Inference of transcription modification in long-live yeast strains from their expression profiles

Background Three kinases: Sch9, PKA and TOR, are suggested to be involved in both the replicative and chronological ageing in yeast. They function in pathways whose down-regulation leads to life span extension. Several stress response proteins, including two transcription factors Msn2 and Msn4, medi...
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Autor*in:	Cheng, Chao [verfasserIn] Fabrizio, Paola Ge, Huanying Longo, Valter D Li, Lei M

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2007

Schlagwörter:	Ribosomal Protein Gene Life Span Extension RAPA Enrich Motif Chronological Ageing

Anmerkung:	© Cheng et al; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (

Übergeordnetes Werk:	Enthalten in: BMC genomics - London : BioMed Central, 2000, 8(2007), 1 vom: 06. Juli
Übergeordnetes Werk:	volume:8 ; year:2007 ; number:1 ; day:06 ; month:07

Links:	Volltext

DOI / URN:	10.1186/1471-2164-8-219

Katalog-ID:	SPR027032701

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520			\|a Background Three kinases: Sch9, PKA and TOR, are suggested to be involved in both the replicative and chronological ageing in yeast. They function in pathways whose down-regulation leads to life span extension. Several stress response proteins, including two transcription factors Msn2 and Msn4, mediate the longevity extension phenotype associated with decreased activity of either Sch9, PKA, or TOR. However, the mechanisms of longevity, especially the underlying transcription program have not been fully understood. Results We measured the gene expression profiles in wild type yeast and three long-lived mutants: sch9 Δ, ras2 Δ, and tor1 Δ. To elucidate the transcription program that may account for the longevity extension, we identified the transcription factors that are systematically and significantly associated with the expression differentiation in these mutants with respect to wild type by integrating microarray expression data with motif and ChIP-chip data, respectively. Our analysis suggests that three stress response transcription factors, Msn2, Msn4 and Gis1, are activated in all the three mutants. We also identify some other transcription factors such as Fhl1 and Hsf1, which may also be involved in the transcriptional modification in the long-lived mutants. Conclusion Combining microarray expression data with other data sources such as motif and ChIP-chip data provides biological insights into the transcription modification that leads to life span extension. In the chronologically long-lived mutant: sch9 Δ, ras2 Δ, and tor1 Δ, several common stress response transcription factors are activated compared with the wild type according to our systematic transcription inference.
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700	1		\|a Longo, Valter D \|4 aut
700	1		\|a Li, Lei M \|4 aut
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allfields	10.1186/1471-2164-8-219 doi (DE-627)SPR027032701 (SPR)1471-2164-8-219-e DE-627 ger DE-627 rakwb eng Cheng, Chao verfasserin aut Inference of transcription modification in long-live yeast strains from their expression profiles 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Cheng et al; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Three kinases: Sch9, PKA and TOR, are suggested to be involved in both the replicative and chronological ageing in yeast. They function in pathways whose down-regulation leads to life span extension. Several stress response proteins, including two transcription factors Msn2 and Msn4, mediate the longevity extension phenotype associated with decreased activity of either Sch9, PKA, or TOR. However, the mechanisms of longevity, especially the underlying transcription program have not been fully understood. Results We measured the gene expression profiles in wild type yeast and three long-lived mutants: sch9 Δ, ras2 Δ, and tor1 Δ. To elucidate the transcription program that may account for the longevity extension, we identified the transcription factors that are systematically and significantly associated with the expression differentiation in these mutants with respect to wild type by integrating microarray expression data with motif and ChIP-chip data, respectively. Our analysis suggests that three stress response transcription factors, Msn2, Msn4 and Gis1, are activated in all the three mutants. We also identify some other transcription factors such as Fhl1 and Hsf1, which may also be involved in the transcriptional modification in the long-lived mutants. Conclusion Combining microarray expression data with other data sources such as motif and ChIP-chip data provides biological insights into the transcription modification that leads to life span extension. In the chronologically long-lived mutant: sch9 Δ, ras2 Δ, and tor1 Δ, several common stress response transcription factors are activated compared with the wild type according to our systematic transcription inference. Ribosomal Protein Gene (dpeaa)DE-He213 Life Span Extension (dpeaa)DE-He213 RAPA (dpeaa)DE-He213 Enrich Motif (dpeaa)DE-He213 Chronological Ageing (dpeaa)DE-He213 Fabrizio, Paola aut Ge, Huanying aut Longo, Valter D aut Li, Lei M aut Enthalten in BMC genomics London : BioMed Central, 2000 8(2007), 1 vom: 06. Juli (DE-627)326644954 (DE-600)2041499-7 1471-2164 nnns volume:8 year:2007 number:1 day:06 month:07 https://dx.doi.org/10.1186/1471-2164-8-219 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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 8 2007 1 06 07
