Recurring cluster and operon assembly for Phenylacetate degradation genes
Background A large number of theories have been advanced to explain why genes involved in the same biochemical processes are often co-located in genomes. Most of these theories have been dismissed because empirical data do not match the expectations of the models. In this work we test the hypothesis...
Ausführliche Beschreibung
Autor*in: |
Martin, Fergal J [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
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2009 |
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Anmerkung: |
© Martin and McInerney; licensee BioMed Central Ltd. 2009 |
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Übergeordnetes Werk: |
Enthalten in: BMC evolutionary biology - London : BioMed Central, 2001, 9(2009), 1 vom: 10. Feb. |
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Übergeordnetes Werk: |
volume:9 ; year:2009 ; number:1 ; day:10 ; month:02 |
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DOI / URN: |
10.1186/1471-2148-9-36 |
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Katalog-ID: |
SPR026964686 |
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520 | |a Background A large number of theories have been advanced to explain why genes involved in the same biochemical processes are often co-located in genomes. Most of these theories have been dismissed because empirical data do not match the expectations of the models. In this work we test the hypothesis that cluster formation is most likely due to a selective pressure to gradually co-localise protein products and that operon formation is not an inevitable conclusion of the process. Results We have selected an exemplar well-characterised biochemical pathway, the phenylacetate degradation pathway, and we show that its complex history is only compatible with a model where a selective advantage accrues from moving genes closer together. This selective pressure is likely to be reasonably weak and only twice in our dataset of 102 genomes do we see independent formation of a complete cluster containing all the catabolic genes in the pathway. Additionally, de novo clustering of genes clearly occurs repeatedly, even though recombination should result in the random dispersal of such genes in their respective genomes. Interspecies gene transfer has frequently replaced in situ copies of genes resulting in clusters that have similar content but very different evolutionary histories. Conclusion Our model for cluster formation in prokaryotes, therefore, consists of a two-stage selection process. The first stage is selection to move genes closer together, either because of macromolecular crowding, chromatin relaxation or transcriptional regulation pressure. This proximity opportunity sets up a separate selection for co-transcription. | ||
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10.1186/1471-2148-9-36 doi (DE-627)SPR026964686 (SPR)1471-2148-9-36-e DE-627 ger DE-627 rakwb eng Martin, Fergal J verfasserin aut Recurring cluster and operon assembly for Phenylacetate degradation genes 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Martin and McInerney; licensee BioMed Central Ltd. 2009 Background A large number of theories have been advanced to explain why genes involved in the same biochemical processes are often co-located in genomes. Most of these theories have been dismissed because empirical data do not match the expectations of the models. In this work we test the hypothesis that cluster formation is most likely due to a selective pressure to gradually co-localise protein products and that operon formation is not an inevitable conclusion of the process. Results We have selected an exemplar well-characterised biochemical pathway, the phenylacetate degradation pathway, and we show that its complex history is only compatible with a model where a selective advantage accrues from moving genes closer together. This selective pressure is likely to be reasonably weak and only twice in our dataset of 102 genomes do we see independent formation of a complete cluster containing all the catabolic genes in the pathway. Additionally, de novo clustering of genes clearly occurs repeatedly, even though recombination should result in the random dispersal of such genes in their respective genomes. Interspecies gene transfer has frequently replaced in situ copies of genes resulting in clusters that have similar content but very different evolutionary histories. Conclusion Our model for cluster formation in prokaryotes, therefore, consists of a two-stage selection process. The first stage is selection to move genes closer together, either because of macromolecular crowding, chromatin relaxation or transcriptional regulation pressure. This proximity opportunity sets up a separate selection for co-transcription. Horizontal Gene Transfer (dpeaa)DE-He213 Gene Content (dpeaa)DE-He213 Catabolic Gene (dpeaa)DE-He213 Operon Structure (dpeaa)DE-He213 Macromolecular Crowding (dpeaa)DE-He213 McInerney, James O aut Enthalten in BMC evolutionary biology London : BioMed Central, 2001 9(2009), 1 vom: 10. Feb. (DE-627)32664489X (DE-600)2041493-6 1471-2148 nnns volume:9 year:2009 number:1 day:10 month:02 https://dx.doi.org/10.1186/1471-2148-9-36 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2009 1 10 02 |
spelling |
