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<big>'''Paper of the month: July 2015'''</big>  
 
<big>'''Paper of the month: July 2015'''</big>  
* The precise functions of serine [[Protein kinases and phosphatases|protein kinases]] in ''B. subtilis'' have largely remained enigmatic until very recently. Now, two studies from the lab of [[Jonathan Dworkin]] describe functions and molecular targets for two of these kinases, [[PrkC]] and [[YabT]]. [http://www.ncbi.nlm.nih.gov/pubmed/26056311 Pereira et al.] have identified the universally conserved [[TufA|elongation factor Tu]] as a target for the protein kinase [[YabT]]. In srarving cells, YabT phosphorylates [[TufA|EF-Tu]] at a conserved threonine residue. Phosphorylation impairs the essential GTPase activity of [[TufA|EF-Tu]], thereby preventing its release from the [[ribosome]]. As a consequence, phosphorylated [[TufA|EF-Tu]] has a dominant-negative effect in [[translation]] elongation, resulting in the overall inhibition of protein synthesis. Importantly, this mechanism allows a quick and robust regulation of one of the [[most abundant proteins|most abundant cellular proteins]]. [http://www.ncbi.nlm.nih.gov/pubmed/26102633 Libby et al.] have uncovered that phosphorylation by PrkC stimulates the activity of the [[essential genes|essential]] [[Two-component systems|two-component transcription factor]] [[WalR]]. This mechanism links the presence of muropeptides that trigger [[PrkC]] activity to the expression of the genes of the [[WalR regulon]] that are involved in [[cell wall synthesis|cell wall metabolism]].
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* The cells in a biofilm experience very different conditions: While the inner cells are well protected from any harm from the environment, they have on the other hand only poor access to nutrients. For the cells on the edge of the biofilm, it is just the other way round. Now, [http://www.ncbi.nlm.nih.gov/pubmed/26200335 Liu et al.] from the lab of [[Gürol M. Süel]] have discovered oscillation in the [[biofilm formation|growth of the biofilm]]. These oscillations serve to provide the inner cells with access to nutrients. These oscillations are caused by metabolic co-dependence between cells in the biofilm periphery and interior that is driven by [[glutamate metabolism|glutamate consumption and ammonium production]], respectively.
* '''Relevant ''Subti''Wiki pages:''' [[Jonathan Dworkin]], [[Protein kinases and phosphatases|protein kinases]], [[YabT]], [[TufA|EF-Tu]], [[PrkC]], [[WalR]], [[cell wall synthesis|cell wall metabolism]]
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* '''Relevant ''Subti''Wiki pages:''' [[Gürol M. Süel]], [[glutamate metabolism|glutamate consumption and ammonium production]], [[biofilm formation]]
<pubmed>26056311 26102633</pubmed>
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* see [http://microbepost.org/2015/08/05/conflict-and-co-operation-in-bacterial-communities/ a blog presenting this paper]
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<pubmed>26200335</pubmed>
 
* [[Previous papers of the month]]
 
* [[Previous papers of the month]]
  

Revision as of 13:14, 10 August 2015

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Paper of the month: July 2015

Jintao Liu, Arthur Prindle, Jacqueline Humphries, Marçal Gabalda-Sagarra, Munehiro Asally, Dong-yeon D Lee, San Ly, Jordi Garcia-Ojalvo, Gürol M Süel
Metabolic co-dependence gives rise to collective oscillations within biofilms.
Nature: 2015, 523(7562);550-4
[PubMed:26200335] [WorldCat.org] [DOI] (I p)


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