User talk:Aparnna suresh
Chemotaxis is a form of signal transduction found in motile cells. It allows the cells to detect environmental changes (like changes in concentration of compounds) and to reorient and move in favourable directions. Cells can either run (move in current direction of motion) or tumble(change direction of motion).
Bacillus subtilis, a major inhabitant of soil, lake and marine habitats, is a rod-shaped, gram positive bacterium of the Bacillus genus.
Signal Transduction[edit]
Chemoattractants bind to the receptor and stimulate CheA(a membrane-bound kinase) which phosphorylates CheY, a chemotaxis protein. Phosphorylated CheY(CheYp) binds to the flagellar motor switch FliY causing the flagella to rotate counterclockwise. This results in a run. A clockwise rotation results in a tumble. Then the motor switch dephosphorylates CheYp. [1]
Adaptation Systems[edit]
The cells adapt to the addition (or removal) of the attractant. This means that over time, the effect of addition of the attractant is nullified. Hence, a still greater concentration of attractant is required to produce a similar response. Hence, the probabilities of running and tumbling depend on the rate of change of the number of attractant(or repellent) ligands bound to the receptor.
B. subtilis achieves this by reversible methylation of the receptors, CheC-CheD-CheYp negative feedback control and CheV negative feed back control.[2] This contributes to the robustness of the system. Gene knockouts leading to malfunctioning of any two systems severely retards chemotaxis at all attractant concentrations This indicates all three contribute to adaptation simultaneously and aren't redundant to each other. Though many models have been developed to predict how the individual systems integrate, it is still an exciting open challenge to biologists. [3]
The Methylation System[edit]
The methylesterase activity of CheB is increased by phosphorylation by CheA. The receptor acts like a binary switch, the identity of the methylated residue influencing CheA activity. Selective methylation is coordinated by CheYp. Methylation of receptors at residue 630 by CheR when CheYp is bound to receptor leads to an active conformation whereas methylation at residue 637 by CheR leads to an inactive conformation.[4] As a result, in B. subtilis, receptors are briskly methylated on attractant binding and slowly remethylated as the addition of attractant continues over time. This process is repeated as the attractant is removed over time. [5]
The CheC-CheD-CheYp System[edit]
B. subtilis has two chemotaxis proteins not found in E. coli: CheC, a CheYp phosphatase and CheD, a positive regulator of CheA kinase activity. CheD deamidates glutamide residues on the receptor to glutamates. CheYp activates CheD sequestering by CheC, and helps form CheC-CheD complex which has a greater phosphatase activity than CheC. When CheD is recruited away from the receptor, CheA kinase activity decreases. The association between CheD and the receptors is unclear, and binding has been shown in the figure for the sake of simplicity. [6]
The CheV System[edit]
CheV (also absent in E.coli) is a negative regulator of receptor activity. CheA kinase phosphorylates CheV while phosphorylated CheV (CheVp) inhibits kinase activity.[7]
Chemotaxis in Eukaryotes[edit]
Due to their size, eukaryotic cells have a different mechanism of sensing the concentration gradient from bacteria. Signalling pathways are diverse and involve eukaryotic components. One mechanism is developing pseudopods, which are formed by the connections between the growing distal end of the actin polymers and the inner surface of the plasma membrane. This signalling pathway is activated by an intracellular PIP3 gradient which is a response to the chemotactic gradient. Another mechanism is Ca++ dependent cilia based chemotaxis. The details of the signaling pathways are still not completely clear. Chemotaxis is significant in early stages of embryogenesis (eg. movement of sperm is guided by the gradient of signal molecules) and in immune competency (eg. movement of lymphocyte to the site of infection). Some cells that are considered to be non-motile have also been observed to attain motility in changed physiological (eg. fibroblasts) and pathological conditions (eg. metastases).[8]
See Also[edit]
Two-component regulatory system
--Aparnna suresh (talk) 11:34, 23 September 2013 (UTC)
- ^ Rao CV, Kirby JR, Arkin AP (2004) Design and Diversity in Bacterial Chemotaxis: A Comparative Study in Escherichia coli and Bacillus subtilis. PLoS Biol 2(2): e49. doi:10.1371/journal.pbio.0020049
- ^ Christopher V. Rao1, George D. Glekas2 and George W. Ordal The three adaptation systems of Bacillus subtilis chemotaxis Trends Microbiol. 2008 Oct;16(10):480-7. doi: 10.1016/j.tim.2008.07.003
- ^ Alon, U. et al. (1999) Robustness in bacterial chemotaxis. Nature 397,168–171
- ^ Ninfa, E.G. et al. (1991) Reconstitution of the bacterial chemotaxis signal transduction system from purified components. J. Biol. Chem. 266, 9764–9770
- ^ Kirby, J.R. et al. (1999) CheY-dependent methylation of the asparagine receptor, McpB, during chemotaxis in Bacillus subtilis. J. Biol. Chem. 274, 11092–11100
- ^ Muff, T.J. and Ordal, G.W. (2007) The CheC phosphatase regulates chemotactic adaptation through CheD. J. Biol. Chem. 282, 34120–34128
- ^ Karatan, E. et al. (2001) Phosphorylation of the response regulator CheV is required for adaptation to attractants during Bacillus subtilis chemotaxis. J. Biol. Chem. 276, 43618–43626
- ^ Anna Bagorda, Carole A. Parent (2008). "Eukaryotic chemotaxis at a glance". J. Cell Science 121 (Pt 16): 2621–4. doi:10.1242/jcs.018077