scholarly journals Receptor-Receptor Coupling in Bacterial Chemotaxis: Evidence for Strongly Coupled Clusters

2006 ◽  
Vol 90 (12) ◽  
pp. 4317-4326 ◽  
Author(s):  
Monica L. Skoge ◽  
Robert G. Endres ◽  
Ned S. Wingreen
2021 ◽  
Author(s):  
Zachary Maschmann ◽  
Siddarth Chandrasekaran ◽  
Brian R Crane

In bacterial chemotaxis chemoreceptors regulate the cytosolic dimeric histidine kinase CheA. To test the role that interdomain linkers play in CheA regulation the linkers that connect the P4 kinase domain to the P3 dimerization domain (L3) and the P5 regulatory domain (L4) were extended and altered in variants of Thermotoga maritima (Tm) CheA. Flexible extensions of the L3 and L4 linkers in CheA-LV1 (linker variant 1) allow for a well-folded kinase domain that retains WT-like binding affinities for nucleotide and normal interactions with the receptor-coupling protein CheW. However, CheA-LV1 autophosphorylation activity registers ~50-fold lower compared to wild-type. Formation of the CheA-LV1 / CheA WT heterodimer fails to rescue CheA-LV1 autophosphorylation and instead reduces the activity of the WT subunit. Neither CheA WT nor CheA-LV1 can phosphorylate P1 in a CheA dimer that contains a single P4 domain. Rescue of autophosphorylation activity in variants with a poly-alanine L3 or an L3 that maintains a heptad repeat suggest that positioning and conformational transitions of P4 depend on L3 assuming helical structure. Pulse dipolar ESR measurements indicate that the CheA-LV1 P4 domains are in close proximity whereas broader distributions in other variants correlate with increased activity. CheA-LV1 has a substantially larger hydrodynamic radius than does CheA WT by SAXS, despite the P4 domains assuming a closed, inhibited conformation. These results explain negative cooperativity in CheA nucleotide binding, demonstrate coupling between P4 disposition and P1 / P2 dynamics and underscore the importance of P4-P4 interactions and an L3 a- helix in CheA activity and regulation.


Author(s):  
Edward Bormashenko ◽  
Alexander A. Fedorets ◽  
Mark Frenkel ◽  
Leonid A. Dombrovsky ◽  
Michael Nosonovsky

Physical properties of clusters, i.e. systems composed of a ‘small’ number of particles, are qualitatively different from those of infinite systems. The general approach to the problem of clustering is suggested. Clusters, as they are seen in the graphs theory, are discussed. Various physical mechanisms of clustering are reviewed. Dimensional properties of clusters are addressed. The dimensionality of clusters governs to a great extent their properties. Weakly and strongly coupled clusters are discussed. Hydrodynamic and capillary interactions giving rise to clusters formation are surveyed. Levitating droplet clusters, turbulent clusters and droplet clusters responsible for the breath-figures self-assembly are considered. Entropy factors influencing clustering are considered. Clustering in biological systems results in non-equilibrium multi-scale assembly, where at each scale, self-driven components come together by consuming energy in order to form the hierarchical structure. This article is part of the theme issue ‘Bioinspired materials and surfaces for green science and technology (part 3)’.


2000 ◽  
Vol 10 (PR5) ◽  
pp. Pr5-271-Pr5-274
Author(s):  
H. Totsuji ◽  
K. Tsuruta ◽  
C. Totsuji ◽  
K. Nakano ◽  
T. Kishimoto ◽  
...  

1985 ◽  
Vol 53 (01) ◽  
pp. 095-098 ◽  
Author(s):  
C R Jones ◽  
R McCabe ◽  
C A Hamilton ◽  
J L Reid

SummaryPaired blood samples were obtained from mothers (venous) and babies (cord venous blood) at the time of delivery by caesarean section under epidural anaesthetic. Fetal platelets failed to aggregate in response to adrenaline in vitro although adrenaline could potentiate the threshold response to adenosine diphosphate (1 μM). Fetal platelet responses to collagen and 8 Arg vasopressin did not differ significantly from maternal responses. Maternal and fetal platelets also showed similar inhibition of aggregation after activation of adenylate cyclase (PGE1 and parathormone), in contrast to the inhibition of adenylate cyclase by adrenaline.Alpha2 adrenoceptors were investigated using [3H] yohimbine binding receptor number and were reduced modestly but significantly on fetal compared to maternal platelets. The failure of fetal platelet aggregation in response to adrenaline appears to be related to a failure of receptor coupling and may represent a delayed maturation of fetal platelet alpha receptors or a response- to increased circulating catecholamines during birth.


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