10.1186/1471-2148-9-36 doi (DE-627)SPR026964686 (SPR)1471-2148-9-36-e DE-627 ger DE-627 rakwb eng Martin, Fergal J verfasserin aut Recurring cluster and operon assembly for Phenylacetate degradation genes 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Martin and McInerney; licensee BioMed Central Ltd. 2009 Background A large number of theories have been advanced to explain why genes involved in the same biochemical processes are often co-located in genomes. Most of these theories have been dismissed because empirical data do not match the expectations of the models. In this work we test the hypothesis that cluster formation is most likely due to a selective pressure to gradually co-localise protein products and that operon formation is not an inevitable conclusion of the process. Results We have selected an exemplar well-characterised biochemical pathway, the phenylacetate degradation pathway, and we show that its complex history is only compatible with a model where a selective advantage accrues from moving genes closer together. This selective pressure is likely to be reasonably weak and only twice in our dataset of 102 genomes do we see independent formation of a complete cluster containing all the catabolic genes in the pathway. Additionally, de novo clustering of genes clearly occurs repeatedly, even though recombination should result in the random dispersal of such genes in their respective genomes. Interspecies gene transfer has frequently replaced in situ copies of genes resulting in clusters that have similar content but very different evolutionary histories. Conclusion Our model for cluster formation in prokaryotes, therefore, consists of a two-stage selection process. The first stage is selection to move genes closer together, either because of macromolecular crowding, chromatin relaxation or transcriptional regulation pressure. This proximity opportunity sets up a separate selection for co-transcription. Horizontal Gene Transfer (dpeaa)DE-He213 Gene Content (dpeaa)DE-He213 Catabolic Gene (dpeaa)DE-He213 Operon Structure (dpeaa)DE-He213 Macromolecular Crowding (dpeaa)DE-He213 McInerney, James O aut Enthalten in BMC evolutionary biology London : BioMed Central, 2001 9(2009), 1 vom: 10. Feb. (DE-627)32664489X (DE-600)2041493-6 1471-2148 nnns volume:9 year:2009 number:1 day:10 month:02 https://dx.doi.org/10.1186/1471-2148-9-36 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2009 1 10 02 |
allfields_unstemmed |
10.1186/1471-2148-9-36 doi (DE-627)SPR026964686 (SPR)1471-2148-9-36-e DE-627 ger DE-627 rakwb eng Martin, Fergal J verfasserin aut Recurring cluster and operon assembly for Phenylacetate degradation genes 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Martin and McInerney; licensee BioMed Central Ltd. 2009 Background A large number of theories have been advanced to explain why genes involved in the same biochemical processes are often co-located in genomes. Most of these theories have been dismissed because empirical data do not match the expectations of the models. In this work we test the hypothesis that cluster formation is most likely due to a selective pressure to gradually co-localise protein products and that operon formation is not an inevitable conclusion of the process. Results We have selected an exemplar well-characterised biochemical pathway, the phenylacetate degradation pathway, and we show that its complex history is only compatible with a model where a selective advantage accrues from moving genes closer together. This selective pressure is likely to be reasonably weak and only twice in our dataset of 102 genomes do we see independent formation of a complete cluster containing all the catabolic genes in the pathway. Additionally, de novo clustering of genes clearly occurs repeatedly, even though recombination should result in the random dispersal of such genes in their respective genomes. Interspecies gene transfer has frequently replaced in situ copies of genes resulting in clusters that have similar content but very different evolutionary histories. Conclusion Our model for cluster formation in prokaryotes, therefore, consists of a two-stage selection process. The first stage is selection to move genes closer together, either because of macromolecular crowding, chromatin relaxation or transcriptional regulation pressure. This proximity opportunity sets up a separate selection for co-transcription. Horizontal Gene Transfer (dpeaa)DE-He213 Gene Content (dpeaa)DE-He213 Catabolic Gene (dpeaa)DE-He213 Operon Structure (dpeaa)DE-He213 Macromolecular Crowding (dpeaa)DE-He213 McInerney, James O aut Enthalten in BMC evolutionary biology London : BioMed Central, 2001 9(2009), 1 vom: 10. Feb. (DE-627)32664489X (DE-600)2041493-6 1471-2148 nnns volume:9 year:2009 number:1 day:10 month:02 https://dx.doi.org/10.1186/1471-2148-9-36 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2009 1 10 02 |
allfieldsGer |
10.1186/1471-2148-9-36 doi (DE-627)SPR026964686 (SPR)1471-2148-9-36-e DE-627 ger DE-627 rakwb eng Martin, Fergal J verfasserin aut Recurring cluster and operon assembly for Phenylacetate degradation genes 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Martin and McInerney; licensee BioMed Central Ltd. 2009 Background A large number of theories have been advanced to explain why genes involved in the same biochemical processes are often co-located in genomes. Most of these theories have been dismissed because empirical data do not match the expectations of the models. In this work we test the hypothesis that cluster formation is most likely due to a selective pressure to gradually co-localise protein products and that operon formation is not an inevitable conclusion of the process. Results We have selected an exemplar well-characterised biochemical pathway, the phenylacetate degradation pathway, and we show that its complex history is only compatible with a model where a selective advantage accrues from moving genes closer together. This selective pressure is likely to be reasonably weak and only twice in our dataset of 102 genomes do we see independent formation of a complete cluster containing all the catabolic genes in the pathway. Additionally, de novo clustering of genes clearly occurs repeatedly, even though recombination should result in the random dispersal of such genes in their respective genomes. Interspecies gene transfer has frequently replaced in situ copies of genes resulting in clusters that have similar content but very different evolutionary histories. Conclusion Our model for cluster formation in prokaryotes, therefore, consists of a two-stage selection process. The first stage is selection to move genes closer together, either because of macromolecular crowding, chromatin relaxation or transcriptional regulation pressure. This proximity opportunity sets up a separate selection for co-transcription. Horizontal Gene Transfer (dpeaa)DE-He213 Gene Content (dpeaa)DE-He213 Catabolic Gene (dpeaa)DE-He213 Operon Structure (dpeaa)DE-He213 Macromolecular Crowding (dpeaa)DE-He213 McInerney, James O aut Enthalten in BMC evolutionary biology London : BioMed Central, 2001 9(2009), 1 vom: 10. Feb. (DE-627)32664489X (DE-600)2041493-6 1471-2148 nnns volume:9 year:2009 number:1 day:10 month:02 https://dx.doi.org/10.1186/1471-2148-9-36 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2009 1 10 02 |
