User:Joshuakrank

My Annotations

Status	Page	Date/Time	GO Term (Aspect)	Reference	Evidence	Notes	Links
updatedbyinstructor	SALTS:A0A0H3NF77	2017-02-26 20:08:33 CST	GO:0098864 modification by symbiont of host occluding cell-cell junction (P)	PMID:25838979	ECO:0000315 mutant phenotype evidence used in manual assertion	Figure 4. AvrA, S. typhimurium in mouse	challenge
acceptable	STRP2:A0A0H2ZQ65	2017-03-23 16:12:46 CDT	GO:0010944 negative regulation of transcription by competitive promoter binding (P)	PMID:17496092	ECO:0000315 mutant phenotype evidence used in manual assertion	Figure 4A: Which describes the negative regulation of B-galactosidase via the ccpa protein in Streptococcus pneumoniae strain D39 serotype 2. In the control, the deletion of catabolite control protein A (ccpa) resulted in an increase in the transcript levels of bga and pts. In the the BgaAC mutant, a decrease in transcription occurred for both bga and pts. Figure 5: Showing that the D39 pts promoter expressed a higher affinity for the CcpA protein rather than the second repressor. The BgaAC mutant bacteria with its pts promoter expressed the higher affinity for the second repressor.	challenge
acceptable	MYCTU:PKNA	2017-03-18 18:13:28 CDT	GO:0009405 pathogenesis (P)	PMID:25713147	ECO:0000315 mutant phenotype evidence used in manual assertion	Figure 5A: The lungs of the animals infected with the wild type Mycobacterium tuberculosis H37Rv and the complemented (containing pknA and pknB placed at the L5 site on the chromosome) strain showed an immense infection and large granulomas where the deleted pknA mutant showed normal lung observation. Figure 5B: looked at lesions in the lungs, showing that the wild type infection caused more damage when compared to the complemented strain. Figure 5c: A histopathological analysis revealed less severe damage in the complemented strain when compared to the wild type strain.	challenge
unacceptable	STAA8:QUEF	2017-03-23 16:08:52 CDT	GO:0043708 cell adhesion involved in biofilm formation (P)	PMID:27144398	ECO:0000315 mutant phenotype evidence used in manual assertion	Figure 1: MgrA is needed for clumping in S. aureus strain RN4220. Wild type, a deleted mutant and an exogenous expressed mutant were incubated in plasma and fibrinogen. The images show clumping in the wild type and mgrA expressed mutant. Figure 2: ebh is a surface protein that blocks clumping. It is repressed by mgrA (Fig 5d and 5a). Other proteins are known to block clumping and are impacted by mgrA, one being sasG and sraP (fig 8+9) Figure 11: Biofilm formation increased in mutants lacking mgrA, with the increase in ebh. This is due to the up-regulation of the protein sasG, which is one of the proteins up-regulated with ebh as a result of the deletion of mgrA. This protein increases intercellular adhesion, meaning clumping decreases but biofilm formation is enhanced (fig 12)	challenge
acceptable	MYCTU:PKNA	2017-03-23 09:57:15 CDT	GO:1990443 peptidyl-threonine autophosphorylation (P)	PMID:25713147	ECO:0000315 mutant phenotype evidence used in manual assertion	Fig 9(b + d): The protein phosphokinase A (pknA) was detected in a wild strain Mycobacterium tuberculosis H37Rv using the antibody alpha-Thr(P), which picks up the threonine residues 172 and 174 in the pkna activation loop. PknA was not detected in the strain pknA(K42M), a strain where kinases were inactivated. This suggested that kinases (like pknA) were being activated by auto-phosphorylation. Fig 9e: In a strain in which the transcription level of pknB is under the control of a pristinamycin inducible promoter, the level of pknA is not impacted whether the strain is grown in the presence or absence of the inducer. This is indicative that pknA is most likely activated through auto-phosphorylation and is independent of pknB	challenge

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