The transcription factors NR5A1 and JUNB cooperate to activate the Axl promoter in mouse Sertoli cell lines

Background The Axl gene is a receptor tyrosine kinase essential for male fertility. With other Tyro3 family members, it regulates cell apoptosis and preserves the organization of seminiferous tubules. However, the regulation of the expression of Axl in testicular Sertoli cells is not entirely unders...

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Veröffentlicht in:Molecular biology reports 2024-12, Vol.51 (1), p.982-982, Article 982
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description Background The Axl gene is a receptor tyrosine kinase essential for male fertility. With other Tyro3 family members, it regulates cell apoptosis and preserves the organization of seminiferous tubules. However, the regulation of the expression of Axl in testicular Sertoli cells is not entirely understood. The transcription factors NR5A1 and JUNB are involved in several male fertility mechanisms such as sex development and steroidogenesis. We hypothesize that Axl promoter activity is regulated by cooperation between JUNB and NR5A1 in Sertoli cells. Methods and Results Following transfections of TM4 Sertoli cells with DsiRNA interference against Axl , our results show that cell morphology may be regulated by AXL . Using transfections of expression plasmids and reporter plasmids containing the Axl promoter, we report that Axl expression is highly activated by cooperation between NR5A1 and JUNB in TM4 and 15P-1 Sertoli cells. Chromatin immunoprecipitation and luciferase reporter assays with 5′ promoter deletions demonstrate that JUNB and NR5A1 are being recruited to DNA regulatory elements in the proximal region of the Axl promoter. The fourth intronic region of Axl also participates in the recruitment of JUNB. Conclusion Thus, Axl expression is regulated by a cooperation between the transcription factors JUNB and NR5A1 and influences the morphology of TM4 Sertoli cells.
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With other Tyro3 family members, it regulates cell apoptosis and preserves the organization of seminiferous tubules. However, the regulation of the expression of Axl in testicular Sertoli cells is not entirely understood. The transcription factors NR5A1 and JUNB are involved in several male fertility mechanisms such as sex development and steroidogenesis. We hypothesize that Axl promoter activity is regulated by cooperation between JUNB and NR5A1 in Sertoli cells. Methods and Results Following transfections of TM4 Sertoli cells with DsiRNA interference against Axl , our results show that cell morphology may be regulated by AXL . Using transfections of expression plasmids and reporter plasmids containing the Axl promoter, we report that Axl expression is highly activated by cooperation between NR5A1 and JUNB in TM4 and 15P-1 Sertoli cells. Chromatin immunoprecipitation and luciferase reporter assays with 5′ promoter deletions demonstrate that JUNB and NR5A1 are being recruited to DNA regulatory elements in the proximal region of the Axl promoter. The fourth intronic region of Axl also participates in the recruitment of JUNB. Conclusion Thus, Axl expression is regulated by a cooperation between the transcription factors JUNB and NR5A1 and influences the morphology of TM4 Sertoli cells.</description><identifier>ISSN: 0301-4851</identifier><identifier>ISSN: 1573-4978</identifier><identifier>EISSN: 1573-4978</identifier><identifier>DOI: 10.1007/s11033-024-09934-3</identifier><identifier>PMID: 39271559</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Animal Anatomy ; Animal Biochemistry ; Animals ; Apoptosis ; Axl protein ; Axl Receptor Tyrosine Kinase ; Biomedical and Life Sciences ; Brief Report ; Cell Line ; Cell lines ; Cell morphology ; cell structures ; Chromatin ; chromatin immunoprecipitation ; Cooperation ; family ; Fertility ; Gene Expression Regulation ; Gene regulation ; Histology ; Immunoprecipitation ; introns ; JunB protein ; Kinases ; Life Sciences ; luciferase ; Male ; male fertility ; Mice ; Morphology ; Plasmids ; Promoter Regions, Genetic - genetics ; Protein-tyrosine kinase receptors ; Proto-Oncogene Proteins - genetics ; Proto-Oncogene Proteins - metabolism ; receptor protein-tyrosine kinase ; Receptor Protein-Tyrosine Kinases - genetics ; Receptor Protein-Tyrosine Kinases - metabolism ; Regulatory sequences ; Sertoli cells ; Sertoli Cells - metabolism ; Steroidogenesis ; Steroidogenic Factor 1 - genetics ; Steroidogenic Factor 1 - metabolism ; Transcription factors ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Tubules</subject><ispartof>Molecular biology reports, 2024-12, Vol.51 (1), p.982-982, Article 982</ispartof><rights>The Author(s), under exclusive licence to Springer Nature B.V. 2024 Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2024. 