Difference between revisions of "Robust gradient formation"
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<newstitle> Robust gradient formation through intermolecular phosphorylation </newstitle> | <newstitle> Robust gradient formation through intermolecular phosphorylation </newstitle> | ||
<teaser> | <teaser> | ||
| − | Together with the lab of Sophie Martin at DMF, we showed that the intracellular gradient of Pom1 in fission yeast achieves robustness to fluctuation through intermolecular auto-phosphorylation. Gradient robustness, how molecular gradient can convey precise positional information despite large fluctuations in molecular dynamics, has been the subject of many conjectures in the last decades. In particular it was hypothesized in 2003 that such robustness could be achieved by super-linear decay. In this work we show that in the Pom1 gradient, super-linear decay is obtained by a very simple and elegant mechanism namely intermolecular auto-phosphorylation. This provides a first telling example of gradient robustness through super-linear decay through auto-catalysis, which could be a widespread phenomenon. The paper | + | Together with the lab of Sophie Martin at DMF, we showed that the intracellular gradient of Pom1 in fission yeast achieves robustness to fluctuation through intermolecular auto-phosphorylation. Gradient robustness, how molecular gradient can convey precise positional information despite large fluctuations in molecular dynamics, has been the subject of many conjectures in the last decades. In particular it was hypothesized in 2003 that such robustness could be achieved by super-linear decay. In this work we show that in the Pom1 gradient, super-linear decay is obtained by a very simple and elegant mechanism namely intermolecular auto-phosphorylation. This provides a first telling example of gradient robustness through super-linear decay through auto-catalysis, which could be a widespread phenomenon. The paper is available in in <a href="http://msb.embopress.org/content/11/7/818.full" target="_blank">Molecular Systems Biology</a>. |
</teaser> | </teaser> | ||
Fission yeast cells are rod-shaped cells that elongate until they reach a certain size (about 14 microns) and then split into two cells of equal size. This seems like a simple thing to do, but it begs the question of how does the cell know it has reached the right size and how can the cell know where its middle is. A few years ago, our collaborator Sophie Martin suggested a model that could explain those two processes, namely the timing (when to divide) and the positioning (where to divide) of cell division. According to that model the Pom1 kinase is constantly brought to the two poles of the cell and diffuses along the cortex of the cell. While it diffuses, it also detaches from the the cortex into the cytoplasm, such that the concentration of Pom1 at the cortex decreases towards the cell middle. In other words, it forms a gradient, or more precisely it forms a double gradient from each pole of the cell. Now, these gradients can be used as rulers, because the further away from the pole, the lower the concentration of Pom1. Indeed a molecular mechanism that is inhibited by Pom1 could only take place when Pom1 is is in sufficiently low concentration, that is when the cell is long enough, and also only in the cell middle, where Pom1 concentration is at its lowest. This molecular mechanism is implemented by the Cdr2 kinase that triggers mitotic entry unless which it inactivated by Pom1 phosphorylation. | Fission yeast cells are rod-shaped cells that elongate until they reach a certain size (about 14 microns) and then split into two cells of equal size. This seems like a simple thing to do, but it begs the question of how does the cell know it has reached the right size and how can the cell know where its middle is. A few years ago, our collaborator Sophie Martin suggested a model that could explain those two processes, namely the timing (when to divide) and the positioning (where to divide) of cell division. According to that model the Pom1 kinase is constantly brought to the two poles of the cell and diffuses along the cortex of the cell. While it diffuses, it also detaches from the the cortex into the cytoplasm, such that the concentration of Pom1 at the cortex decreases towards the cell middle. In other words, it forms a gradient, or more precisely it forms a double gradient from each pole of the cell. Now, these gradients can be used as rulers, because the further away from the pole, the lower the concentration of Pom1. Indeed a molecular mechanism that is inhibited by Pom1 could only take place when Pom1 is is in sufficiently low concentration, that is when the cell is long enough, and also only in the cell middle, where Pom1 concentration is at its lowest. This molecular mechanism is implemented by the Cdr2 kinase that triggers mitotic entry unless which it inactivated by Pom1 phosphorylation. | ||
| − | This is all nice ( | + | This is all nice (but still somewhat debated), but there is one issue. The amount of Pom1 that is brought to the cell tips is highly variable between cell and even within cells, such that the mechanism described above should be very imprecise. |
Revision as of 12:18, 14 July 2015
Fission yeast cells are rod-shaped cells that elongate until they reach a certain size (about 14 microns) and then split into two cells of equal size. This seems like a simple thing to do, but it begs the question of how does the cell know it has reached the right size and how can the cell know where its middle is. A few years ago, our collaborator Sophie Martin suggested a model that could explain those two processes, namely the timing (when to divide) and the positioning (where to divide) of cell division. According to that model the Pom1 kinase is constantly brought to the two poles of the cell and diffuses along the cortex of the cell. While it diffuses, it also detaches from the the cortex into the cytoplasm, such that the concentration of Pom1 at the cortex decreases towards the cell middle. In other words, it forms a gradient, or more precisely it forms a double gradient from each pole of the cell. Now, these gradients can be used as rulers, because the further away from the pole, the lower the concentration of Pom1. Indeed a molecular mechanism that is inhibited by Pom1 could only take place when Pom1 is is in sufficiently low concentration, that is when the cell is long enough, and also only in the cell middle, where Pom1 concentration is at its lowest. This molecular mechanism is implemented by the Cdr2 kinase that triggers mitotic entry unless which it inactivated by Pom1 phosphorylation.
This is all nice (but still somewhat debated), but there is one issue. The amount of Pom1 that is brought to the cell tips is highly variable between cell and even within cells, such that the mechanism described above should be very imprecise.
