Biased exonization of transposed elements in duplicated genes: A lesson from the TIF-IA gene

Background Gene duplication and exonization of intronic transposed elements are two mechanisms that enhance genomic diversity. We examined whether there is less selection against exonization of transposed elements in duplicated genes than in single-copy genes. Results Genome-wide analysis of exoniza...
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Autor*in:	Amit, Maayan [verfasserIn] Sela, Noa Keren, Hadas Melamed, Ze'ev Muler, Inna Shomron, Noam Izraeli, Shai Ast, Gil

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2007

Schlagwörter:	Alternative Splice Transpose Element Gene Duplication Duplicate Gene Chronic Granulomatous Disease

Anmerkung:	© Amit et al; licensee BioMed Central Ltd. 2007

Übergeordnetes Werk:	Enthalten in: BMC molecular biology - London : BioMed Central, 2000, 8(2007), 1 vom: 29. Nov.
Übergeordnetes Werk:	volume:8 ; year:2007 ; number:1 ; day:29 ; month:11

Links:	Volltext

DOI / URN:	10.1186/1471-2199-8-109

Katalog-ID:	SPR027215806

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245	1	0	\|a Biased exonization of transposed elements in duplicated genes: A lesson from the TIF-IA gene
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520			\|a Background Gene duplication and exonization of intronic transposed elements are two mechanisms that enhance genomic diversity. We examined whether there is less selection against exonization of transposed elements in duplicated genes than in single-copy genes. Results Genome-wide analysis of exonization of transposed elements revealed a higher rate of exonization within duplicated genes relative to single-copy genes. The gene for TIF-IA, an RNA polymerase I transcription initiation factor, underwent a humanoid-specific triplication, all three copies of the gene are active transcriptionally, although only one copy retains the ability to generate the TIF-IA protein. Prior to TIF-IA triplication, an Alu element was inserted into the first intron. In one of the non-protein coding copies, this Alu is exonized. We identified a single point mutation leading to exonization in one of the gene duplicates. When this mutation was introduced into the TIF-IA coding copy, exonization was activated and the level of the protein-coding mRNA was reduced substantially. A very low level of exonization was detected in normal human cells. However, this exonization was abundant in most leukemia cell lines evaluated, although the genomic sequence is unchanged in these cancerous cells compared to normal cells. Conclusion The definition of the Alu element within the TIF-IA gene as an exon is restricted to certain types of cancers; the element is not exonized in normal human cells. These results further our understanding of the delicate interplay between gene duplication and alternative splicing and of the molecular evolutionary mechanisms leading to genetic innovations. This implies the existence of purifying selection against exonization in single copy genes, with duplicate genes free from such constrains.
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700	1		\|a Shomron, Noam \|4 aut
700	1		\|a Izraeli, Shai \|4 aut
700	1		\|a Ast, Gil \|4 aut
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Indexfelder

