Neural expression and post-transcriptional dosage compensation of the steroid metabolic enzyme 17β-HSD type 4
Background Steroids affect many tissues, including the brain. In the zebra finch, the estrogenic steroid estradiol ($ E_{2} $) is especially effective at promoting growth of the neural circuit specialized for song. In this species, only the males sing and they have a much larger and more interconnec...
Ausführliche Beschreibung
Autor*in: |
London, Sarah E [verfasserIn] |
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Englisch |
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2010 |
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Anmerkung: |
© London et al; licensee BioMed Central Ltd. 2010 |
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Übergeordnetes Werk: |
Enthalten in: BMC neuroscience - London : BioMed Central, 2000, 11(2010), 1 vom: 01. Apr. |
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volume:11 ; year:2010 ; number:1 ; day:01 ; month:04 |
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DOI / URN: |
10.1186/1471-2202-11-47 |
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SPR027238075 |
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520 | |a Background Steroids affect many tissues, including the brain. In the zebra finch, the estrogenic steroid estradiol ($ E_{2} $) is especially effective at promoting growth of the neural circuit specialized for song. In this species, only the males sing and they have a much larger and more interconnected song circuit than females. Thus, it was surprising that the gene for 17β-hydroxysteroid dehydrogenase type 4 (HSD17B4), an enzyme that converts $ E_{2} $ to a less potent estrogen, had been mapped to the Z sex chromosome. As a consequence, it was likely that HSD17B4 was differentially expressed in males (ZZ) and females (ZW) because dosage compensation of Z chromosome genes is incomplete in birds. If a higher abundance of HSD17B4 mRNA in males than females was translated into functional enzyme in the brain, then contrary to expectation, males could produce less $ E_{2} $ in their brains than females. Results Here, we used molecular and biochemical techniques to confirm the HSD17B4 Z chromosome location in the zebra finch and to determine that HSD17B4 mRNA and activity were detectable in the early developing and adult brain. As expected, HSD17B4 mRNA expression levels were higher in males compared to females. This provides further evidence of the incomplete Z chromosome inactivation mechanisms in birds. We detected HSD17B4 mRNA in regions that suggested a role for this enzyme in the early organization and adult function of song nuclei. We did not, however, detect significant sex differences in HSD17B4 activity levels in the adult brain. Conclusions Our results demonstrate that the HSD17B4 gene is expressed and active in the zebra finch brain as an $ E_{2} $ metabolizing enzyme, but that dosage compensation of this Z-linked gene may occur via post-transcriptional mechanisms. | ||
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700 | 1 | |a Lance, Valentin A |4 aut | |
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700 | 1 | |a Oyama, Randi K |4 aut | |
700 | 1 | |a Arnold, Arthur P |4 aut | |
700 | 1 | |a Schlinger, Barney A |4 aut | |
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10.1186/1471-2202-11-47 doi (DE-627)SPR027238075 (SPR)1471-2202-11-47-e DE-627 ger DE-627 rakwb eng London, Sarah E verfasserin aut Neural expression and post-transcriptional dosage compensation of the steroid metabolic enzyme 17β-HSD type 4 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © London et al; licensee BioMed Central Ltd. 2010 Background Steroids affect many tissues, including the brain. In the zebra finch, the estrogenic steroid estradiol ($ E_{2} $) is especially effective at promoting growth of the neural circuit specialized for song. In this species, only the males sing and they have a much larger and more interconnected song circuit than females. Thus, it was surprising that the gene for 17β-hydroxysteroid dehydrogenase type 4 (HSD17B4), an enzyme that converts $ E_{2} $ to a less potent estrogen, had been mapped to the Z sex chromosome. As a consequence, it was likely that HSD17B4 was differentially expressed in males (ZZ) and females (ZW) because dosage compensation of Z chromosome genes is incomplete in birds. If a higher abundance of HSD17B4 mRNA in males than females was translated into functional enzyme in the brain, then contrary to expectation, males could produce less $ E_{2} $ in their brains than females. Results Here, we used molecular and biochemical techniques to confirm the HSD17B4 Z chromosome location in the zebra finch and to determine that HSD17B4 mRNA and activity were detectable in