28 12:19:44 CDT||GO:0005982 starch metabolic process (P)||PMID:19141707||ECO:0000315 mutant phenotype evidence used in manual assertion|
Figure 1 shows SEX4 incubated with different amounts of prephosphorylated starch granules caused dephosphorylates the starch granule surface. Activity increased with starch added. Activity decreased when leaf extracts from mutants sex4 when compared to wild type extracts.