author_variant	m a ma n s ns h k hk z m zm i m im n s ns s i si g a ga
matchkey_str	article:14712199:2007----::isdxnztootasoeeeetidpiaegnsl
hierarchy_sort_str	2007
publishDate	2007
allfields	10.1186/1471-2199-8-109 doi (DE-627)SPR027215806 (SPR)1471-2199-8-109-e DE-627 ger DE-627 rakwb eng Amit, Maayan verfasserin aut Biased exonization of transposed elements in duplicated genes: A lesson from the TIF-IA gene 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Amit et al; licensee BioMed Central Ltd. 2007 Background Gene duplication and exonization of intronic transposed elements are two mechanisms that enhance genomic diversity. We examined whether there is less selection against exonization of transposed elements in duplicated genes than in single-copy genes. Results Genome-wide analysis of exonization of transposed elements revealed a higher rate of exonization within duplicated genes relative to single-copy genes. The gene for TIF-IA, an RNA polymerase I transcription initiation factor, underwent a humanoid-specific triplication, all three copies of the gene are active transcriptionally, although only one copy retains the ability to generate the TIF-IA protein. Prior to TIF-IA triplication, an Alu element was inserted into the first intron. In one of the non-protein coding copies, this Alu is exonized. We identified a single point mutation leading to exonization in one of the gene duplicates. When this mutation was introduced into the TIF-IA coding copy, exonization was activated and the level of the protein-coding mRNA was reduced substantially. A very low level of exonization was detected in normal human cells. However, this exonization was abundant in most leukemia cell lines evaluated, although the genomic sequence is unchanged in these cancerous cells compared to normal cells. Conclusion The definition of the Alu element within the TIF-IA gene as an exon is restricted to certain types of cancers; the element is not exonized in normal human cells. These results further our understanding of the delicate interplay between gene duplication and alternative splicing and of the molecular evolutionary mechanisms leading to genetic innovations. This implies the existence of purifying selection against exonization in single copy genes, with duplicate genes free from such constrains. Alternative Splice (dpeaa)DE-He213 Transpose Element (dpeaa)DE-He213 Gene Duplication (dpeaa)DE-He213 Duplicate Gene (dpeaa)DE-He213 Chronic Granulomatous Disease (dpeaa)DE-He213 Sela, Noa aut Keren, Hadas aut Melamed, Ze'ev aut Muler, Inna aut Shomron, Noam aut Izraeli, Shai aut Ast, Gil aut Enthalten in BMC molecular biology London : BioMed Central, 2000 8(2007), 1 vom: 29. Nov. (DE-627)326645004 (DE-600)2041506-0 1471-2199 nnns volume:8 year:2007 number:1 day:29 month:11 https://dx.doi.org/10.1186/1471-2199-8-109 kostenfrei 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_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 8 2007 1 29 11
spelling	10.1186/1471-2199-8-109 doi (DE-627)SPR027215806 (SPR)1471-2199-8-109-e DE-627 ger DE-627 rakwb eng Amit, Maayan verfasserin aut Biased exonization of transposed elements in duplicated genes: A lesson from the TIF-IA gene 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Amit et al; licensee BioMed Central Ltd. 2007 Background Gene duplication and exonization of intronic transposed elements are two mechanisms that enhance genomic diversity. We examined whether there is less selection against exonization of transposed elements in duplicated genes than in single-copy genes. Results Genome-wide analysis of exonization of transposed elements revealed a higher rate of exonization within duplicated genes relative to single-copy genes. The gene for TIF-IA, an RNA polymerase I transcription initiation factor, underwent a humanoid-specific triplication, all three copies of the gene are active transcriptionally, although only one copy retains the ability to generate the TIF-IA protein. Prior to TIF-IA triplication, an Alu element was inserted into the first intron. In one of the non-protein coding copies, this Alu is exonized. We identified a single point mutation leading to exonization in one of the gene duplicates. When this mutation was introduced into the TIF-IA coding copy, exonization was activated and the level of the protein-coding mRNA was reduced substantially. A very low level of exonization was detected in normal human cells. However, this exonization was abundant in most leukemia cell lines evaluated, although the genomic sequence is unchanged in these cancerous cells compared to normal cells. Conclusion The definition of the Alu element within the TIF-IA gene as an exon is restricted to certain types of cancers; the