the early developing and adult brain. As expected, HSD17B4 mRNA expression levels were higher in males compared to females. This provides further evidence of the incomplete Z chromosome inactivation mechanisms in birds. We detected HSD17B4 mRNA in regions that suggested a role for this enzyme in the early organization and adult function of song nuclei. We did not, however, detect significant sex differences in HSD17B4 activity levels in the adult brain. Conclusions Our results demonstrate that the HSD17B4 gene is expressed and active in the zebra finch brain as an $ E_{2} $ metabolizing enzyme, but that dosage compensation of this Z-linked gene may occur via post-transcriptional mechanisms. Zebra Finch (dpeaa)DE-He213 Dosage Compensation (dpeaa)DE-He213 HSD17B4 Activity (dpeaa)DE-He213 HSD17B4 Expression (dpeaa)DE-He213 HSD17B4 Gene (dpeaa)DE-He213 Itoh, Yuichiro aut Lance, Valentin A aut Wise, Petra M aut Ekanayake, Preethika S aut Oyama, Randi K aut Arnold, Arthur P aut Schlinger, Barney A aut Enthalten in BMC neuroscience London : BioMed Central, 2000 11(2010), 1 vom: 01. Apr. (DE-627)326643648 (DE-600)2041344-0 1471-2202 nnns volume:11 year:2010 number:1 day:01 month:04 https://dx.doi.org/10.1186/1471-2202-11-47 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 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 11 2010 1 01 04 |
spelling |
10.1186/1471-2202-11-47 doi (DE-627)SPR027238075 (SPR)1471-2202-11-47-e DE-627 ger DE-627 rakwb eng London, Sarah E verfasserin aut Neural expression and post-transcriptional dosage compensation of the steroid metabolic enzyme 17β-HSD type 4 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © London et al; licensee BioMed Central Ltd. 2010 Background Steroids affect many tissues, including the brain. In the zebra finch, the estrogenic steroid estradiol ($ E_{2} $) is especially effective at promoting growth of the neural circuit specialized for song. In this species, only the males sing and they have a much larger and more interconnected song circuit than females. Thus, it was surprising that the gene for 17β-hydroxysteroid dehydrogenase type 4 (HSD17B4), an enzyme that converts $ E_{2} $ to a less potent estrogen, had been mapped to the Z sex chromosome. As a consequence, it was likely that HSD17B4 was differentially expressed in males (ZZ) and females (ZW) because dosage compensation of Z chromosome genes is incomplete in birds. If a higher abundance of HSD17B4 mRNA in males than females was translated into functional enzyme in the brain, then contrary to expectation, males could produce less $ E_{2} $ in their brains than females. Results Here, we used molecular and biochemical techniques to confirm the HSD17B4 Z chromosome location in the zebra finch and to determine that HSD17B4 mRNA and activity were detectable in the early developing and adult brain. As expected, HSD17B4 mRNA expression levels were higher in males compared to females. This provides further evidence of the incomplete Z chromosome inactivation mechanisms in birds. We detected HSD17B4 mRNA in regions that suggested a role for this enzyme in the early organization and adult function of song nuclei. We did not, however, detect significant sex differences in HSD17B4 activity levels in the adult brain. Conclusions Our results demonstrate that the HSD17B4 gene is expressed and active in the zebra finch brain as an $ E_{2} $ metabolizing enzyme, but that dosage compensation of this Z-linked gene may occur via post-transcriptional mechanisms. Zebra Finch (dpeaa)DE-He213 Dosage Compensation (dpeaa)DE-He213 HSD17B4 Activity (dpeaa)DE-He213 HSD17B4 Expression (dpeaa)DE-He213 HSD17B4 Gene (dpeaa)DE-He213 Itoh, Yuichiro aut Lance, Valentin A aut Wise, Petra M aut Ekanayake, Preethika S aut Oyama, Randi K aut Arnold, Arthur P aut Schlinger, Barney A aut Enthalten in BMC neuroscience London : BioMed Central, 2000 11(2010), 1 vom: 01. Apr. (DE-627)326643648 (DE-600)2041344-0 1471-2202 nnns volume:11 year:2010 number:1 day:01 month:04 https://dx.doi.org/10.1186/1471-2202-11-47 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 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 11 2010 1 01 04 |
allfields_unstemmed |
