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v-erbA oncogene initiates ultrastructural changes characteristic of early and intermediate events of meiotic maturation in Xenopus oocytes
The growth‐promoting properties of the retroviral v‐erbA oncogene, a highly mutated version of the chicken thyroid hormone receptor (TR) α, have so far exclusively been linked to dominant repression of the antimitogenic roles of TR and retinoic acid receptors. Here we show that when expressed in Xen...
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Published in: | Journal of cellular biochemistry 1997-11, Vol.67 (2), p.184-200 |
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creator | Nagl, Sylvia B. Bunn, Caroline F. Allison, Lizabeth A. |
description | The growth‐promoting properties of the retroviral v‐erbA oncogene, a highly mutated version of the chicken thyroid hormone receptor (TR) α, have so far exclusively been linked to dominant repression of the antimitogenic roles of TR and retinoic acid receptors. Here we show that when expressed in Xenopus oocytes v‐ErbA induced ultrastructural changes characteristic of early and intermediate events of meiotic maturation by activating gene transcription. v‐ErbA–induced maturation events occurred without activation of the cAMP/maturation‐promoting factor signal pathway and were arrested prior to meiotic spindle formation. The effects of v‐ErbA were not mimicked by a dominant negative in vitro–generated mutant of human TR, suggesting that v‐ErbA can contribute to cell cycle reentry by interference with regulatory pathways distinct from those involving TR. Interestingly, a portion of v‐ErbA expressed in oocytes was present at the cytoplasmic fibrils of the nuclear pore complexes, suggesting that in addition to its intranuclear function v‐ErbA may modulate nucleocytoplasmic transport. J. Cell. Biochem. 67:184–200, 1997. © 1997 Wiley‐Liss, Inc. |
doi_str_mv | 10.1002/(SICI)1097-4644(19971101)67:2<184::AID-JCB4>3.0.CO;2-T |
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Here we show that when expressed in Xenopus oocytes v‐ErbA induced ultrastructural changes characteristic of early and intermediate events of meiotic maturation by activating gene transcription. v‐ErbA–induced maturation events occurred without activation of the cAMP/maturation‐promoting factor signal pathway and were arrested prior to meiotic spindle formation. The effects of v‐ErbA were not mimicked by a dominant negative in vitro–generated mutant of human TR, suggesting that v‐ErbA can contribute to cell cycle reentry by interference with regulatory pathways distinct from those involving TR. Interestingly, a portion of v‐ErbA expressed in oocytes was present at the cytoplasmic fibrils of the nuclear pore complexes, suggesting that in addition to its intranuclear function v‐ErbA may modulate nucleocytoplasmic transport. J. Cell. Biochem. 67:184–200, 1997. © 1997 Wiley‐Liss, Inc.</description><identifier>ISSN: 0730-2312</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/(SICI)1097-4644(19971101)67:2<184::AID-JCB4>3.0.CO;2-T</identifier><identifier>PMID: 9328824</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Animals ; Biological Transport ; Cell Nucleus - metabolism ; Cell Nucleus - ultrastructure ; Cyclic AMP - physiology ; Cytoplasm - metabolism ; Female ; Gene Expression ; Gene Transfer Techniques ; Genes, erbA ; Humans ; maturation-promoting factor ; Maturation-Promoting Factor - physiology ; meiosis ; Meiosis - genetics ; Meiosis - physiology ; Microinjections ; Microscopy, Electron ; Mutation ; Nuclear Envelope - chemistry ; Nuclear Envelope - ultrastructure ; nuclear pore complex ; nucleocytoplasmic transport ; Oncogene Proteins v-erbA - analysis ; Oncogene Proteins v-erbA - pharmacology ; Oncogene Proteins v-erbA - physiology ; Oocytes - physiology ; Oocytes - ultrastructure ; Receptors, Thyroid Hormone - antagonists & inhibitors ; Receptors, Thyroid Hormone - genetics ; thyroid hormone receptor ; Xenopus laevis</subject><ispartof>Journal of cellular biochemistry, 1997-11, Vol.67 (2), p.184-200</ispartof><rights>Copyright © 1997 Wiley‐Liss, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9328824$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nagl, Sylvia B.