allfieldsSound |
10.1186/1471-2148-9-36 doi (DE-627)SPR026964686 (SPR)1471-2148-9-36-e DE-627 ger DE-627 rakwb eng Martin, Fergal J verfasserin aut Recurring cluster and operon assembly for Phenylacetate degradation genes 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Martin and McInerney; licensee BioMed Central Ltd. 2009 Background A large number of theories have been advanced to explain why genes involved in the same biochemical processes are often co-located in genomes. Most of these theories have been dismissed because empirical data do not match the expectations of the models. In this work we test the hypothesis that cluster formation is most likely due to a selective pressure to gradually co-localise protein products and that operon formation is not an inevitable conclusion of the process. Results We have selected an exemplar well-characterised biochemical pathway, the phenylacetate degradation pathway, and we show that its complex history is only compatible with a model where a selective advantage accrues from moving genes closer together. This selective pressure is likely to be reasonably weak and only twice in our dataset of 102 genomes do we see independent formation of a complete cluster containing all the catabolic genes in the pathway. Additionally, de novo clustering of genes clearly occurs repeatedly, even though recombination should result in the random dispersal of such genes in their respective genomes. Interspecies gene transfer has frequently replaced in situ copies of genes resulting in clusters that have similar content but very different evolutionary histories. Conclusion Our model for cluster formation in prokaryotes, therefore, consists of a two-stage selection process. The first stage is selection to move genes closer together, either because of macromolecular crowding, chromatin relaxation or transcriptional regulation pressure. This proximity opportunity sets up a separate selection for co-transcription. Horizontal Gene Transfer (dpeaa)DE-He213 Gene Content (dpeaa)DE-He213 Catabolic Gene (dpeaa)DE-He213 Operon Structure (dpeaa)DE-He213 Macromolecular Crowding (dpeaa)DE-He213 McInerney, James O aut Enthalten in BMC evolutionary biology London : BioMed Central, 2001 9(2009), 1 vom: 10. Feb. (DE-627)32664489X (DE-600)2041493-6 1471-2148 nnns volume:9 year:2009 number:1 day:10 month:02 https://dx.doi.org/10.1186/1471-2148-9-36 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2009 1 10 02 |
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Enthalten in BMC evolutionary biology 9(2009), 1 vom: 10. Feb. volume:9 year:2009 number:1 day:10 month:02 |
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Recurring cluster and operon assembly for Phenylacetate degradation genes Horizontal Gene Transfer (dpeaa)DE-He213 Gene Content (dpeaa)DE-He213 Catabolic Gene (dpeaa)DE-He213 Operon Structure (dpeaa)DE-He213 Macromolecular Crowding (dpeaa)DE-He213 |
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recurring cluster and operon assembly for phenylacetate degradation genes |
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Recurring cluster and operon assembly for Phenylacetate degradation genes |
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Background A large number of theories have been advanced to explain why genes involved in the same biochemical processes are often co-located in genomes. Most of these theories have been dismissed because empirical data do not match the expectations of the models. In this work we test the hypothesis that cluster formation is most likely due to a selective pressure to gradually co-localise protein products and that operon formation is not an inevitable conclusion of the process. Results We have selected an exemplar well-characterised biochemical pathway, the phenylacetate degradation pathway, and we show that its complex history is only compatible with a model where a selective advantage accrues from moving genes closer together. This selective pressure is likely to be reasonably weak and only twice in our dataset of 102 genomes do we see independent formation of a complete cluster containing all the catabolic genes in the pathway. Additionally, de novo clustering of genes clearly occurs repeatedly, even though recombination should result in the random dispersal of such genes in their respective genomes. Interspecies gene transfer has frequently replaced in situ copies of genes resulting in clusters that have similar content but very different evolutionary histories. Conclusion Our model for cluster formation in prokaryotes, therefore, consists of a two-stage selection process. The first stage is selection to move genes closer together, either because of macromolecular crowding, chromatin relaxation or transcriptional regulation pressure. This proximity opportunity sets up a separate selection for co-transcription. © Martin and McInerney; licensee BioMed Central Ltd. 2009 |
abstractGer |
