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|Status||Page||User||Date/Time||GO Term (Aspect)||Reference||Evidence||Notes||Links|
|TREDE:Q73JV3||Polaske4, MichSt14A 17||2014-04-06 17:02:22 CDT||GO:0030155 regulation of cell adhesion (P)||PMID:24586498||ECO:0000315 mutant phenotype evidence used in manual assertion|
In Figure 8 the TDE2508-deficient Mutant and the wild type, T. denticola, were both incubated with Ca9-22 epithelial cells for 1 hour. After one hour the Mutant showed significantly more adherence to human gingival epithelial cells at both high and low MOI. Since the figure shows the mutant, which is TDE2508-deficient, as having superior adherence compared to the wild-type, it is clear that the TDE2508 protein plays an important role in regulating cell adhesion.
|TREDE:Q73JV3||Polaske4, MichSt14A 17||2014-04-06 16:45:04 CDT||GO:1900191 negative regulation of single-species biofilm formation (P)||PMID:24586498||ECO:0000315 mutant phenotype evidence used in manual assertion|
In Figure 7 the TDE2508-deficient Mutant and the wild type, T. denticola, were both incubated on a polystyrene plate for 2 days. After two days, the amount of biofilm formation and development of bacterial aggregates were measured. The mutant, which was TDE2508-deficient, had a substantial amount of biofilm formation and bacterial aggregates compared to the wild-type. The mutant's ability to produce more biofilm than the wild-type because of the deletion of TDE2508, supports the claim that TDE2508 is involved in the regulation of biofilm formation.
|STALU:E6MC21||Polaske4, MichSt14A 17||2014-04-06 16:03:56 CDT||GO:0042710 biofilm formation (Figure 4 is able to demonstrate how one or more proteins expressed by the isd locus are involved in biofilm formation in iron deficient environments, due to the ability of the mutant with the isd locus deleted to produce the same amount of biofilm as the wild-type. The only mutant strand without the isd locus that shows growth on iron deficient media contains the IsdC protein. This illustrates the fact that IsdC is sufficient, all alone, in promoting biofilm formation in minimal iron conditions.)||PMID:24686057||IMP: Inferred from Mutant Phenotype||challenge|
|9STAP:A0A1F1MBJ8||Polaske4, MichSt14A 17||2014-04-06 15:51:56 CDT||GO:1900233 positive regulation of single-species biofilm formation on inanimate substrate (P)||PMID:24686057||ECO:0000315 mutant phenotype evidence used in manual assertion|
Figure 4 first demonstrates how one or more proteins expressed by the isd locus are involved in biofilm formation in iron deficient environments, due to the ability of the mutant with the isd locus deleted to produce the same amount of biofilm as the wild-type. Furthermore in Figure 4, the isd mutant that lacked the entire isd locus bore an isdc gene engineered to express IsdC protein expression. Similar levels of biofilm formed in this mutant and the wild type. Therefore, IsdC is sufficient in promoting biofilm formation in low-iron environments all alone.
|HUMAN:DCTN1||Polaske4, MichSt14A 17||2014-04-06 15:09:16 CDT||GO:0007399 nervous system development (P)||PMID:24676999||ECO:0000315 mutant phenotype evidence used in manual assertion|
Figure 1E is a graphical result of the affect that a mutation in DCTN1 for p150 has on microtubule growth and communication. This is supported by the evidence that p150, when grown in the presence of microtubules, increases microtubule development. In contrast the mutant protein results in a decrease in microtubule affinity leading to neurodegeneration.
|MOUSE:Q6IS31||Polaske4, MichSt14A 17||2014-04-06 14:16:41 CDT||GO:1902412 regulation of mitotic cytokinesis (P)||PMID:24681957||ECO:0000315 mutant phenotype evidence used in manual assertion|
Figure 3 demonstrates how cells without PINK1 protein are halted at G2/M phase of cell division and can no longer divide. Specifically in Figure 3b, it can be observed using double immunoﬂuorescence, that cells lacking PINK1 did not divide even two hours after release from the nocodazole block. This illustrates that PINK1 is involved in regulation of cell division, because without it division halts.