spelling	10.1186/1471-2164-8-219 doi (DE-627)SPR027032701 (SPR)1471-2164-8-219-e DE-627 ger DE-627 rakwb eng Cheng, Chao verfasserin aut Inference of transcription modification in long-live yeast strains from their expression profiles 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Cheng et al; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Three kinases: Sch9, PKA and TOR, are suggested to be involved in both the replicative and chronological ageing in yeast. They function in pathways whose down-regulation leads to life span extension. Several stress response proteins, including two transcription factors Msn2 and Msn4, mediate the longevity extension phenotype associated with decreased activity of either Sch9, PKA, or TOR. However, the mechanisms of longevity, especially the underlying transcription program have not been fully understood. Results We measured the gene expression profiles in wild type yeast and three long-lived mutants: sch9 Δ, ras2 Δ, and tor1 Δ. To elucidate the transcription program that may account for the longevity extension, we identified the transcription factors that are systematically and significantly associated with the expression differentiation in these mutants with respect to wild type by integrating microarray expression data with motif and ChIP-chip data, respectively. Our analysis suggests that three stress response transcription factors, Msn2, Msn4 and Gis1, are activated in all the three mutants. We also identify some other transcription factors such as Fhl1 and Hsf1, which may also be involved in the transcriptional modification in the long-lived mutants. Conclusion Combining microarray expression data with other data sources such as motif and ChIP-chip data provides biological insights into the transcription modification that leads to life span extension. In the chronologically long-lived mutant: sch9 Δ, ras2 Δ, and tor1 Δ, several common stress response transcription factors are activated compared with the wild type according to our systematic transcription inference. Ribosomal Protein Gene (dpeaa)DE-He213 Life Span Extension (dpeaa)DE-He213 RAPA (dpeaa)DE-He213 Enrich Motif (dpeaa)DE-He213 Chronological Ageing (dpeaa)DE-He213 Fabrizio, Paola aut Ge, Huanying aut Longo, Valter D aut Li, Lei M aut Enthalten in BMC genomics London : BioMed Central, 2000 8(2007), 1 vom: 06. Juli (DE-627)326644954 (DE-600)2041499-7 1471-2164 nnns volume:8 year:2007 number:1 day:06 month:07 https://dx.doi.org/10.1186/1471-2164-8-219 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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 8 2007 1 06 07
allfields_unstemmed	10.1186/1471-2164-8-219 doi (DE-627)SPR027032701 (SPR)1471-2164-8-219-e DE-627 ger DE-627 rakwb eng Cheng, Chao verfasserin aut Inference of transcription modification in long-live yeast strains from their expression profiles 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Cheng et al; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Three kinases: Sch9, PKA and TOR, are suggested to be involved in both the replicative and chronological ageing in yeast. They function in pathways whose down-regulation leads to life span extension. Several stress response proteins, including two transcription factors Msn2 and Msn4, mediate the longevity extension phenotype associated with decreased activity of either Sch9, PKA, or TOR. However, the mechanisms of longevity, especially the underlying transcription program have not been fully understood. Results We measured the gene expression profiles in wild type yeast and three long-lived mutants: sch9 Δ, ras2 Δ, and tor1 Δ. To elucidate the transcription program that may account for the longevity extension, we identified the transcription factors that are systematically and significantly associated with the expression differentiation in these mutants with respect to wild type by integrating microarray expression data with motif and ChIP-chip data, respectively. Our analysis suggests that three stress response transcription factors, Msn2, Msn4 and Gis1, are activated in all the three mutants. We also identify some other transcription factors such as Fhl1 and Hsf1, which may also be involved in the transcriptional modification in the long-lived mutants. Conclusion Combining microarray expression data with other data sources such as motif and ChIP-chip data provides biological insights into the transcription modification that leads to life span extension. In the chronologically long-lived mutant: sch9 Δ, ras2 Δ, and tor1 Δ, several common stress response transcription factors are activated compared with the wild type according to our systematic transcription inference. Ribosomal Protein Gene (dpeaa)DE-He213 Life Span Extension (dpeaa)DE-He213 RAPA (dpeaa)DE-He213 Enrich Motif (dpeaa)DE-He213 Chronological Ageing (dpeaa)DE-He213 Fabrizio, Paola aut Ge, Huanying aut Longo, Valter D aut Li, Lei M aut Enthalten in BMC genomics London : BioMed Central, 2000 8(2007), 1 vom: 06. Juli (DE-627)326644954 (DE-600)2041499-7 1471-2164 nnns volume:8 year:2007 number:1 day:06 month:07 https://dx.doi.org/10.1186/1471-2164-8-219 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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 8 2007 1 06 07