10.1186/1471-2202-11-47 doi (DE-627)SPR027238075 (SPR)1471-2202-11-47-e DE-627 ger DE-627 rakwb eng London, Sarah E verfasserin aut Neural expression and post-transcriptional dosage compensation of the steroid metabolic enzyme 17β-HSD type 4 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © London et al; licensee BioMed Central Ltd. 2010 Background Steroids affect many tissues, including the brain. In the zebra finch, the estrogenic steroid estradiol ($ E_{2} $) is especially effective at promoting growth of the neural circuit specialized for song. In this species, only the males sing and they have a much larger and more interconnected song circuit than females. Thus, it was surprising that the gene for 17β-hydroxysteroid dehydrogenase type 4 (HSD17B4), an enzyme that converts $ E_{2} $ to a less potent estrogen, had been mapped to the Z sex chromosome. As a consequence, it was likely that HSD17B4 was differentially expressed in males (ZZ) and females (ZW) because dosage compensation of Z chromosome genes is incomplete in birds. If a higher abundance of HSD17B4 mRNA in males than females was translated into functional enzyme in the brain, then contrary to expectation, males could produce less $ E_{2} $ in their brains than females. Results Here, we used molecular and biochemical techniques to confirm the HSD17B4 Z chromosome location in the zebra finch and to determine that HSD17B4 mRNA and activity were detectable in the early developing and adult brain. As expected, HSD17B4 mRNA expression levels were higher in males compared to females. This provides further evidence of the incomplete Z chromosome inactivation mechanisms in birds. We detected HSD17B4 mRNA in regions that suggested a role for this enzyme in the early organization and adult function of song nuclei. We did not, however, detect significant sex differences in HSD17B4 activity levels in the adult brain. Conclusions Our results demonstrate that the HSD17B4 gene is expressed and active in the zebra finch brain as an $ E_{2} $ metabolizing enzyme, but that dosage compensation of this Z-linked gene may occur via post-transcriptional mechanisms. Zebra Finch (dpeaa)DE-He213 Dosage Compensation (dpeaa)DE-He213 HSD17B4 Activity (dpeaa)DE-He213 HSD17B4 Expression (dpeaa)DE-He213 HSD17B4 Gene (dpeaa)DE-He213 Itoh, Yuichiro aut Lance, Valentin A aut Wise, Petra M aut Ekanayake, Preethika S aut Oyama, Randi K aut Arnold, Arthur P aut Schlinger, Barney A aut Enthalten in BMC neuroscience London : BioMed Central, 2000 11(2010), 1 vom: 01. Apr. (DE-627)326643648 (DE-600)2041344-0 1471-2202 nnns volume:11 year:2010 number:1 day:01 month:04 https://dx.doi.org/10.1186/1471-2202-11-47 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 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 11 2010 1 01 04 |
allfieldsGer |
10.1186/1471-2202-11-47 doi (DE-627)SPR027238075 (SPR)1471-2202-11-47-e DE-627 ger DE-627 rakwb eng London, Sarah E verfasserin aut Neural expression and post-transcriptional dosage compensation of the steroid metabolic enzyme 17β-HSD type 4 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © London et al; licensee BioMed Central Ltd. 2010 Background Steroids affect many tissues, including the brain. In the zebra finch, the estrogenic steroid estradiol ($ E_{2} $) is especially effective at promoting growth of the neural circuit specialized for song. In this species, only the males sing and they have a much larger and more interconnected song circuit than females. Thus, it was surprising that the gene for 17β-hydroxysteroid dehydrogenase type 4 (HSD17B4), an enzyme that converts $ E_{2} $ to a less potent estrogen, had been mapped to the Z sex chromosome. As a consequence, it was likely that HSD17B4 was differentially expressed in males (ZZ) and females (ZW) because dosage compensation of Z chromosome genes is incomplete in birds. If a higher abundance of HSD17B4 mRNA in males than females was translated into functional enzyme in the brain, then contrary to expectation, males could produce less $ E_{2} $ in their brains than females. Results Here, we used molecular and biochemical techniques to confirm the HSD17B4 Z chromosome location in the zebra finch and to determine that HSD17B4 mRNA and activity were detectable in the early developing and adult brain. As expected, HSD17B4 mRNA expression levels were higher in males compared to females. This provides further evidence of the incomplete Z chromosome inactivation mechanisms in birds. We detected HSD17B4 mRNA in regions that suggested a role for this enzyme in the early organization and adult function of song nuclei. We did not, however, detect significant sex differences in HSD17B4 activity levels in the adult brain. Conclusions Our results demonstrate that the HSD17B4 gene is expressed and active in the zebra finch brain as an $ E_{2} $ metabolizing enzyme, but that dosage compensation of this Z-linked gene may occur via post-transcriptional mechanisms. Zebra Finch (dpeaa)DE-He213 Dosage Compensation (dpeaa)DE-He213 HSD17B4 Activity (dpeaa)DE-He213 HSD17B4 Expression (dpeaa)DE-He213 HSD17B4 Gene (dpeaa)DE-He213 Itoh, Yuichiro aut Lance, Valentin A aut Wise, Petra M aut Ekanayake, Preethika S aut Oyama, Randi K aut Arnold, Arthur P aut Schlinger, Barney A aut Enthalten in BMC neuroscience London : BioMed Central, 2000 11(2010), 1 vom: 01. Apr. (DE-627)326643648 (DE-600)2041344-0 1471-2202 nnns volume:11 year:2010 number:1 day:01 month:04 https://dx.doi.org/10.1186/1471-2202-11-47 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 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 11 2010 1 01 04 |
