8t4c - Revision history

OCA at 10:54, 22 May 2024

2024-05-22T10:54:10Z

←Older revision		Revision as of 10:54, 22 May 2024
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	Campylobacter jejuni is a leading cause of bacterial gastroenteritis worldwide. Acute infection can be antecedent to highly debilitating long-term sequelae. Expression of iron acquisition systems is vital for C. jejuni to survive the low iron availability within the human gut. The C. jejuni fetMP-fetABCDEF gene cluster is known to be upregulated during human infection and under iron limitation. While FetM and FetP have been functionally linked to iron transport in prior work, here we assess the contribution by each of the downstream genes ( fetABCDEF ) to C. jejuni growth during both iron-depleted and iron-replete conditions. Significant growth impairment was observed upon disruption of fetA , fetB, fetC , and fetD , suggesting a role in iron acquisition for each encoded protein. FetA expression was modulated by iron-availability but not dependent on the presence of FetB, FetC, FetD, FetE or FetF. Functions of the putative thioredoxins FetE and FetF were redundant in iron scavenging, requiring a double deletion (Delta fetEF ) to exhibit a growth defect. C. jejuni FetE was expressed and the structure solved to 1.50 A, revealing structural similarity to thiol-disulfide oxidases. Functional characterization in biochemical assays showed that FetE reduced insulin at a slower rate than E. coli Trx and that together, FetEF promoted substrate oxidation in cell extracts, suggesting that FetE (and presumably FetF) are oxidoreductases that can mediate oxidation in vivo . This study advances our understanding of the contributions by the fetMP-fetABCDEF gene cluster to virulence at a genetic and functional level, providing foundational knowledge towards mitigating C. jejuni -related morbidity and mortality.		Campylobacter jejuni is a leading cause of bacterial gastroenteritis worldwide. Acute infection can be antecedent to highly debilitating long-term sequelae. Expression of iron acquisition systems is vital for C. jejuni to survive the low iron availability within the human gut. The C. jejuni fetMP-fetABCDEF gene cluster is known to be upregulated during human infection and under iron limitation. While FetM and FetP have been functionally linked to iron transport in prior work, here we assess the contribution by each of the downstream genes ( fetABCDEF ) to C. jejuni growth during both iron-depleted and iron-replete conditions. Significant growth impairment was observed upon disruption of fetA , fetB, fetC , and fetD , suggesting a role in iron acquisition for each encoded protein. FetA expression was modulated by iron-availability but not dependent on the presence of FetB, FetC, FetD, FetE or FetF. Functions of the putative thioredoxins FetE and FetF were redundant in iron scavenging, requiring a double deletion (Delta fetEF ) to exhibit a growth defect. C. jejuni FetE was expressed and the structure solved to 1.50 A, revealing structural similarity to thiol-disulfide oxidases. Functional characterization in biochemical assays showed that FetE reduced insulin at a slower rate than E. coli Trx and that together, FetEF promoted substrate oxidation in cell extracts, suggesting that FetE (and presumably FetF) are oxidoreductases that can mediate oxidation in vivo . This study advances our understanding of the contributions by the fetMP-fetABCDEF gene cluster to virulence at a genetic and functional level, providing foundational knowledge towards mitigating C. jejuni -related morbidity and mortality.

-	Dissecting components of the Campylobacter jejuni fetMP-fetABCDEF gene cluster in iron scavenging.,Richardson-Sanchez T, Chan ACK, Sabatino B, Lin H, Gaynor EC, Murphy MEP bioRxiv. 2023 Jul 5:2023.07.05.547857. doi: 10.1101/2023.07.05.547857~~. Preprint~~. PMID:37461706<ref>PMID:37461706</ref>	+	Dissecting components of the Campylobacter jejuni fetMP-fetABCDEF gene cluster in iron scavenging.,Richardson-Sanchez T, Chan ACK, Sabatino B, Lin H, Gaynor EC, Murphy MEP bioRxiv [Preprint]. 2023 Jul 5:2023.07.05.547857. doi: 10.1101/2023.07.05.547857. PMID:37461706<ref>PMID:37461706</ref>

	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>		From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>

OCA at 05:32, 9 August 2023

2023-08-09T05:32:45Z

←Older revision		Revision as of 05:32, 9 August 2023
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-	'''Unreleased structure'''