|CANO9:H8WVX6||Polaske4, MichSt14A 17||2014-04-05 04:54:12 CDT||GO:0010992 ubiquitin homeostasis (P)||PMID:21321079||ECO:0000315 mutant phenotype evidence used in manual assertion|
Figure 1 demonstrates the importance of Not4 for ubiquitin homeostasis in a cell. In normal wild type cells with Not4 ubiquitin levels were stable, but in cells lacking Not4 there was a reduction in production of ubiquitin and increased synthesis leading to cell death. Without Not4 to regulate homeostasis, ubiquitin levels were unregulated causing cell death.
|YEAST:WHI3||Polaske4, MichSt14A 17||2014-04-05 04:22:26 CDT||GO:0071554 cell wall organization or biogenesis (P)||PMID:18667435||ECO:0000315 mutant phenotype evidence used in manual assertion|
Figure 4 demonstrates that in cell walls that are deficient of WHI3 protein, significant deterioration occurs. In Figure 4, WHI3 deficient cells, as well as other mutants and controls, were treated with cell wall inhibitors resulting in horrible degradation in those cells without WHI3. The degradation in cells missing WHI3 can affect development and even survival of the cell. Cells with the protein were relatively unscathed by the cell wall inhibitors.
|HUMAN:PACA||Polaske4, MichSt14A 17||2014-04-05 03:44:19 CDT||GO:0071651 positive regulation of chemokine (C-C motif) ligand 5 production (P)||PMID:24696163||ECO:0000314 direct assay evidence used in manual assertion|
|ECOLI:BSSS||Polaske4, MichSt14A 17||2014-04-05 02:09:55 CDT||GO:1900191 negative regulation of single-species biofilm formation (P)||PMID:23667443||ECO:0000314 direct assay evidence used in manual assertion|
Table 4 demonstrates that Biofilm regulator BssS protein negatively regulates biofilm formation. This table illustrates that when biofilm is attacked by a pathogen and infected, the production of Biofilm regulator BssS protein or yceP protein is induced to stop further biofilm production. By regulating and halting the production of biofilm it stops the spread of the pathogen. So, therefore, we see that with BssS protein there is negative regulation in biofilm production in contrast to other proteins, which have the opposite effect on formation of biofilm, even when exposed to a pathogen.
|YEAST:CCW12||Polaske4, MichSt14A 17||2014-04-05 01:31:17 CDT||GO:0005199 structural constituent of cell wall (F)||PMID:21320323||ECO:0000315 mutant phenotype evidence used in manual assertion|
Figure 5A demonstrates that cells without the ccw12 protein underwent lysis when introduced to hypotonic shock conditions at a rate of 41%. Wild type cells which produced ccw12 protein only experienced lysis and cell death at a rate of 8% when moving from an osmotically stable environment to that of a hypotonic environment. This figure shows that without ccw12 protein present, cell lysis in daughter yeast cells occurs much more frequently during bud formation. Due to the low rate of cell death in the wild type, it can be inferred that the ccw12 protein plays a major role in stabilizing the cell wall and protecting against lysis.
|ECOBD:C6EIU7||Polaske4, MichSt14A 17||2014-04-04 23:35:56 CDT||GO:1900191 negative regulation of single-species biofilm formation (P)||PMID:16597943||ECO:0000315 mutant phenotype evidence used in manual assertion|
Figure 1: Demonstrates how the deletion of yliH has a positive effect on biofilm formation, compared to wild type strains, when plated on multiple media. When yliH was deleted biofilm formation grew exponentially when compared to bacteria in which yliH was present, including the wild type. This demonstrates how the presence of yliH negatively regulates biofilm formation, causing an overall decrease in biofilm mass.
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Pages in category "MichSt14A 17"
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