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Tinri Aegerter-Wilmsen

Publications and source records attributed to Tinri Aegerter-Wilmsen.

3 recordsLinked to original sources

Comment on "Precise domain specification in the developing Drosophila embryo".

In a recent paper, Houchmandzadeh [Phys. Rev. E 72, 061920 (2005)] introduce a correlated bigradient model in order to explain the robust scaling of the boundary of hunchback (hb) expression in the early Drosophila embryo. In particular, they stress that recent experiments by Lucchetta [Nature (London) 434, 1134 (2005)], where embryos whose anterior and posterior halves develop at different temperatures still show excellent precision in the hb boundary, are in good agreement with such a model. We would like to show here that this conclusion is unwarranted. This is because the experiments of Lucchetta were done at different temperatures from those studied in the model. Since in other temperature combinations the model does not produce precise boundaries and there are no systematic trends in these deviations, a comparison to the experiment is not possible. Furthermore, we would like to point out that any correlated bigradient model should also take into account the fluctuations of the bicoid profile within an embryo. When forming correlated bigradients of experimental profiles from an online library, we observe that these intraembryo variations destroy robustness of the hb boundary even in the wild-type situation.

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Model for the robust establishment of precise proportions in the early Drosophila embryo.

During embryonic development, a spatial pattern is formed in which proportions are established precisely. As an early pattern formation step in Drosophila embryos, an anterior-posterior gradient of Bicoid (Bcd) induces hunchback (hb) expression (Nature 337 (1989) 138; Nature 332 (1988) 281). In contrast to the Bcd gradient, the Hb profile includes information about the scale of the embryo. Furthermore, the resulting hb expression pattern shows a much lower embryo-to-embryo variability than the Bcd gradient (Nature 415 (2002) 798). An additional graded posterior repressing activity could theoretically account for the observed scaling. However, we show that such a model cannot produce the observed precision in the Hb boundary, such that a fundamentally different mechanism must be at work. We describe and simulate a model that can account for the observed precise generation of the scaled Hb profile in a highly robust manner. The proposed mechanism includes Staufen (Stau), an RNA binding protein that appears essential to precision scaling (Nature 415 (2002) 798). In the model, Stau is released from both ends of the embryo and relocalizes hb RNA by increasing its mobility. This leads to an effective transport of hb away from the respective Stau sources. The balance between these opposing effects then gives rise to scaling and precision. Considering the biological importance of robust precision scaling and the simplicity of the model, the same principle may be employed more often during development.

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