-	~~The entry~~ 8t4c is ~~ON HOLD until Paper~~ Publication	+	==Membrane-associated thioredoxin oxidoreductase FetE from Campylobacter jejuni==
		+	<StructureSection load='8t4c' size='340' side='right'caption='[[8t4c]], [[Resolution\|resolution]] 1.50Å' scene=''>
		+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[8t4c]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Campylobacter_jejuni_subsp._jejuni_81-176 Campylobacter jejuni subsp. jejuni 81-176]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=8T4C OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=8T4C FirstGlance]. <br>
		+	</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models\|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution\|Resolution]] 1.5Å</td></tr>
		+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
		+	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=8t4c FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8t4c OCA], [https://pdbe.org/8t4c PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8t4c RCSB], [https://www.ebi.ac.uk/pdbsum/8t4c PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8t4c ProSAT]</span></td></tr>
		+	</table>
		+	== Function ==
		+	[https://www.uniprot.org/uniprot/A0A0H3PAZ9_CAMJJ A0A0H3PAZ9_CAMJJ]
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Campylobacter jejuni is a leading cause of bacterial gastroenteritis worldwide. Acute infection can be antecedent to highly debilitating long-term sequelae. Expression of iron acquisition systems is vital for C. jejuni to survive the low iron availability within the human gut. The C. jejuni fetMP-fetABCDEF gene cluster is known to be upregulated during human infection and under iron limitation. While FetM and FetP have been functionally linked to iron transport in prior work, here we assess the contribution by each of the downstream genes ( fetABCDEF ) to C. jejuni growth during both iron-depleted and iron-replete conditions. Significant growth impairment was observed upon disruption of fetA , fetB, fetC , and fetD , suggesting a role in iron acquisition for each encoded protein. FetA expression was modulated by iron-availability but not dependent on the presence of FetB, FetC, FetD, FetE or FetF. Functions of the putative thioredoxins FetE and FetF were redundant in iron scavenging, requiring a double deletion (Delta fetEF ) to exhibit a growth defect. C. jejuni FetE was expressed and the structure solved to 1.50 A, revealing structural similarity to thiol-disulfide oxidases. Functional characterization in biochemical assays showed that FetE reduced insulin at a slower rate than E. coli Trx and that together, FetEF promoted substrate oxidation in cell extracts, suggesting that FetE (and presumably FetF) are oxidoreductases that can mediate oxidation in vivo . This study advances our understanding of the contributions by the fetMP-fetABCDEF gene cluster to virulence at a genetic and functional level, providing foundational knowledge towards mitigating C. jejuni -related morbidity and mortality.

-	~~Authors~~:	+	Dissecting components of the Campylobacter jejuni fetMP-fetABCDEF gene cluster in iron scavenging.,Richardson-Sanchez T, Chan ACK, Sabatino B, Lin H, Gaynor EC, Murphy MEP bioRxiv. 2023 Jul 5:2023.07.05.547857. doi: 10.1101/2023.07.05.547857. Preprint. PMID:37461706<ref>PMID:37461706</ref>

-	~~Description~~:	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	[[Category: ~~Unreleased~~ Structures]]	+	</div>
		+	<div class="pdbe-citations 8t4c" style="background-color:#fffaf0;"></div>
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
		+	[[Category: Campylobacter jejuni subsp. jejuni 81-176]]
		+	[[Category: Large Structures]]
		+	[[Category: Chan AC]]
		+	[[Category: Murphy ME]]

OCA at 11:08, 26 July 2023

2023-07-26T11:08:09Z

←Older revision		Revision as of 11:08, 26 July 2023
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	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 8t4c is ON HOLD	+	The entry 8t4c is ON HOLD until Paper Publication

	Authors:		Authors:

OCA: Protected "8t4c" [edit=sysop:move=sysop]

2023-06-14T06:56:16Z

Protected "8t4c" [edit=sysop:move=sysop]

←Older revision

Revision as of 06:56, 14 June 2023

OCA: New page: '''Unreleased structure''' The entry 8t4c is ON HOLD Authors: Description: Category: Unreleased Structures

2023-06-14T06:56:15Z

New page: '''Unreleased structure''' The entry 8t4c is ON HOLD Authors: Description: Category: Unreleased Structures

New page

'''Unreleased structure'''

The entry 8t4c is ON HOLD

Authors:

Description:
[[Category: Unreleased Structures]]