Neural expression and post-transcriptional dosage compensation of the steroid metabolic enzyme 17β-HSD type 4

<p<Abstract</p< <p<Background</p< <p<Steroids affect many tissues, including the brain. In the zebra finch, the estrogenic steroid estradiol (E<sub<2</sub<) is especially effective at promoting growth of the neural circuit specialized for song. In this speci...
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Autor*in:	Wise Petra M [verfasserIn] Lance Valentin A [verfasserIn] Itoh Yuichiro [verfasserIn] London Sarah E [verfasserIn] Ekanayake Preethika S [verfasserIn] Oyama Randi K [verfasserIn] Arnold Arthur P [verfasserIn] Schlinger Barney A [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2010

Übergeordnetes Werk:	In: BMC Neuroscience - BMC, 2003, 11(2010), 1, p 47
Übergeordnetes Werk:	volume:11 ; year:2010 ; number:1, p 47

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/1471-2202-11-47

Katalog-ID:	DOAJ072619457

Internformat


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520			\|a <p<Abstract</p< <p<Background</p< <p<Steroids affect many tissues, including the brain. In the zebra finch, the estrogenic steroid estradiol (E<sub<2</sub<) 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<sub<2 </sub<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<sub<2 </sub<in their brains than females.</p< <p<Results</p< <p<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.</p< <p<Conclusions</p< <p<Our results demonstrate that the HSD17B4 gene is expressed and active in the zebra finch brain as an E<sub<2 </sub<metabolizing enzyme, but that dosage compensation of this Z-linked gene may occur via post-transcriptional mechanisms.</p<
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allfields	10.1186/1471-2202-11-47 doi (DE-627)DOAJ072619457 (DE-599)DOAJ0ee3f6b03a9e47edb83489b8099b3431 DE-627 ger DE-627 rakwb eng RC321-571 QP351-495 Wise Petra M 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 <p<Abstract</p< <p<Background</p< <p<Steroids affect many tissues, including the brain. In the zebra finch, the estrogenic steroid estradiol (E<sub<2</sub<) 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<sub<2 </sub<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<sub<2 </sub<in their brains than females.</p< <p<Results</p< <p<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.</p< <p<Conclusions</p< <p<Our results demonstrate that the HSD17B4 gene is expressed and active in the zebra finch brain as an E<sub<2 </sub<metabolizing enzyme, but that dosage compensation of this Z-linked gene may occur via post-transcriptional mechanisms.</p< Neurosciences. Biological psychiatry. Neuropsychiatry Neurophysiology and neuropsychology Lance Valentin A verfasserin aut Itoh Yuichiro verfasserin aut London Sarah E verfasserin aut Ekanayake Preethika S verfasserin aut Oyama Randi K verfasserin aut Arnold Arthur P verfasserin aut Schlinger Barney A verfasserin aut In BMC Neuroscience BMC, 2003 11(2010), 1, p 47 (DE-627)326643648 (DE-600)2041344-0 14712202 nnns volume:11 year:2010 number:1, p 47 https://doi.org/10.1186/1471-2202-11-47 kostenfrei https://doaj.org/article/0ee3f6b03a9e47edb83489b8099b3431 kostenfrei http://www.biomedcentral.com/1471-2202/11/47 kostenfrei https://doaj.org/toc/1471-2202 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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, p 47
spelling	10.1186/1471-2202-11-47 doi (DE-627)DOAJ072619457 (DE-599)DOAJ0ee3f6b03a9e47edb83489b8099b3431 DE-627 ger DE-627 rakwb eng RC321-571 QP351-495 Wise Petra M 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 <p<Abstract</p< <p<Background</p< <p<Steroids affect many tissues, including the brain. In the zebra finch, the estrogenic steroid estradiol (E<sub<2</sub<) 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<sub<2 </sub<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<sub<2 </sub<in their brains than females.</p< <p<Results</p< <p<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.</p< <p<Conclusions</p< <p<Our results demonstrate that the HSD17B4 gene is expressed and active in the zebra finch brain as an E<sub<2 </sub<metabolizing enzyme, but that dosage compensation of this Z-linked gene may occur via post-transcriptional mechanisms.</p< Neurosciences. Biological psychiatry. Neuropsychiatry Neurophysiology and neuropsychology Lance Valentin A verfasserin aut Itoh Yuichiro verfasserin aut London Sarah E verfasserin aut Ekanayake Preethika S verfasserin aut Oyama Randi K verfasserin aut Arnold Arthur P verfasserin aut Schlinger Barney A verfasserin aut In BMC Neuroscience BMC, 2003 11(2010), 1, p 47 (DE-627)326643648 (DE-600)2041344-0 14712202 nnns volume:11 year:2010 number:1, p 47 https://doi.org/10.1186/1471-2202-11-47 kostenfrei https://doaj.org/article/0ee3f6b03a9e47edb83489b8099b3431 kostenfrei http://www.biomedcentral.com/1471-2202/11/47 kostenfrei https://doaj.org/toc/1471-2202 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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, p 47