allfieldsGer	10.1186/1471-2164-8-219 doi (DE-627)SPR027032701 (SPR)1471-2164-8-219-e DE-627 ger DE-627 rakwb eng Cheng, Chao verfasserin aut Inference of transcription modification in long-live yeast strains from their expression profiles 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Cheng et al; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Three kinases: Sch9, PKA and TOR, are suggested to be involved in both the replicative and chronological ageing in yeast. They function in pathways whose down-regulation leads to life span extension. Several stress response proteins, including two transcription factors Msn2 and Msn4, mediate the longevity extension phenotype associated with decreased activity of either Sch9, PKA, or TOR. However, the mechanisms of longevity, especially the underlying transcription program have not been fully understood. Results We measured the gene expression profiles in wild type yeast and three long-lived mutants: sch9 Δ, ras2 Δ, and tor1 Δ. To elucidate the transcription program that may account for the longevity extension, we identified the transcription factors that are systematically and significantly associated with the expression differentiation in these mutants with respect to wild type by integrating microarray expression data with motif and ChIP-chip data, respectively. Our analysis suggests that three stress response transcription factors, Msn2, Msn4 and Gis1, are activated in all the three mutants. We also identify some other transcription factors such as Fhl1 and Hsf1, which may also be involved in the transcriptional modification in the long-lived mutants. Conclusion Combining microarray expression data with other data sources such as motif and ChIP-chip data provides biological insights into the transcription modification that leads to life span extension. In the chronologically long-lived mutant: sch9 Δ, ras2 Δ, and tor1 Δ, several common stress response transcription factors are activated compared with the wild type according to our systematic transcription inference. Ribosomal Protein Gene (dpeaa)DE-He213 Life Span Extension (dpeaa)DE-He213 RAPA (dpeaa)DE-He213 Enrich Motif (dpeaa)DE-He213 Chronological Ageing (dpeaa)DE-He213 Fabrizio, Paola aut Ge, Huanying aut Longo, Valter D aut Li, Lei M aut Enthalten in BMC genomics London : BioMed Central, 2000 8(2007), 1 vom: 06. Juli (DE-627)326644954 (DE-600)2041499-7 1471-2164 nnns volume:8 year:2007 number:1 day:06 month:07 https://dx.doi.org/10.1186/1471-2164-8-219 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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 8 2007 1 06 07
allfieldsSound	10.1186/1471-2164-8-219 doi (DE-627)SPR027032701 (SPR)1471-2164-8-219-e DE-627 ger DE-627 rakwb eng Cheng, Chao verfasserin aut Inference of transcription modification in long-live yeast strains from their expression profiles 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Cheng et al; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Three kinases: Sch9, PKA and TOR, are suggested to be involved in both the replicative and chronological ageing in yeast. They function in pathways whose down-regulation leads to life span extension. Several stress response proteins, including two transcription factors Msn2 and Msn4, mediate the longevity extension phenotype associated with decreased activity of either Sch9, PKA, or TOR. However, the mechanisms of longevity, especially the underlying transcription program have not been fully understood. Results We measured the gene expression profiles in wild type yeast and three long-lived mutants: sch9 Δ, ras2 Δ, and tor1 Δ. To elucidate the transcription program that may account for the longevity extension, we identified the transcription factors that are systematically and significantly associated with the expression differentiation in these mutants with respect to wild type by integrating microarray expression data with motif and ChIP-chip data, respectively. Our analysis suggests that three stress response transcription factors, Msn2, Msn4 and Gis1, are activated in all the three mutants. We also identify some other transcription factors such as Fhl1 and Hsf1, which may also be involved in the transcriptional modification in the long-lived mutants. Conclusion Combining microarray expression data with other data sources such as motif and ChIP-chip data provides biological insights into the transcription modification that leads to life span extension. In the chronologically long-lived mutant: sch9 Δ, ras2 Δ, and tor1 Δ, several common stress response transcription factors are activated compared with the wild type according to our systematic transcription inference. Ribosomal Protein Gene (dpeaa)DE-He213 Life Span Extension (dpeaa)DE-He213 RAPA (dpeaa)DE-He213 Enrich Motif (dpeaa)DE-He213 Chronological Ageing (dpeaa)DE-He213 Fabrizio, Paola aut Ge, Huanying aut Longo, Valter D aut Li, Lei M aut Enthalten in BMC genomics London : BioMed Central, 2000 8(2007), 1 vom: 06. Juli (DE-627)326644954 (DE-600)2041499-7 1471-2164 nnns volume:8 year:2007 number:1 day:06 month:07 https://dx.doi.org/10.1186/1471-2164-8-219 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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 8 2007 1 06 07