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10.1186/1471-2202-11-47 doi (DE-627)SPR027238075 (SPR)1471-2202-11-47-e DE-627 ger DE-627 rakwb eng London, Sarah E verfasserin aut Neural expression and post-transcriptional dosage compensation of the steroid metabolic enzyme 17β-HSD type 4 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © London et al; licensee BioMed Central Ltd. 2010 Background Steroids affect many tissues, including the brain. In the zebra finch, the estrogenic steroid estradiol ($ E_{2} $) is especially effective at promoting growth of the neural circuit specialized for song. In this species, only the males sing and they have a much larger and more interconnected song circuit than females. Thus, it was surprising that the gene for 17β-hydroxysteroid dehydrogenase type 4 (HSD17B4), an enzyme that converts $ E_{2} $ to a less potent estrogen, had been mapped to the Z sex chromosome. As a consequence, it was likely that HSD17B4 was differentially expressed in males (ZZ) and females (ZW) because dosage compensation of Z chromosome genes is incomplete in birds. If a higher abundance of HSD17B4 mRNA in males than females was translated into functional enzyme in the brain, then contrary to expectation, males could produce less $ E_{2} $ in their brains than females. Results Here, we used molecular and biochemical techniques to confirm the HSD17B4 Z chromosome location in the zebra finch and to determine that HSD17B4 mRNA and activity were detectable in the early developing and adult brain. As expected, HSD17B4 mRNA expression levels were higher in males compared to females. This provides further evidence of the incomplete Z chromosome inactivation mechanisms in birds. We detected HSD17B4 mRNA in regions that suggested a role for this enzyme in the early organization and adult function of song nuclei. We did not, however, detect significant sex differences in HSD17B4 activity levels in the adult brain. Conclusions Our results demonstrate that the HSD17B4 gene is expressed and active in the zebra finch brain as an $ E_{2} $ metabolizing enzyme, but that dosage compensation of this Z-linked gene may occur via post-transcriptional mechanisms. Zebra Finch (dpeaa)DE-He213 Dosage Compensation (dpeaa)DE-He213 HSD17B4 Activity (dpeaa)DE-He213 HSD17B4 Expression (dpeaa)DE-He213 HSD17B4 Gene (dpeaa)DE-He213 Itoh, Yuichiro aut Lance, Valentin A aut Wise, Petra M aut Ekanayake, Preethika S aut Oyama, Randi K aut Arnold, Arthur P aut Schlinger, Barney A aut Enthalten in BMC neuroscience London : BioMed Central, 2000 11(2010), 1 vom: 01. Apr. (DE-627)326643648 (DE-600)2041344-0 1471-2202 nnns volume:11 year:2010 number:1 day:01 month:04 https://dx.doi.org/10.1186/1471-2202-11-47 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 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 11 2010 1 01 04 |
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Neural expression and post-transcriptional dosage compensation of the steroid metabolic enzyme 17β-HSD type 4 |
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Neural expression and post-transcriptional dosage compensation of the steroid metabolic enzyme 17β-HSD type 4 |
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London, Sarah E Itoh, Yuichiro Lance, Valentin A Wise, Petra M Ekanayake, Preethika S Oyama, Randi K Arnold, Arthur P Schlinger, Barney A |
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neural expression and post-transcriptional dosage compensation of the steroid metabolic enzyme 17β-hsd type 4 |
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Neural expression and post-transcriptional dosage compensation of the steroid metabolic enzyme 17β-HSD type 4 |
abstract |
Background Steroids affect many tissues, including the brain. In the zebra finch, the estrogenic steroid estradiol ($ E_{2} $) is especially effective at promoting growth of the neural circuit specialized for song. In this species, only the males sing and they have a much larger and more interconnected song circuit than females. Thus, it was surprising that the gene for 17β-hydroxysteroid dehydrogenase type 4 (HSD17B4), an enzyme that converts $ E_{2} $ to a less potent estrogen, had been mapped to the Z sex chromosome. As a consequence, it was likely that HSD17B4 was differentially expressed in males (ZZ) and females (ZW) because dosage compensation of Z chromosome genes is incomplete in birds. If a higher abundance of HSD17B4 mRNA in males than females was translated into functional enzyme in the brain, then contrary to expectation, males