allfields_unstemmed	10.1186/1471-2202-11-47 doi (DE-627)DOAJ072619457 (DE-599)DOAJ0ee3f6b03a9e47edb83489b8099b3431 DE-627 ger DE-627 rakwb eng RC321-571 QP351-495 Wise Petra M 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 <p<Abstract</p< <p<Background</p< <p<Steroids affect many tissues, including the brain. In the zebra finch, the estrogenic steroid estradiol (E<sub<2</sub<) 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<sub<2 </sub<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<sub<2 </sub<in their brains than females.</p< <p<Results</p< <p<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.</p< <p<Conclusions</p< <p<Our results demonstrate that the HSD17B4 gene is expressed and active in the zebra finch brain as an E<sub<2 </sub<metabolizing enzyme, but that dosage compensation of this Z-linked gene may occur via post-transcriptional mechanisms.</p< Neurosciences. Biological psychiatry. Neuropsychiatry Neurophysiology and neuropsychology Lance Valentin A verfasserin aut Itoh Yuichiro verfasserin aut London Sarah E verfasserin aut Ekanayake Preethika S verfasserin aut Oyama Randi K verfasserin aut Arnold Arthur P verfasserin aut Schlinger Barney A verfasserin aut In BMC Neuroscience BMC, 2003 11(2010), 1, p 47 (DE-627)326643648 (DE-600)2041344-0 14712202 nnns volume:11 year:2010 number:1, p 47 https://doi.org/10.1186/1471-2202-11-47 kostenfrei https://doaj.org/article/0ee3f6b03a9e47edb83489b8099b3431 kostenfrei http://www.biomedcentral.com/1471-2202/11/47 kostenfrei https://doaj.org/toc/1471-2202 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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, p 47
allfieldsGer	10.1186/1471-2202-11-47 doi (DE-627)DOAJ072619457 (DE-599)DOAJ0ee3f6b03a9e47edb83489b8099b3431 DE-627 ger DE-627 rakwb eng RC321-571 QP351-495 Wise Petra M 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 <p<Abstract</p< <p<Background</p< <p<Steroids affect many tissues, including the brain. In the zebra finch, the estrogenic steroid estradiol (E<sub<2</sub<) 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<sub<2 </sub<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<sub<2 </sub<in their brains than females.</p< <p<Results</p< <p<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.</p< <p<Conclusions</p< <p<Our results demonstrate that the HSD17B4 gene is expressed and active in the zebra finch brain as an E<sub<2 </sub<metabolizing enzyme, but that dosage compensation of this Z-linked gene may occur via post-transcriptional mechanisms.</p< Neurosciences. Biological psychiatry. Neuropsychiatry Neurophysiology and neuropsychology Lance Valentin A verfasserin aut Itoh Yuichiro verfasserin aut London Sarah E verfasserin aut Ekanayake Preethika S verfasserin aut Oyama Randi K verfasserin aut Arnold Arthur P verfasserin aut Schlinger Barney A verfasserin aut In BMC Neuroscience BMC, 2003 11(2010), 1, p 47 (DE-627)326643648 (DE-600)2041344-0 14712202 nnns volume:11 year:2010 number:1, p 47 https://doi.org/10.1186/1471-2202-11-47 kostenfrei https://doaj.org/article/0ee3f6b03a9e47edb83489b8099b3431 kostenfrei http://www.biomedcentral.com/1471-2202/11/47 kostenfrei https://doaj.org/toc/1471-2202 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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, p 47
allfieldsSound	10.1186/1471-2202-11-47 doi (DE-627)DOAJ072619457 (DE-599)DOAJ0ee3f6b03a9e47edb83489b8099b3431 DE-627 ger DE-627 rakwb eng RC321-571 QP351-495 Wise Petra M 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 <p<Abstract</p< <p<Background</p< <p<Steroids affect many tissues, including the brain. In the zebra finch, the estrogenic steroid estradiol (E<sub<2</sub<) 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<sub<2 </sub<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<sub<2 </sub<in their brains than females.</p< <p<Results</p< <p<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.</p< <p<Conclusions</p< <p<Our results demonstrate that the HSD17B4 gene is expressed and active in the zebra finch brain as an E<sub<2 </sub<metabolizing enzyme, but that dosage compensation of this Z-linked gene may occur via post-transcriptional mechanisms.</p< Neurosciences. Biological psychiatry. Neuropsychiatry Neurophysiology and neuropsychology Lance Valentin A verfasserin aut Itoh Yuichiro verfasserin aut London Sarah E verfasserin aut Ekanayake Preethika S verfasserin aut Oyama Randi K verfasserin aut Arnold Arthur P verfasserin aut Schlinger Barney A verfasserin aut In BMC Neuroscience BMC, 2003 11(2010), 1, p 47 (DE-627)326643648 (DE-600)2041344-0 14712202 nnns volume:11 year:2010 number:1, p 47 https://doi.org/10.1186/1471-2202-11-47 kostenfrei https://doaj.org/article/0ee3f6b03a9e47edb83489b8099b3431 kostenfrei http://www.biomedcentral.com/1471-2202/11/47 kostenfrei https://doaj.org/toc/1471-2202 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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, p 47