element is not exonized in normal human cells. These results further our understanding of the delicate interplay between gene duplication and alternative splicing and of the molecular evolutionary mechanisms leading to genetic innovations. This implies the existence of purifying selection against exonization in single copy genes, with duplicate genes free from such constrains. Alternative Splice (dpeaa)DE-He213 Transpose Element (dpeaa)DE-He213 Gene Duplication (dpeaa)DE-He213 Duplicate Gene (dpeaa)DE-He213 Chronic Granulomatous Disease (dpeaa)DE-He213 Sela, Noa aut Keren, Hadas aut Melamed, Ze'ev aut Muler, Inna aut Shomron, Noam aut Izraeli, Shai aut Ast, Gil aut Enthalten in BMC molecular biology London : BioMed Central, 2000 8(2007), 1 vom: 29. Nov. (DE-627)326645004 (DE-600)2041506-0 1471-2199 nnns volume:8 year:2007 number:1 day:29 month:11 https://dx.doi.org/10.1186/1471-2199-8-109 kostenfrei 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_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 8 2007 1 29 11
allfields_unstemmed	10.1186/1471-2199-8-109 doi (DE-627)SPR027215806 (SPR)1471-2199-8-109-e DE-627 ger DE-627 rakwb eng Amit, Maayan verfasserin aut Biased exonization of transposed elements in duplicated genes: A lesson from the TIF-IA gene 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Amit et al; licensee BioMed Central Ltd. 2007 Background Gene duplication and exonization of intronic transposed elements are two mechanisms that enhance genomic diversity. We examined whether there is less selection against exonization of transposed elements in duplicated genes than in single-copy genes. Results Genome-wide analysis of exonization of transposed elements revealed a higher rate of exonization within duplicated genes relative to single-copy genes. The gene for TIF-IA, an RNA polymerase I transcription initiation factor, underwent a humanoid-specific triplication, all three copies of the gene are active transcriptionally, although only one copy retains the ability to generate the TIF-IA protein. Prior to TIF-IA triplication, an Alu element was inserted into the first intron. In one of the non-protein coding copies, this Alu is exonized. We identified a single point mutation leading to exonization in one of the gene duplicates. When this mutation was introduced into the TIF-IA coding copy, exonization was activated and the level of the protein-coding mRNA was reduced substantially. A very low level of exonization was detected in normal human cells. However, this exonization was abundant in most leukemia cell lines evaluated, although the genomic sequence is unchanged in these cancerous cells compared to normal cells. Conclusion The definition of the Alu element within the TIF-IA gene as an exon is restricted to certain types of cancers; the element is not exonized in normal human cells. These results further our understanding of the delicate interplay between gene duplication and alternative splicing and of the molecular evolutionary mechanisms leading to genetic innovations. This implies the existence of purifying selection against exonization in single copy genes, with duplicate genes free from such constrains. Alternative Splice (dpeaa)DE-He213 Transpose Element (dpeaa)DE-He213 Gene Duplication (dpeaa)DE-He213 Duplicate Gene (dpeaa)DE-He213 Chronic Granulomatous Disease (dpeaa)DE-He213 Sela, Noa aut Keren, Hadas aut Melamed, Ze'ev aut Muler, Inna aut Shomron, Noam aut Izraeli, Shai aut Ast, Gil aut Enthalten in BMC molecular biology London : BioMed Central, 2000 8(2007), 1 vom: 29. Nov. (DE-627)326645004 (DE-600)2041506-0 1471-2199 nnns volume:8 year:2007 number:1 day:29 month:11 https://dx.doi.org/10.1186/1471-2199-8-109 kostenfrei 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_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 8 2007 1 29 11
allfieldsGer	10.1186/1471-2199-8-109 doi (DE-627)SPR027215806 (SPR)1471-2199-8-109-e DE-627 ger DE-627 rakwb eng Amit, Maayan verfasserin aut Biased exonization of transposed elements in duplicated genes: A lesson from the TIF-IA gene 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Amit et al; licensee BioMed Central Ltd. 2007 Background Gene duplication and exonization of intronic transposed elements are two mechanisms that enhance genomic diversity. We examined whether there is less selection against exonization of transposed elements in duplicated genes than in single-copy genes. Results Genome-wide analysis of exonization of transposed elements revealed a higher rate of exonization within duplicated genes relative to single-copy genes. The gene for TIF-IA, an RNA polymerase I transcription initiation factor, underwent a humanoid-specific triplication, all three copies of the