language	English
source	Enthalten in BMC genomics 8(2007), 1 vom: 06. Juli volume:8 year:2007 number:1 day:06 month:07
sourceStr	Enthalten in BMC genomics 8(2007), 1 vom: 06. Juli volume:8 year:2007 number:1 day:06 month:07
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Ribosomal Protein Gene Life Span Extension RAPA Enrich Motif Chronological Ageing
isfreeaccess_bool	false
container_title	BMC genomics
authorswithroles_txt_mv	Cheng, Chao @@aut@@ Fabrizio, Paola @@aut@@ Ge, Huanying @@aut@@ Longo, Valter D @@aut@@ Li, Lei M @@aut@@
publishDateDaySort_date	2007-07-06T00:00:00Z
hierarchy_top_id	326644954
id	SPR027032701
language_de	englisch
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This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background Three kinases: Sch9, PKA and TOR, are suggested to be involved in both the replicative and chronological ageing in yeast. They function in pathways whose down-regulation leads to life span extension. Several stress response proteins, including two transcription factors Msn2 and Msn4, mediate the longevity extension phenotype associated with decreased activity of either Sch9, PKA, or TOR. However, the mechanisms of longevity, especially the underlying transcription program have not been fully understood. Results We measured the gene expression profiles in wild type yeast and three long-lived mutants: sch9 Δ, ras2 Δ, and tor1 Δ. To elucidate the transcription program that may account for the longevity extension, we identified the transcription factors that are systematically and significantly associated with the expression differentiation in these mutants with respect to wild type by integrating microarray expression data with motif and ChIP-chip data, respectively. Our analysis suggests that three stress response transcription factors, Msn2, Msn4 and Gis1, are activated in all the three mutants. We also identify some other transcription factors such as Fhl1 and Hsf1, which may also be involved in the transcriptional modification in the long-lived mutants. Conclusion Combining microarray expression data with other data sources such as motif and ChIP-chip data provides biological insights into the transcription modification that leads to life span extension. 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author	Cheng, Chao
spellingShingle	Cheng, Chao misc Ribosomal Protein Gene misc Life Span Extension misc RAPA misc Enrich Motif misc Chronological Ageing Inference of transcription modification in long-live yeast strains from their expression profiles
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topic_title	Inference of transcription modification in long-live yeast strains from their expression profiles Ribosomal Protein Gene (dpeaa)DE-He213 Life Span Extension (dpeaa)DE-He213 RAPA (dpeaa)DE-He213 Enrich Motif (dpeaa)DE-He213 Chronological Ageing (dpeaa)DE-He213
topic	misc Ribosomal Protein Gene misc Life Span Extension misc RAPA misc Enrich Motif misc Chronological Ageing
topic_unstemmed	misc Ribosomal Protein Gene misc Life Span Extension misc RAPA misc Enrich Motif misc Chronological Ageing
topic_browse	misc Ribosomal Protein Gene misc Life Span Extension misc RAPA misc Enrich Motif misc Chronological Ageing
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title	Inference of transcription modification in long-live yeast strains from their expression profiles
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title_full	Inference of transcription modification in long-live yeast strains from their expression profiles
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author_browse	Cheng, Chao Fabrizio, Paola Ge, Huanying Longo, Valter D Li, Lei M
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title_sort	inference of transcription modification in long-live yeast strains from their expression profiles
title_auth	Inference of transcription modification in long-live yeast strains from their expression profiles