</creatorcontrib><creatorcontrib>Bunn, Caroline F.</creatorcontrib><creatorcontrib>Allison, Lizabeth A.</creatorcontrib><title>v-erbA oncogene initiates ultrastructural changes characteristic of early and intermediate events of meiotic maturation in Xenopus oocytes</title><title>Journal of cellular biochemistry</title><addtitle>J. Cell. Biochem</addtitle><description>The growth‐promoting properties of the retroviral v‐erbA oncogene, a highly mutated version of the chicken thyroid hormone receptor (TR) α, have so far exclusively been linked to dominant repression of the antimitogenic roles of TR and retinoic acid receptors. Here we show that when expressed in Xenopus oocytes v‐ErbA induced ultrastructural changes characteristic of early and intermediate events of meiotic maturation by activating gene transcription. v‐ErbA–induced maturation events occurred without activation of the cAMP/maturation‐promoting factor signal pathway and were arrested prior to meiotic spindle formation. The effects of v‐ErbA were not mimicked by a dominant negative in vitro–generated mutant of human TR, suggesting that v‐ErbA can contribute to cell cycle reentry by interference with regulatory pathways distinct from those involving TR. Interestingly, a portion of v‐ErbA expressed in oocytes was present at the cytoplasmic fibrils of the nuclear pore complexes, suggesting that in addition to its intranuclear function v‐ErbA may modulate nucleocytoplasmic transport. J. Cell. Biochem. 67:184–200, 1997. © 1997 Wiley‐Liss, Inc.</description><subject>Animals</subject><subject>Biological Transport</subject><subject>Cell Nucleus - metabolism</subject><subject>Cell Nucleus - ultrastructure</subject><subject>Cyclic AMP - physiology</subject><subject>Cytoplasm - metabolism</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Gene Transfer Techniques</subject><subject>Genes, erbA</subject><subject>Humans</subject><subject>maturation-promoting factor</subject><subject>Maturation-Promoting Factor - physiology</subject><subject>meiosis</subject><subject>Meiosis - genetics</subject><subject>Meiosis - physiology</subject><subject>Microinjections</subject><subject>Microscopy, Electron</subject><subject>Mutation</subject><subject>Nuclear Envelope - chemistry</subject><subject>Nuclear Envelope - ultrastructure</subject><subject>nuclear pore complex</subject><subject>nucleocytoplasmic transport</subject><subject>Oncogene Proteins v-erbA - analysis</subject><subject>Oncogene Proteins v-erbA - pharmacology</subject><subject>Oncogene Proteins v-erbA - physiology</subject><subject>Oocytes - physiology</subject><subject>Oocytes - ultrastructure</subject><subject>Receptors, Thyroid Hormone - antagonists & inhibitors</subject><subject>Receptors, Thyroid Hormone - genetics</subject><subject>thyroid hormone receptor</subject><subject>Xenopus laevis</subject><issn>0730-2312</issn><issn>1097-4644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><recordid>eNo9kV1v0zAUhi0EGmXwE5ByhbaLdP5qnBQ0qQS2FVXrxcrH3ZGTnAxDPortDPoX-NU4a-mNj_ye97yWz0PIJaNTRim_OLtb5stzRjMVy0TKM5ZlijHKzhM15-9YKufzxfJD_Cl_Ly_FlE7z9Vseb56QyXHkKZlQJWjMBePPyQvnflBKs0zwE3ISzjTlckL-PsRoi0XUd2V_jx1GpjPeaI8uGhpvtfN2KP1gdROV33V3H_RQrS49WuO8KaO-jlDbZhfprgrTQW-xGhMifMDOu9HQoulHb6vHKG_6Ljijb9j12yEY-nIXHnxJntW6cfjqUE_J56uPm_wmXq2vl_liFRsuUhlXXAmtWCFpXadVkYoaOaY6VVhJRnlBi5mSQmEp6oTVWSGo5rM640WtZcYqJU7Jm33u1va_BnQeWuNKbBrdYT84UJkIOZwH4-uDcSjCn2BrTavtDg7LC_0v-_5v0-Du2GYURoIwAoSRBow04D9ASBRwCAAh8IORHwigkK-Dunm8h-B4Hxw2jH-Owdr-DMNCzeDr7TWs1CrPb5M7mIl_EpCl4g</recordid><startdate>19971101</startdate><enddate>19971101</enddate><creator>Nagl, Sylvia B.</creator><creator>Bunn, Caroline F.</creator><creator>Allison, Lizabeth A.