gene are active transcriptionally, although only one copy retains the ability to generate the TIF-IA protein. Prior to TIF-IA triplication, an Alu element was inserted into the first intron. In one of the non-protein coding copies, this Alu is exonized. We identified a single point mutation leading to exonization in one of the gene duplicates. When this mutation was introduced into the TIF-IA coding copy, exonization was activated and the level of the protein-coding mRNA was reduced substantially. A very low level of exonization was detected in normal human cells. However, this exonization was abundant in most leukemia cell lines evaluated, although the genomic sequence is unchanged in these cancerous cells compared to normal cells. Conclusion The definition of the Alu element within the TIF-IA gene as an exon is restricted to certain types of cancers; the element is not exonized in normal human cells. These results further our understanding of the delicate interplay between gene duplication and alternative splicing and of the molecular evolutionary mechanisms leading to genetic innovations. This implies the existence of purifying selection against exonization in single copy genes, with duplicate genes free from such constrains. Alternative Splice (dpeaa)DE-He213 Transpose Element (dpeaa)DE-He213 Gene Duplication (dpeaa)DE-He213 Duplicate Gene (dpeaa)DE-He213 Chronic Granulomatous Disease (dpeaa)DE-He213 Sela, Noa aut Keren, Hadas aut Melamed, Ze'ev aut Muler, Inna aut Shomron, Noam aut Izraeli, Shai aut Ast, Gil aut Enthalten in BMC molecular biology London : BioMed Central, 2000 8(2007), 1 vom: 29. Nov. (DE-627)326645004 (DE-600)2041506-0 1471-2199 nnns volume:8 year:2007 number:1 day:29 month:11 https://dx.doi.org/10.1186/1471-2199-8-109 kostenfrei 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_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 8 2007 1 29 11
allfieldsSound	10.1186/1471-2199-8-109 doi (DE-627)SPR027215806 (SPR)1471-2199-8-109-e DE-627 ger DE-627 rakwb eng Amit, Maayan verfasserin aut Biased exonization of transposed elements in duplicated genes: A lesson from the TIF-IA gene 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Amit et al; licensee BioMed Central Ltd. 2007 Background Gene duplication and exonization of intronic transposed elements are two mechanisms that enhance genomic diversity. We examined whether there is less selection against exonization of transposed elements in duplicated genes than in single-copy genes. Results Genome-wide analysis of exonization of transposed elements revealed a higher rate of exonization within duplicated genes relative to single-copy genes. The gene for TIF-IA, an RNA polymerase I transcription initiation factor, underwent a humanoid-specific triplication, all three copies of the gene are active transcriptionally, although only one copy retains the ability to generate the TIF-IA protein. Prior to TIF-IA triplication, an Alu element was inserted into the first intron. In one of the non-protein coding copies, this Alu is exonized. We identified a single point mutation leading to exonization in one of the gene duplicates. When this mutation was introduced into the TIF-IA coding copy, exonization was activated and the level of the protein-coding mRNA was reduced substantially. A very low level of exonization was detected in normal human cells. However, this exonization was abundant in most leukemia cell lines evaluated, although the genomic sequence is unchanged in these cancerous cells compared to normal cells. Conclusion The definition of the Alu element within the TIF-IA gene as an exon is restricted to certain types of cancers; the element is not exonized in normal human cells. These results further our understanding of the delicate interplay between gene duplication and alternative splicing and of the molecular evolutionary mechanisms leading to genetic innovations. This implies the existence of purifying selection against exonization in single copy genes, with duplicate genes free from such constrains. Alternative Splice (dpeaa)DE-He213 Transpose Element (dpeaa)DE-He213 Gene Duplication (dpeaa)DE-He213 Duplicate Gene (dpeaa)DE-He213 Chronic Granulomatous Disease (dpeaa)DE-He213 Sela, Noa aut Keren, Hadas aut Melamed, Ze'ev aut Muler, Inna aut Shomron, Noam aut Izraeli, Shai aut Ast, Gil aut Enthalten in BMC molecular biology London : BioMed Central, 2000 8(2007), 1 vom: 29. Nov. (DE-627)326645004 (DE-600)2041506-0 1471-2199 nnns volume:8 year:2007 number:1 day:29 month:11 https://dx.doi.org/10.1186/1471-2199-8-109 kostenfrei 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_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 8 2007 1 29 11
language	English