could produce less $ E_{2} $ in their brains than females. Results Here, we used molecular and biochemical techniques to confirm the HSD17B4 Z chromosome location in the zebra finch and to determine that HSD17B4 mRNA and activity were detectable in the early developing and adult brain. As expected, HSD17B4 mRNA expression levels were higher in males compared to females. This provides further evidence of the incomplete Z chromosome inactivation mechanisms in birds. We detected HSD17B4 mRNA in regions that suggested a role for this enzyme in the early organization and adult function of song nuclei. We did not, however, detect significant sex differences in HSD17B4 activity levels in the adult brain. Conclusions Our results demonstrate that the HSD17B4 gene is expressed and active in the zebra finch brain as an $ E_{2} $ metabolizing enzyme, but that dosage compensation of this Z-linked gene may occur via post-transcriptional mechanisms. © London et al; licensee BioMed Central Ltd. 2010 |
abstractGer |
Background Steroids affect many tissues, including the brain. In the zebra finch, the estrogenic steroid estradiol ($ E_{2} $) is especially effective at promoting growth of the neural circuit specialized for song. In this species, only the males sing and they have a much larger and more interconnected song circuit than females. Thus, it was surprising that the gene for 17β-hydroxysteroid dehydrogenase type 4 (HSD17B4), an enzyme that converts $ E_{2} $ to a less potent estrogen, had been mapped to the Z sex chromosome. As a consequence, it was likely that HSD17B4 was differentially expressed in males (ZZ) and females (ZW) because dosage compensation of Z chromosome genes is incomplete in birds. If a higher abundance of HSD17B4 mRNA in males than females was translated into functional enzyme in the brain, then contrary to expectation, males could produce less $ E_{2} $ in their brains than females. Results Here, we used molecular and biochemical techniques to confirm the HSD17B4 Z chromosome location in the zebra finch and to determine that HSD17B4 mRNA and activity were detectable in the early developing and adult brain. As expected, HSD17B4 mRNA expression levels were higher in males compared to females. This provides further evidence of the incomplete Z chromosome inactivation mechanisms in birds. We detected HSD17B4 mRNA in regions that suggested a role for this enzyme in the early organization and adult function of song nuclei. We did not, however, detect significant sex differences in HSD17B4 activity levels in the adult brain. Conclusions Our results demonstrate that the HSD17B4 gene is expressed and active in the zebra finch brain as an $ E_{2} $ metabolizing enzyme, but that dosage compensation of this Z-linked gene may occur via post-transcriptional mechanisms. © London et al; licensee BioMed Central Ltd. 2010 |
abstract_unstemmed |
Background Steroids affect many tissues, including the brain. In the zebra finch, the estrogenic steroid estradiol ($ E_{2} $) is especially effective at promoting growth of the neural circuit specialized for song. In this species, only the males sing and they have a much larger and more interconnected song circuit than females. Thus, it was surprising that the gene for 17β-hydroxysteroid dehydrogenase type 4 (HSD17B4), an enzyme that converts $ E_{2} $ to a less potent estrogen, had been mapped to the Z sex chromosome. As a consequence, it was likely that HSD17B4 was differentially expressed in males (ZZ) and females (ZW) because dosage compensation of Z chromosome genes is incomplete in birds. If a higher abundance of HSD17B4 mRNA in males than females was translated into functional enzyme in the brain, then contrary to expectation, males could produce less $ E_{2} $ in their brains than females. Results Here, we used molecular and biochemical techniques to confirm the HSD17B4 Z chromosome location in the zebra finch and to determine that HSD17B4 mRNA and activity were detectable in the early developing and adult brain. As expected, HSD17B4 mRNA expression levels were higher in males compared to females. This provides further evidence of the incomplete Z chromosome inactivation mechanisms in birds. We detected HSD17B4 mRNA in regions that suggested a role for this enzyme in the early organization and adult function of song nuclei. We did not, however, detect significant sex differences in HSD17B4 activity levels in the adult brain. Conclusions Our results demonstrate that the HSD17B4 gene is expressed and active in the zebra finch brain as an $ E_{2} $ metabolizing enzyme, but that dosage compensation of this Z-linked gene may occur via post-transcriptional mechanisms. © London et al; licensee BioMed Central Ltd. 2010 |
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