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Category:MichSt14A 51

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StatusPageUserDate/TimeGO Term (Aspect)ReferenceEvidenceNotesLinks
updatedbyinstructorMOUSE:Q99M68Tuckerem, MichSt14A 512014-04-06 14:48:27 CDTGO:0035176 social behavior (P)PMID:22231481ECO:0000316 genetic interaction evidence used in manual assertion

Figure 6a shows that the mice who have already received social deficits through mutation are able to regain social behavior function through reducing the Oprm1 gene. This graph shows wild type mice having the highest amount of socialization time and the mutated mice with the most reduction of the Oprm1 gene regaining a lot of their lost socialization skills.

acceptableBUNLC:D3K4J9Tuckerem, MichSt14A 512014-04-06 13:08:33 CDTGO:0046774 suppression by virus of host intracellular interferon activity (P)PMID:17344298ECO:0000315 mutant phenotype evidence used in manual assertion

Figure 5B shows that when the nonstructural protein was expressed, the interferon induction system was suppressed, thus suppressing the innate immune system of the host. The function of the NSs is to suppress the innate immune system of the host and to allow the infection of the virus to take hold.

requireschangesECOLW:E0IYJ0Tuckerem, MichSt14A 512014-04-06 12:15:12 CDTGO:0004045 aminoacyl-tRNA hydrolase activity (F)PMID:24322300ECO:0000315 mutant phenotype evidence used in manual assertion

Figure 4 shows several yaeJ mutants that all show significantly less peptidyl-tRNA hydrolysis (PTH) activity than the wild type. The PTH activity occurs when a ribosome is stalled and the activity prompts the ribosome to complete release.

unacceptableBORPT:O07076Tuckerem, MichSt14A 512014-04-06 11:17:18 CDTGO:0008920 lipopolysaccharide heptosyltransferase activity (F)PMID:9422589ECO:0000315 mutant phenotype evidence used in manual assertion

Figure 4 shows that the mutant waaF gene of B. pertussis produces a lipopolysaccharide that has a deep, rough phenotype, which leads to the explanation that waaF finds its function in lipopolysaccharide biosynthesis.

unacceptableTRYCR:Q03876Tuckerem, MichSt14A 512014-04-06 08:31:33 CDTGO:0050839 cell adhesion molecule binding (F)PMID:8126090ECO:0000315 mutant phenotype evidence used in manual assertion

Figure 4A shows the wildtype flagellum completely attached to the cell body, while Figure 4B shows the Gp72 null mutant with a partially detached flagellum. These figures show that the protein Gp72 is necessary for complete flagellum attachment to the cell body of Trypanosoma cruzi.


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