source	Enthalten in BMC molecular biology 8(2007), 1 vom: 29. Nov. volume:8 year:2007 number:1 day:29 month:11
sourceStr	Enthalten in BMC molecular biology 8(2007), 1 vom: 29. Nov. volume:8 year:2007 number:1 day:29 month:11
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Alternative Splice Transpose Element Gene Duplication Duplicate Gene Chronic Granulomatous Disease
isfreeaccess_bool	true
container_title	BMC molecular biology
authorswithroles_txt_mv	Amit, Maayan @@aut@@ Sela, Noa @@aut@@ Keren, Hadas @@aut@@ Melamed, Ze'ev @@aut@@ Muler, Inna @@aut@@ Shomron, Noam @@aut@@ Izraeli, Shai @@aut@@ Ast, Gil @@aut@@
publishDateDaySort_date	2007-11-29T00:00:00Z
hierarchy_top_id	326645004
id	SPR027215806
language_de	englisch
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A very low level of exonization was detected in normal human cells. However, this exonization was abundant in most leukemia cell lines evaluated, although the genomic sequence is unchanged in these cancerous cells compared to normal cells. Conclusion The definition of the Alu element within the TIF-IA gene as an exon is restricted to certain types of cancers; the element is not exonized in normal human cells. These results further our understanding of the delicate interplay between gene duplication and alternative splicing and of the molecular evolutionary mechanisms leading to genetic innovations. 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author	Amit, Maayan
spellingShingle	Amit, Maayan misc Alternative Splice misc Transpose Element misc Gene Duplication misc Duplicate Gene misc Chronic Granulomatous Disease Biased exonization of transposed elements in duplicated genes: A lesson from the TIF-IA gene
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topic_title	Biased exonization of transposed elements in duplicated genes: A lesson from the TIF-IA gene Alternative Splice (dpeaa)DE-He213 Transpose Element (dpeaa)DE-He213 Gene Duplication (dpeaa)DE-He213 Duplicate Gene (dpeaa)DE-He213 Chronic Granulomatous Disease (dpeaa)DE-He213
topic	misc Alternative Splice misc Transpose Element misc Gene Duplication misc Duplicate Gene misc Chronic Granulomatous Disease
topic_unstemmed	misc Alternative Splice misc Transpose Element misc Gene Duplication misc Duplicate Gene misc Chronic Granulomatous Disease
topic_browse	misc Alternative Splice misc Transpose Element misc Gene Duplication misc Duplicate Gene misc Chronic Granulomatous Disease
format_facet	Elektronische Aufsätze Aufsätze Elektronische Ressource
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title	Biased exonization of transposed elements in duplicated genes: A lesson from the TIF-IA gene
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title_full	Biased exonization of transposed elements in duplicated genes: A lesson from the TIF-IA gene
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author_browse	Amit, Maayan Sela, Noa Keren, Hadas Melamed, Ze'ev Muler, Inna Shomron, Noam Izraeli, Shai Ast, Gil
container_volume	8
format_se	Elektronische Aufsätze
author-letter	Amit, Maayan
doi_str_mv	10.1186/1471-2199-8-109
title_sort	biased exonization of transposed elements in duplicated genes: a lesson from the tif-ia gene
title_auth	Biased exonization of transposed elements in duplicated genes: A lesson from the TIF-IA gene
abstract	Background Gene duplication and exonization of intronic transposed elements are two mechanisms that enhance genomic diversity. We examined whether there is less selection against exonization of transposed elements in duplicated genes than in single-copy genes. Results Genome-wide analysis of exonization of transposed elements revealed a higher rate of exonization within duplicated genes relative to single-copy genes. The gene for TIF-IA, an RNA polymerase I transcription initiation factor, underwent a humanoid-specific triplication, all three copies of the gene are active transcriptionally, although only one copy retains the ability to generate the TIF-IA protein. Prior to TIF-IA triplication, an Alu element was inserted into the first intron. In one of the non-protein coding copies, this Alu is exonized. We identified a single point mutation leading to exonization in one of the gene duplicates. When this mutation was introduced into the TIF-IA coding copy, exonization was activated and the level of the protein-coding mRNA was reduced substantially. A very low level of exonization was detected in normal human cells. However, this exonization was abundant in most leukemia cell lines evaluated, although the genomic sequence is unchanged in these cancerous cells compared to normal cells. Conclusion The definition of the Alu element within the TIF-IA gene as an exon is restricted to certain types of cancers; the element is not exonized in normal human cells. These results further our understanding of the delicate interplay between gene duplication and alternative splicing and of the molecular evolutionary mechanisms leading to genetic innovations. This implies the existence of purifying selection against exonization in single copy genes, with duplicate genes free from such constrains. © Amit et al; licensee BioMed Central Ltd. 2007