language	English
source	In BMC Neuroscience 11(2010), 1, p 47 volume:11 year:2010 number:1, p 47
sourceStr	In BMC Neuroscience 11(2010), 1, p 47 volume:11 year:2010 number:1, p 47
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Neurosciences. Biological psychiatry. Neuropsychiatry Neurophysiology and neuropsychology
isfreeaccess_bool	true
container_title	BMC Neuroscience
authorswithroles_txt_mv	Wise Petra M @@aut@@ Lance Valentin A @@aut@@ Itoh Yuichiro @@aut@@ London Sarah E @@aut@@ Ekanayake Preethika S @@aut@@ Oyama Randi K @@aut@@ Arnold Arthur P @@aut@@ Schlinger Barney A @@aut@@
publishDateDaySort_date	2010-01-01T00:00:00Z
hierarchy_top_id	326643648
id	DOAJ072619457
language_de	englisch
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callnumber-first	R - Medicine
author	Wise Petra M
spellingShingle	Wise Petra M misc RC321-571 misc QP351-495 misc Neurosciences. Biological psychiatry. Neuropsychiatry misc Neurophysiology and neuropsychology Neural expression and post-transcriptional dosage compensation of the steroid metabolic enzyme 17β-HSD type 4
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topic_title	RC321-571 QP351-495 Neural expression and post-transcriptional dosage compensation of the steroid metabolic enzyme 17β-HSD type 4
topic	misc RC321-571 misc QP351-495 misc Neurosciences. Biological psychiatry. Neuropsychiatry misc Neurophysiology and neuropsychology
topic_unstemmed	misc RC321-571 misc QP351-495 misc Neurosciences. Biological psychiatry. Neuropsychiatry misc Neurophysiology and neuropsychology
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title	Neural expression and post-transcriptional dosage compensation of the steroid metabolic enzyme 17β-HSD type 4
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title_full	Neural expression and post-transcriptional dosage compensation of the steroid metabolic enzyme 17β-HSD type 4
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author_browse	Wise Petra M Lance Valentin A Itoh Yuichiro London Sarah E Ekanayake Preethika S Oyama Randi K Arnold Arthur P Schlinger Barney A
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title_sort	neural expression and post-transcriptional dosage compensation of the steroid metabolic enzyme 17β-hsd type 4
callnumber	RC321-571
title_auth	Neural expression and post-transcriptional dosage compensation of the steroid metabolic enzyme 17β-HSD type 4
abstract	<p<Abstract</p< <p<Background</p< <p<Steroids affect many tissues, including the brain. In the zebra finch, the estrogenic steroid estradiol (E<sub<2</sub<) 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<sub<2 </sub<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<sub<2 </sub<in their brains than females.</p< <p<Results</p< <p<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.</p< <p<Conclusions</p< <p<Our results demonstrate that the HSD17B4 gene is expressed and active in the zebra finch brain as an E<sub<2 </sub<metabolizing enzyme, but that dosage compensation of this Z-linked gene may occur via post-transcriptional mechanisms.</p<
abstractGer	<p<Abstract</p< <p<Background</p< <p<Steroids affect many tissues, including the brain. In the zebra finch, the estrogenic steroid estradiol (E<sub<2</sub<) 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<sub<2 </sub<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<sub<2 </sub<in their brains than females.</p< <p<Results</p< <p<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.</p< <p<Conclusions</p< <p<Our results demonstrate that the HSD17B4 gene is expressed and active in the zebra finch brain as an E<sub<2 </sub<metabolizing enzyme, but that dosage compensation of this Z-linked gene may occur via post-transcriptional mechanisms.</p<
abstract_unstemmed	<p<Abstract</p< <p<Background</p< <p<Steroids affect many tissues, including the brain. In the zebra finch, the estrogenic steroid estradiol (E<sub<2</sub<) 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<sub<2 </sub<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<sub<2 </sub<in their brains than females.</p< <p<Results</p< <p<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.</p< <p<Conclusions</p< <p<Our results demonstrate that the HSD17B4 gene is expressed and active in the zebra finch brain as an E<sub<2 </sub<metabolizing enzyme, but that dosage compensation of this Z-linked gene may occur via post-transcriptional mechanisms.</p<
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title_short	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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