Showing posts with label Qurom sensing. Show all posts
Showing posts with label Qurom sensing. Show all posts

Myxococcus xanthus - Life cycle - C-signal (simplified)

The C signal functions after the A-signal. And it functions after 6 hours of post starvation. The C-signal is the surface protein at the poles, which binds to other receptors at the poles.

The C-signal is regulated by the Act operon.

The Act operon codes for 4 different proteins, ActA and ActB which are involved in contorl of the Act operon and ActC and ActD are involved in the timing of the csgA gene.

The product of csgA gene is CsgA, which is a 25kDa protein.

This protein is processed by a cell surface protease to a 17kDa protein. The 17kDa protein is the actual C-signal.

Increased C-signal results in activation of a cognate FruA Histidine protein kinase.

This kinase phosphorylates FruA to FruA-P.

FruA-P has two main functions. First, to activate the frz (frequency of reversal) operon and aggregation and second to activate dev operon (developnmental and sporulation genes).


Myxococcus xanthus - Life cycle - A-signal (simplified)

Myxococcus xanthus Life cycle - A signal

The A-signal is also known as cell density signal. When the cells are starving and the cell density is sufficiently high for fruiting body formation and aggregation an A-signal is produced.


  • The A-signal begins when there is a nutrient limitation; starvation for amino acids, carbon, phosphorus etc.
  • An intracellular signal is activated and an intracellular signaling molecule ppGpp is synthesized.[ppGpp stands for guanosine 3'-diphosphate 5'-diphosphate]
  • This intracellular signal activates a putative DNA binding protein called AsgB and a sigma factor for it called AsgC.
  • AsgB (and AsgC as sigma factor) activate genes required for synthesis for certain proteases.
  • Various proteases are made and are secreted. These proteases degrade the cell surface proteins into various amino-acids which are known as the A-signal.
  • When the concentration of A-signal rises above 10 microM, a membrane bound histidine kinase is activated which is called SasS.
  • SasS is autophosphorylated and it then phosophorylates a response regulator protein named SasR.
  • SasR-P (phosphorylated SasR) stimulates transcription of gene named fruA.
  • fruA gene makes FruA product. After which FruA is phosphorylated to form FruA-P by a putative histidine protein kinase(HPK).
  • FruA-P activates various developmental genes which will lead to fruiting body formation and aggregation.

Blog by Mufaddal Dewaswala

Chemotaxis in Borrelia

Chemotaxis, in simple words, is the movement of an organism towards a chemical stimulus. Borrelia burgdorferi which causes Lymes disease in Humans, completes its Enzootic life cycle in both humans and ticks.

A two-component system mediates the direction or speed of flagellar rotation. The CheA gene product is a Histidine kinase receptor. When this histidine kinase receptor comes in contact with an chemical stimulus, such as N-acetyl-d-glucosamine, it gets phosphorylated and this in turn phosphorylates another molecule which is the product of the gene CheY.

This CheY when phosphorylated interacts with the motor switch proteins and controls the rotational direction of flagellar motors. In this way chemotaxis plays an important role in pathogenesis of Borrelia burgdorferi.