abstractGer	Background Gene duplication and exonization of intronic transposed elements are two mechanisms that enhance genomic diversity. We examined whether there is less selection against exonization of transposed elements in duplicated genes than in single-copy genes. Results Genome-wide analysis of exonization of transposed elements revealed a higher rate of exonization within duplicated genes relative to single-copy genes. The gene for TIF-IA, an RNA polymerase I transcription initiation factor, underwent a humanoid-specific triplication, all three copies of the gene are active transcriptionally, although only one copy retains the ability to generate the TIF-IA protein. Prior to TIF-IA triplication, an Alu element was inserted into the first intron. In one of the non-protein coding copies, this Alu is exonized. We identified a single point mutation leading to exonization in one of the gene duplicates. When this mutation was introduced into the TIF-IA coding copy, exonization was activated and the level of the protein-coding mRNA was reduced substantially. A very low level of exonization was detected in normal human cells. However, this exonization was abundant in most leukemia cell lines evaluated, although the genomic sequence is unchanged in these cancerous cells compared to normal cells. Conclusion The definition of the Alu element within the TIF-IA gene as an exon is restricted to certain types of cancers; the element is not exonized in normal human cells. These results further our understanding of the delicate interplay between gene duplication and alternative splicing and of the molecular evolutionary mechanisms leading to genetic innovations. This implies the existence of purifying selection against exonization in single copy genes, with duplicate genes free from such constrains. © Amit et al; licensee BioMed Central Ltd. 2007
abstract_unstemmed	Background Gene duplication and exonization of intronic transposed elements are two mechanisms that enhance genomic diversity. We examined whether there is less selection against exonization of transposed elements in duplicated genes than in single-copy genes. Results Genome-wide analysis of exonization of transposed elements revealed a higher rate of exonization within duplicated genes relative to single-copy genes. The gene for TIF-IA, an RNA polymerase I transcription initiation factor, underwent a humanoid-specific triplication, all three copies of the gene are active transcriptionally, although only one copy retains the ability to generate the TIF-IA protein. Prior to TIF-IA triplication, an Alu element was inserted into the first intron. In one of the non-protein coding copies, this Alu is exonized. We identified a single point mutation leading to exonization in one of the gene duplicates. When this mutation was introduced into the TIF-IA coding copy, exonization was activated and the level of the protein-coding mRNA was reduced substantially. A very low level of exonization was detected in normal human cells. However, this exonization was abundant in most leukemia cell lines evaluated, although the genomic sequence is unchanged in these cancerous cells compared to normal cells. Conclusion The definition of the Alu element within the TIF-IA gene as an exon is restricted to certain types of cancers; the element is not exonized in normal human cells. These results further our understanding of the delicate interplay between gene duplication and alternative splicing and of the molecular evolutionary mechanisms leading to genetic innovations. This implies the existence of purifying selection against exonization in single copy genes, with duplicate genes free from such constrains. © Amit et al; licensee BioMed Central Ltd. 2007
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title_short	Biased exonization of transposed elements in duplicated genes: A lesson from the TIF-IA gene
url	https://dx.doi.org/10.1186/1471-2199-8-109
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author2	Sela, Noa Keren, Hadas Melamed, Ze'ev Muler, Inna Shomron, Noam Izraeli, Shai Ast, Gil
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Biased exonization of transposed elements in duplicated genes: A lesson from the TIF-IA gene

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