4yg7: Difference between revisions

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'''Unreleased structure'''
==Structure of FL autorepression promoter complex==
 
<StructureSection load='4yg7' size='340' side='right' caption='[[4yg7]], [[Resolution|resolution]] 3.77&Aring;' scene=''>
The entry 4yg7 is ON HOLD  until Paper Publication
== Structural highlights ==
 
<table><tr><td colspan='2'>[[4yg7]] is a 8 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4YG7 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4YG7 FirstGlance]. <br>
Authors: Schumacher, M.A.
</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[4yg1|4yg1]], [[4yg4|4yg4]]</td></tr>
 
<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Non-specific_serine/threonine_protein_kinase Non-specific serine/threonine protein kinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.11.1 2.7.11.1] </span></td></tr>
Description:  
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4yg7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4yg7 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=4yg7 RCSB], [http://www.ebi.ac.uk/pdbsum/4yg7 PDBsum]</span></td></tr>
[[Category: Unreleased Structures]]
</table>
[[Category: Schumacher, M.A]]
== Function ==
[[http://www.uniprot.org/uniprot/HIPB_ECOLI HIPB_ECOLI]] Antitoxin component of a toxin-antitoxin (TA) module. Neutralizes the toxic effect of cognate toxin HipA. Binds to operator sites with the consensus sequence 5-'TATCCN(8)GGATA-3' to repress the hipBA operon promoter. [[http://www.uniprot.org/uniprot/HIPA_ECOLI HIPA_ECOLI]] Toxic component of a toxin-antitoxin (TA) module. Autophosphorylates (Ser-150) and phosphorylates EF-Tu in vitro (on 'Thr-383'), may act on other proteins as well. The hipA7 mutation leads to increased generation of persister cells, cells that survive antibiotic treatment probably by entering into a dormant state. Wild-type cells produce persisters at a frequency of 10-6 to 10-5 whereas mutant hipA7 cells produce persisters at a frequency of 10-2. Generation of persister cells requires (p)ppGpp as cells lacking relA or relA/spoT generate fewer or no persister cells respectively compared to hipA7. Low level expression of HipA causes cell filamentation and depending on the protein level is toxic enough to reduce cell growth or even kill cells. Expression of wild-type HipA also leads to high antibiotic tolerance of the survivor cells. The toxic effect of HipA is neutralized by its cognate antitoxin HipB. With HipB acts as a corepressor for transcription of the hipBA promoter.<ref>PMID:17041039</ref> <ref>PMID:6348026</ref> <ref>PMID:8021189</ref> <ref>PMID:14622409</ref> <ref>PMID:19150849</ref> 
== References ==
<references/>
__TOC__
</StructureSection>
[[Category: Non-specific serine/threonine protein kinase]]
[[Category: Schumacher, M A]]
[[Category: Autorepression]]
[[Category: Multidrug tolerance]]
[[Category: Persistence]]
[[Category: Promoter]]
[[Category: Transcription]]
[[Category: Transferase-dna complex]]

Revision as of 17:51, 29 July 2015

Structure of FL autorepression promoter complexStructure of FL autorepression promoter complex

Structural highlights

4yg7 is a 8 chain structure. Full crystallographic information is available from OCA. For a guided tour on the structure components use FirstGlance.
Activity:Non-specific serine/threonine protein kinase, with EC number 2.7.11.1
Resources:FirstGlance, OCA, RCSB, PDBsum

Function

[HIPB_ECOLI] Antitoxin component of a toxin-antitoxin (TA) module. Neutralizes the toxic effect of cognate toxin HipA. Binds to operator sites with the consensus sequence 5-'TATCCN(8)GGATA-3' to repress the hipBA operon promoter. [HIPA_ECOLI] Toxic component of a toxin-antitoxin (TA) module. Autophosphorylates (Ser-150) and phosphorylates EF-Tu in vitro (on 'Thr-383'), may act on other proteins as well. The hipA7 mutation leads to increased generation of persister cells, cells that survive antibiotic treatment probably by entering into a dormant state. Wild-type cells produce persisters at a frequency of 10-6 to 10-5 whereas mutant hipA7 cells produce persisters at a frequency of 10-2. Generation of persister cells requires (p)ppGpp as cells lacking relA or relA/spoT generate fewer or no persister cells respectively compared to hipA7. Low level expression of HipA causes cell filamentation and depending on the protein level is toxic enough to reduce cell growth or even kill cells. Expression of wild-type HipA also leads to high antibiotic tolerance of the survivor cells. The toxic effect of HipA is neutralized by its cognate antitoxin HipB. With HipB acts as a corepressor for transcription of the hipBA promoter.[1] [2] [3] [4] [5]

References

  1. Correia FF, D'Onofrio A, Rejtar T, Li L, Karger BL, Makarova K, Koonin EV, Lewis K. Kinase activity of overexpressed HipA is required for growth arrest and multidrug tolerance in Escherichia coli. J Bacteriol. 2006 Dec;188(24):8360-7. Epub 2006 Oct 13. PMID:17041039 doi:10.1128/JB.01237-06
  2. Moyed HS, Bertrand KP. hipA, a newly recognized gene of Escherichia coli K-12 that affects frequency of persistence after inhibition of murein synthesis. J Bacteriol. 1983 Aug;155(2):768-75. PMID:6348026
  3. Black DS, Irwin B, Moyed HS. Autoregulation of hip, an operon that affects lethality due to inhibition of peptidoglycan or DNA synthesis. J Bacteriol. 1994 Jul;176(13):4081-91. PMID:8021189
  4. Korch SB, Henderson TA, Hill TM. Characterization of the hipA7 allele of Escherichia coli and evidence that high persistence is governed by (p)ppGpp synthesis. Mol Microbiol. 2003 Nov;50(4):1199-213. PMID:14622409
  5. Schumacher MA, Piro KM, Xu W, Hansen S, Lewis K, Brennan RG. Molecular mechanisms of HipA-mediated multidrug tolerance and its neutralization by HipB. Science. 2009 Jan 16;323(5912):396-401. PMID:19150849 doi:323/5912/396

4yg7, resolution 3.77Å

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