abstract	Background Three kinases: Sch9, PKA and TOR, are suggested to be involved in both the replicative and chronological ageing in yeast. They function in pathways whose down-regulation leads to life span extension. Several stress response proteins, including two transcription factors Msn2 and Msn4, mediate the longevity extension phenotype associated with decreased activity of either Sch9, PKA, or TOR. However, the mechanisms of longevity, especially the underlying transcription program have not been fully understood. Results We measured the gene expression profiles in wild type yeast and three long-lived mutants: sch9 Δ, ras2 Δ, and tor1 Δ. To elucidate the transcription program that may account for the longevity extension, we identified the transcription factors that are systematically and significantly associated with the expression differentiation in these mutants with respect to wild type by integrating microarray expression data with motif and ChIP-chip data, respectively. Our analysis suggests that three stress response transcription factors, Msn2, Msn4 and Gis1, are activated in all the three mutants. We also identify some other transcription factors such as Fhl1 and Hsf1, which may also be involved in the transcriptional modification in the long-lived mutants. Conclusion Combining microarray expression data with other data sources such as motif and ChIP-chip data provides biological insights into the transcription modification that leads to life span extension. In the chronologically long-lived mutant: sch9 Δ, ras2 Δ, and tor1 Δ, several common stress response transcription factors are activated compared with the wild type according to our systematic transcription inference. © Cheng et al; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
abstractGer	Background Three kinases: Sch9, PKA and TOR, are suggested to be involved in both the replicative and chronological ageing in yeast. They function in pathways whose down-regulation leads to life span extension. Several stress response proteins, including two transcription factors Msn2 and Msn4, mediate the longevity extension phenotype associated with decreased activity of either Sch9, PKA, or TOR. However, the mechanisms of longevity, especially the underlying transcription program have not been fully understood. Results We measured the gene expression profiles in wild type yeast and three long-lived mutants: sch9 Δ, ras2 Δ, and tor1 Δ. To elucidate the transcription program that may account for the longevity extension, we identified the transcription factors that are systematically and significantly associated with the expression differentiation in these mutants with respect to wild type by integrating microarray expression data with motif and ChIP-chip data, respectively. Our analysis suggests that three stress response transcription factors, Msn2, Msn4 and Gis1, are activated in all the three mutants. We also identify some other transcription factors such as Fhl1 and Hsf1, which may also be involved in the transcriptional modification in the long-lived mutants. Conclusion Combining microarray expression data with other data sources such as motif and ChIP-chip data provides biological insights into the transcription modification that leads to life span extension. In the chronologically long-lived mutant: sch9 Δ, ras2 Δ, and tor1 Δ, several common stress response transcription factors are activated compared with the wild type according to our systematic transcription inference. © Cheng et al; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
abstract_unstemmed	Background Three kinases: Sch9, PKA and TOR, are suggested to be involved in both the replicative and chronological ageing in yeast. They function in pathways whose down-regulation leads to life span extension. Several stress response proteins, including two transcription factors Msn2 and Msn4, mediate the longevity extension phenotype associated with decreased activity of either Sch9, PKA, or TOR. However, the mechanisms of longevity, especially the underlying transcription program have not been fully understood. Results We measured the gene expression profiles in wild type yeast and three long-lived mutants: sch9 Δ, ras2 Δ, and tor1 Δ. To elucidate the transcription program that may account for the longevity extension, we identified the transcription factors that are systematically and significantly associated with the expression differentiation in these mutants with respect to wild type by integrating microarray expression data with motif and ChIP-chip data, respectively. Our analysis suggests that three stress response transcription factors, Msn2, Msn4 and Gis1, are activated in all the three mutants. We also identify some other transcription factors such as Fhl1 and Hsf1, which may also be involved in the transcriptional modification in the long-lived mutants. Conclusion Combining microarray expression data with other data sources such as motif and ChIP-chip data provides biological insights into the transcription modification that leads to life span extension. In the chronologically long-lived mutant: sch9 Δ, ras2 Δ, and tor1 Δ, several common stress response transcription factors are activated compared with the wild type according to our systematic transcription inference. © Cheng et al; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
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title_short	Inference of transcription modification in long-live yeast strains from their expression profiles
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Inference of transcription modification in long-live yeast strains from their expression profiles

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