Background A large number of theories have been advanced to explain why genes involved in the same biochemical processes are often co-located in genomes. Most of these theories have been dismissed because empirical data do not match the expectations of the models. In this work we test the hypothesis that cluster formation is most likely due to a selective pressure to gradually co-localise protein products and that operon formation is not an inevitable conclusion of the process. Results We have selected an exemplar well-characterised biochemical pathway, the phenylacetate degradation pathway, and we show that its complex history is only compatible with a model where a selective advantage accrues from moving genes closer together. This selective pressure is likely to be reasonably weak and only twice in our dataset of 102 genomes do we see independent formation of a complete cluster containing all the catabolic genes in the pathway. Additionally, de novo clustering of genes clearly occurs repeatedly, even though recombination should result in the random dispersal of such genes in their respective genomes. Interspecies gene transfer has frequently replaced in situ copies of genes resulting in clusters that have similar content but very different evolutionary histories. Conclusion Our model for cluster formation in prokaryotes, therefore, consists of a two-stage selection process. The first stage is selection to move genes closer together, either because of macromolecular crowding, chromatin relaxation or transcriptional regulation pressure. This proximity opportunity sets up a separate selection for co-transcription. © Martin and McInerney; licensee BioMed Central Ltd. 2009 |
abstract_unstemmed |
Background A large number of theories have been advanced to explain why genes involved in the same biochemical processes are often co-located in genomes. Most of these theories have been dismissed because empirical data do not match the expectations of the models. In this work we test the hypothesis that cluster formation is most likely due to a selective pressure to gradually co-localise protein products and that operon formation is not an inevitable conclusion of the process. Results We have selected an exemplar well-characterised biochemical pathway, the phenylacetate degradation pathway, and we show that its complex history is only compatible with a model where a selective advantage accrues from moving genes closer together. This selective pressure is likely to be reasonably weak and only twice in our dataset of 102 genomes do we see independent formation of a complete cluster containing all the catabolic genes in the pathway. Additionally, de novo clustering of genes clearly occurs repeatedly, even though recombination should result in the random dispersal of such genes in their respective genomes. Interspecies gene transfer has frequently replaced in situ copies of genes resulting in clusters that have similar content but very different evolutionary histories. Conclusion Our model for cluster formation in prokaryotes, therefore, consists of a two-stage selection process. The first stage is selection to move genes closer together, either because of macromolecular crowding, chromatin relaxation or transcriptional regulation pressure. This proximity opportunity sets up a separate selection for co-transcription. © Martin and McInerney; licensee BioMed Central Ltd. 2009 |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR026964686</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519185723.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201007s2009 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1186/1471-2148-9-36</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR026964686</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)1471-2148-9-36-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Martin, Fergal J</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Recurring cluster and operon assembly for Phenylacetate degradation genes</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2009</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© Martin and McInerney; licensee BioMed Central Ltd. 2009</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background A large number of theories have been advanced to explain why genes involved in the same biochemical processes are often co-located in genomes. Most of these theories have been dismissed because empirical data do not match the expectations of the models. In this work we test the hypothesis that cluster formation is most likely due to a selective pressure to gradually co-localise protein products and that operon formation is not an inevitable conclusion of the process. Results We have selected an exemplar well-characterised biochemical pathway, the phenylacetate degradation pathway, and we show that its complex history is only compatible with a model where a selective advantage accrues from moving genes closer together. This selective pressure is likely to be reasonably weak and only twice in our dataset of 102 genomes do we see independent formation of a complete cluster containing all the catabolic genes in the pathway. Additionally, de novo clustering of genes clearly occurs repeatedly, even though recombination should result in the random dispersal of such genes in their respective genomes. Interspecies gene transfer has frequently replaced in situ copies of genes resulting in clusters that have similar content but very different evolutionary histories. Conclusion Our model for cluster formation in prokaryotes, therefore, consists of a two-stage selection process. The first stage is selection to move genes closer together, either because of macromolecular crowding, chromatin relaxation or transcriptional regulation pressure. This proximity opportunity sets up a separate selection for co-transcription.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Horizontal Gene Transfer</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Gene Content</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Catabolic Gene</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Operon Structure</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Macromolecular Crowding</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">McInerney, James O</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">BMC evolutionary biology</subfield><subfield code="d">London : BioMed Central, 2001</subfield><subfield code="g">9(2009), 1 vom: 10. 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