Adenosine Triphosphate and Guanosine Triphosphate Determinations in Intertidal Sediments

2009 ◽  
pp. 5-5-16 ◽  
Author(s):  
DM Karl
Keyword(s):  
Adenosine Triphosphate ◽  
Intertidal Sediments ◽  
Guanosine Triphosphate

scholarly journals A widespread toxin−antitoxin system exploiting growth control via alarmone signaling

2020 ◽  
Vol 117 (19) ◽  
pp. 10500-10510 ◽  
Author(s):  
Steffi Jimmy ◽  
Chayan Kumar Saha ◽  
Tatsuaki Kurata ◽  
Constantine Stavropoulos ◽  
Sofia Raquel Alves Oliveira ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Adenosine Triphosphate ◽  
Bacterial Growth ◽  
Growth Control ◽  
Genomic Context ◽  
Guanosine Triphosphate ◽  
Functional Roles ◽  
Bacterial Transcription ◽  
Signaling Mechanisms ◽  
High Concentrations

Under stressful conditions, bacterial RelA-SpoT Homolog (RSH) enzymes synthesize the alarmone (p)ppGpp, a nucleotide second messenger. (p)ppGpp rewires bacterial transcription and metabolism to cope with stress, and, at high concentrations, inhibits the process of protein synthesis and bacterial growth to save and redirect resources until conditions improve. Single-domain small alarmone synthetases (SASs) are RSH family members that contain the (p)ppGpp synthesis (SYNTH) domain, but lack the hydrolysis (HD) domain and regulatory C-terminal domains of the long RSHs such as Rel, RelA, and SpoT. We asked whether analysis of the genomic context of SASs can indicate possible functional roles. Indeed, multiple SAS subfamilies are encoded in widespread conserved bicistronic operon architectures that are reminiscent of those typically seen in toxin−antitoxin (TA) operons. We have validated five of these SASs as being toxic (toxSASs), with neutralization by the protein products of six neighboring antitoxin genes. The toxicity of Cellulomonas marina toxSAS FaRel is mediated by the accumulation of alarmones ppGpp and ppApp, and an associated depletion of cellular guanosine triphosphate and adenosine triphosphate pools, and is counteracted by its HD domain-containing antitoxin. Thus, the ToxSAS–antiToxSAS system with its multiple different antitoxins exemplifies how ancient nucleotide-based signaling mechanisms can be repurposed as TA modules during evolution, potentially multiple times independently.

Cerebral high-energy compounds: changes in anoxia

1962 ◽  
Vol 202 (1) ◽  
pp. 77-79 ◽  
Author(s):  
Richard N. Lolley ◽  
Frederick E. Samson
Keyword(s):  
Ion Exchange ◽  
Rat Brain ◽  
Adenosine Triphosphate ◽  
Energy Flow ◽  
Inorganic Phosphate ◽  
High Energy ◽  
High Energy Phosphate ◽  
Guanosine Triphosphate ◽  
Inosine Monophosphate ◽  
Flow Through

Acid-soluble phosphates of rat brain during anoxia were determined by ion-exchange and chemical procedures. There is a general shift during anoxia of triphosphate nucleotides to monophosphates and a very rapid breakdown of phosphoryl-creatine. However, total phosphate leaving the high-energy phosphate pool is not equal to the changes in inorganic phosphate; inorganic phosphate change is much larger than high-energy phosphate change in early anoxia and much smaller in extended anoxia. The patterns of guanosine triphosphate and uridine triphosphate changes are more complex than adenosine triphosphate changes. Nicotinamideadenine dinucleotide levels are steady until late anoxia, at which time they decrease slightly. Cytidine monophosphate is the only cytidine nucleotide detected. Inosine nucleotide concentrations in control animals were below the limit of the method, but in late anoxia inosine monophosphate appeared. The data show that the energy flow through the phosphates in brain is rapid and involves phosphate compounds other than the acid-soluble nucleotides and phosphoryl-creatine.

Sign in / Sign up

Export Citation Format

Share Document