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The dynamic interplay between a cell fate determinant and a lysozyme homolog drives the asymmetric division cycle of Caulobacter crescentus
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Zeitschriftentitel: | Genes & Development |
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Personen und Körperschaften: | , , |
In: | Genes & Development, 22, 2008, 2, S. 212-225 |
Format: | E-Article |
Sprache: | Englisch |
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Cold Spring Harbor Laboratory
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author_facet |
Radhakrishnan, Sunish Kumar Thanbichler, Martin Viollier, Patrick H. Radhakrishnan, Sunish Kumar Thanbichler, Martin Viollier, Patrick H. |
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author |
Radhakrishnan, Sunish Kumar Thanbichler, Martin Viollier, Patrick H. |
spellingShingle |
Radhakrishnan, Sunish Kumar Thanbichler, Martin Viollier, Patrick H. Genes & Development The dynamic interplay between a cell fate determinant and a lysozyme homolog drives the asymmetric division cycle of Caulobacter crescentus Developmental Biology Genetics |
author_sort |
radhakrishnan, sunish kumar |
spelling |
Radhakrishnan, Sunish Kumar Thanbichler, Martin Viollier, Patrick H. 0890-9369 1549-5477 Cold Spring Harbor Laboratory Developmental Biology Genetics http://dx.doi.org/10.1101/gad.1601808 <jats:p><jats:italic>Caulobacter crescentus</jats:italic> divides asymmetrically into a swarmer cell and a stalked cell, a process that is governed by the imbalance in phosphorylated levels of the DivK cell fate determinant in the two cellular compartments. The asymmetric polar localization of the DivJ kinase results in its specific inheritance in the stalked daughter cell where it phosphorylates DivK. The mechanism for the polar positioning of DivJ is poorly understood. SpmX, an uncharacterized lysozyme homolog, is shown here to control DivJ localization and activation. In the absence of SpmX, DivJ is delocalized and dysfunctional, resulting in developmental defects caused by an insufficiency in phospho-DivK. While SpmX stimulates DivK phosphorylation in the stalked cell, unphosphorylated DivK in the swarmer cell activates an intricate transcriptional cascade that leads to the production of the <jats:italic>spmX</jats:italic> message. This event primes the swarmer cell for the impending transition into a stalked cell, a transition that is sparked by the abrupt accumulation and localization of SpmX to the future stalked cell pole. Localized SpmX then recruits and stimulates DivJ, and the resulting phospho-DivK implements the stalked cell fate. The dynamic interplay between SpmX and DivK is at the heart of the molecular circuitry that sustains the <jats:italic>Caulobacter</jats:italic> developmental cycle.</jats:p> The dynamic interplay between a cell fate determinant and a lysozyme homolog drives the asymmetric division cycle of <i>Caulobacter crescentus</i> Genes & Development |
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Cold Spring Harbor Laboratory, 2008 |
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title |
The dynamic interplay between a cell fate determinant and a lysozyme homolog drives the asymmetric division cycle of Caulobacter crescentus |
title_unstemmed |
The dynamic interplay between a cell fate determinant and a lysozyme homolog drives the asymmetric division cycle of Caulobacter crescentus |
title_full |
The dynamic interplay between a cell fate determinant and a lysozyme homolog drives the asymmetric division cycle of Caulobacter crescentus |
title_fullStr |
The dynamic interplay between a cell fate determinant and a lysozyme homolog drives the asymmetric division cycle of Caulobacter crescentus |
title_full_unstemmed |
The dynamic interplay between a cell fate determinant and a lysozyme homolog drives the asymmetric division cycle of Caulobacter crescentus |
title_short |
The dynamic interplay between a cell fate determinant and a lysozyme homolog drives the asymmetric division cycle of Caulobacter crescentus |
title_sort |
the dynamic interplay between a cell fate determinant and a lysozyme homolog drives the asymmetric division cycle of <i>caulobacter crescentus</i> |
topic |
Developmental Biology Genetics |
url |
http://dx.doi.org/10.1101/gad.1601808 |
publishDate |
2008 |
physical |
212-225 |
description |
<jats:p><jats:italic>Caulobacter crescentus</jats:italic> divides asymmetrically into a swarmer cell and a stalked cell, a process that is governed by the imbalance in phosphorylated levels of the DivK cell fate determinant in the two cellular compartments. The asymmetric polar localization of the DivJ kinase results in its specific inheritance in the stalked daughter cell where it phosphorylates DivK. The mechanism for the polar positioning of DivJ is poorly understood. SpmX, an uncharacterized lysozyme homolog, is shown here to control DivJ localization and activation. In the absence of SpmX, DivJ is delocalized and dysfunctional, resulting in developmental defects caused by an insufficiency in phospho-DivK. While SpmX stimulates DivK phosphorylation in the stalked cell, unphosphorylated DivK in the swarmer cell activates an intricate transcriptional cascade that leads to the production of the <jats:italic>spmX</jats:italic> message. This event primes the swarmer cell for the impending transition into a stalked cell, a transition that is sparked by the abrupt accumulation and localization of SpmX to the future stalked cell pole. Localized SpmX then recruits and stimulates DivJ, and the resulting phospho-DivK implements the stalked cell fate. The dynamic interplay between SpmX and DivK is at the heart of the molecular circuitry that sustains the <jats:italic>Caulobacter</jats:italic> developmental cycle.</jats:p> |