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>19971101</creationdate><title>v-erbA oncogene initiates ultrastructural changes characteristic of early and intermediate events of meiotic maturation in Xenopus oocytes</title><author>Nagl, Sylvia B. ; Bunn, Caroline F. ; Allison, Lizabeth A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-i2384-d273a71b40ff8db83fe2e8a87ed4102b0b57437ec3f61f9b30a25f92bfa491d73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Animals</topic><topic>Biological Transport</topic><topic>Cell Nucleus - metabolism</topic><topic>Cell Nucleus - ultrastructure</topic><topic>Cyclic AMP - physiology</topic><topic>Cytoplasm - metabolism</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Gene Transfer Techniques</topic><topic>Genes, erbA</topic><topic>Humans</topic><topic>maturation-promoting factor</topic><topic>Maturation-Promoting Factor - physiology</topic><topic>meiosis</topic><topic>Meiosis - genetics</topic><topic>Meiosis - physiology</topic><topic>Microinjections</topic><topic>Microscopy, Electron</topic><topic>Mutation</topic><topic>Nuclear Envelope - chemistry</topic><topic>Nuclear Envelope - ultrastructure</topic><topic>nuclear pore complex</topic><topic>nucleocytoplasmic transport</topic><topic>Oncogene Proteins v-erbA - analysis</topic><topic>Oncogene Proteins v-erbA - pharmacology</topic><topic>Oncogene Proteins v-erbA - physiology</topic><topic>Oocytes - physiology</topic><topic>Oocytes - ultrastructure</topic><topic>Receptors, Thyroid Hormone - antagonists & inhibitors</topic><topic>Receptors, Thyroid Hormone - genetics</topic><topic>thyroid hormone receptor</topic><topic>Xenopus laevis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nagl, Sylvia B.</creatorcontrib><creatorcontrib>Bunn, Caroline F.</creatorcontrib><creatorcontrib>Allison, Lizabeth A.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nagl, Sylvia B.</au><au>Bunn, Caroline F.</au><au>Allison, Lizabeth A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>v-erbA oncogene initiates ultrastructural changes characteristic of early and intermediate events of meiotic maturation in Xenopus oocytes</atitle><jtitle>Journal of cellular biochemistry</jtitle><addtitle>J. Cell. Biochem</addtitle><date>1997-11-01</date><risdate>1997</risdate><volume>67</volume><issue>2</issue><spage>184</spage><epage>200</epage><pages>184-200</pages><issn>0730-2312</issn><eissn>1097-4644</eissn><abstract>The growth‐promoting properties of the retroviral v‐erbA oncogene, a highly mutated version of the chicken thyroid hormone receptor (TR) α, have so far exclusively been linked to dominant repression of the antimitogenic roles of TR and retinoic acid receptors. Here we show that when expressed in Xenopus oocytes v‐ErbA induced ultrastructural changes characteristic of early and intermediate events of meiotic maturation by activating gene transcription. v‐ErbA–induced maturation events occurred without activation of the cAMP/maturation‐promoting factor signal pathway and were arrested prior to meiotic spindle formation. The effects of v‐ErbA were not mimicked by a dominant negative in vitro–generated mutant of human TR, suggesting that v‐ErbA can contribute to cell cycle reentry by interference with regulatory pathways distinct from those involving TR. Interestingly, a portion of v‐ErbA expressed in oocytes was present at the cytoplasmic fibrils of the nuclear pore complexes, suggesting that in addition to its intranuclear function v‐ErbA may modulate nucleocytoplasmic transport. J. Cell. Biochem. 67:184–200, 1997. © 1997 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>9328824</pmid><doi>10.1002/(SICI)1097-4644(19971101)67:2<184::AID-JCB4>3.0.CO;2-T</doi><tpages>17</tpages></addata></record> |
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subjects | Animals Biological Transport Cell Nucleus - metabolism Cell Nucleus - ultrastructure Cyclic AMP - physiology Cytoplasm - metabolism Female Gene Expression Gene Transfer Techniques Genes, erbA Humans maturation-promoting factor Maturation-Promoting Factor - physiology meiosis Meiosis - genetics Meiosis - physiology Microinjections Microscopy, Electron Mutation Nuclear Envelope - chemistry Nuclear Envelope - ultrastructure nuclear pore complex nucleocytoplasmic transport Oncogene Proteins v-erbA - analysis Oncogene Proteins v-erbA - pharmacology Oncogene Proteins v-erbA - physiology Oocytes - physiology Oocytes - ultrastructure Receptors, Thyroid Hormone - antagonists & inhibitors Receptors, Thyroid Hormone - genetics thyroid hormone receptor Xenopus laevis |
title | v-erbA oncogene initiates ultrastructural changes characteristic of early and intermediate events of meiotic maturation in Xenopus oocytes |
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