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author | Radhakrishnan, Sunish Kumar, Thanbichler, Martin, Viollier, Patrick H. |
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description | <jats:p><jats:italic>Caulobacter crescentus</jats:italic> divides asymmetrically into a swarmer cell and a stalked cell, a process that is governed by the imbalance in phosphorylated levels of the DivK cell fate determinant in the two cellular compartments. The asymmetric polar localization of the DivJ kinase results in its specific inheritance in the stalked daughter cell where it phosphorylates DivK. The mechanism for the polar positioning of DivJ is poorly understood. SpmX, an uncharacterized lysozyme homolog, is shown here to control DivJ localization and activation. In the absence of SpmX, DivJ is delocalized and dysfunctional, resulting in developmental defects caused by an insufficiency in phospho-DivK. While SpmX stimulates DivK phosphorylation in the stalked cell, unphosphorylated DivK in the swarmer cell activates an intricate transcriptional cascade that leads to the production of the <jats:italic>spmX</jats:italic> message. This event primes the swarmer cell for the impending transition into a stalked cell, a transition that is sparked by the abrupt accumulation and localization of SpmX to the future stalked cell pole. Localized SpmX then recruits and stimulates DivJ, and the resulting phospho-DivK implements the stalked cell fate. The dynamic interplay between SpmX and DivK is at the heart of the molecular circuitry that sustains the <jats:italic>Caulobacter</jats:italic> developmental cycle.</jats:p> |
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spelling | Radhakrishnan, Sunish Kumar Thanbichler, Martin Viollier, Patrick H. 0890-9369 1549-5477 Cold Spring Harbor Laboratory Developmental Biology Genetics http://dx.doi.org/10.1101/gad.1601808 <jats:p><jats:italic>Caulobacter crescentus</jats:italic> divides asymmetrically into a swarmer cell and a stalked cell, a process that is governed by the imbalance in phosphorylated levels of the DivK cell fate determinant in the two cellular compartments. The asymmetric polar localization of the DivJ kinase results in its specific inheritance in the stalked daughter cell where it phosphorylates DivK. The mechanism for the polar positioning of DivJ is poorly understood. SpmX, an uncharacterized lysozyme homolog, is shown here to control DivJ localization and activation. In the absence of SpmX, DivJ is delocalized and dysfunctional, resulting in developmental defects caused by an insufficiency in phospho-DivK. While SpmX stimulates DivK phosphorylation in the stalked cell, unphosphorylated DivK in the swarmer cell activates an intricate transcriptional cascade that leads to the production of the <jats:italic>spmX</jats:italic> message. This event primes the swarmer cell for the impending transition into a stalked cell, a transition that is sparked by the abrupt accumulation and localization of SpmX to the future stalked cell pole. Localized SpmX then recruits and stimulates DivJ, and the resulting phospho-DivK implements the stalked cell fate. The dynamic interplay between SpmX and DivK is at the heart of the molecular circuitry that sustains the <jats:italic>Caulobacter</jats:italic> developmental cycle.</jats:p> The dynamic interplay between a cell fate determinant and a lysozyme homolog drives the asymmetric division cycle of <i>Caulobacter crescentus</i> Genes & Development |
spellingShingle | Radhakrishnan, Sunish Kumar, Thanbichler, Martin, Viollier, Patrick H., Genes & Development, The dynamic interplay between a cell fate determinant and a lysozyme homolog drives the asymmetric division cycle of Caulobacter crescentus, Developmental Biology, Genetics |
title | The dynamic interplay between a cell fate determinant and a lysozyme homolog drives the asymmetric division cycle of Caulobacter crescentus |
title_full | The dynamic interplay between a cell fate determinant and a lysozyme homolog drives the asymmetric division cycle of Caulobacter crescentus |
title_fullStr | The dynamic interplay between a cell fate determinant and a lysozyme homolog drives the asymmetric division cycle of Caulobacter crescentus |
title_full_unstemmed | The dynamic interplay between a cell fate determinant and a lysozyme homolog drives the asymmetric division cycle of Caulobacter crescentus |
title_short | The dynamic interplay between a cell fate determinant and a lysozyme homolog drives the asymmetric division cycle of Caulobacter crescentus |
title_sort | the dynamic interplay between a cell fate determinant and a lysozyme homolog drives the asymmetric division cycle of <i>caulobacter crescentus</i> |
title_unstemmed | The dynamic interplay between a cell fate determinant and a lysozyme homolog drives the asymmetric division cycle of Caulobacter crescentus |
topic | Developmental Biology, Genetics |
url | http://dx.doi.org/10.1101/gad.1601808 |