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With other Tyro3 family members, it regulates cell apoptosis and preserves the organization of seminiferous tubules. However, the regulation of the expression of Axl in testicular Sertoli cells is not entirely understood. The transcription factors NR5A1 and JUNB are involved in several male fertility mechanisms such as sex development and steroidogenesis. We hypothesize that Axl promoter activity is regulated by cooperation between JUNB and NR5A1 in Sertoli cells. Methods and Results Following transfections of TM4 Sertoli cells with DsiRNA interference against Axl , our results show that cell morphology may be regulated by AXL . Using transfections of expression plasmids and reporter plasmids containing the Axl promoter, we report that Axl expression is highly activated by cooperation between NR5A1 and JUNB in TM4 and 15P-1 Sertoli cells. Chromatin immunoprecipitation and luciferase reporter assays with 5′ promoter deletions demonstrate that JUNB and NR5A1 are being recruited to DNA regulatory elements in the proximal region of the Axl promoter. The fourth intronic region of Axl also participates in the recruitment of JUNB. 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Martin, Luc J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c289t-d700730cd6264ebc65c8beeb854c116fef9606e40fe20eeaab25c0eaaca58e7d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Animal Anatomy</topic><topic>Animal Biochemistry</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Axl protein</topic><topic>Axl Receptor Tyrosine Kinase</topic><topic>Biomedical and Life Sciences</topic><topic>Brief Report</topic><topic>Cell Line</topic><topic>Cell lines</topic><topic>Cell morphology</topic><topic>cell structures</topic><topic>Chromatin</topic><topic>chromatin immunoprecipitation</topic><topic>Cooperation</topic><topic>family</topic><topic>Fertility</topic><topic>Gene Expression Regulation</topic><topic>Gene regulation</topic><topic>Histology</topic><topic>Immunoprecipitation</topic><topic>introns</topic><topic>JunB protein</topic><topic>Kinases</topic><topic>Life Sciences</topic><topic>luciferase</topic><topic>Male</topic><topic>male fertility</topic><topic>Mice</topic><topic>Morphology</topic><topic>Plasmids</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>Protein-tyrosine kinase receptors</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>receptor protein-tyrosine kinase</topic><topic>Receptor Protein-Tyrosine Kinases - genetics</topic><topic>Receptor Protein-Tyrosine Kinases - metabolism</topic><topic>Regulatory sequences</topic><topic>Sertoli cells</topic><topic>Sertoli Cells - metabolism</topic><topic>Steroidogenesis</topic><topic>Steroidogenic Factor 1 - genetics</topic><topic>Steroidogenic Factor 1 - metabolism</topic><topic>Transcription factors</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><topic>Tubules</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Diawara, Mariama</creatorcontrib><creatorcontrib>Martin, Luc J.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health &amp; 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With other Tyro3 family members, it regulates cell apoptosis and preserves the organization of seminiferous tubules. However, the regulation of the expression of Axl in testicular Sertoli cells is not entirely understood. The transcription factors NR5A1 and JUNB are involved in several male fertility mechanisms such as sex development and steroidogenesis. We hypothesize that Axl promoter activity is regulated by cooperation between JUNB and NR5A1 in Sertoli cells. Methods and Results Following transfections of TM4 Sertoli cells with DsiRNA interference against Axl , our results show that cell morphology may be regulated by AXL . Using transfections of expression plasmids and reporter plasmids containing the Axl promoter, we report that Axl expression is highly activated by cooperation between NR5A1 and JUNB in TM4 and 15P-1 Sertoli cells. Chromatin immunoprecipitation and luciferase reporter assays with 5′ promoter deletions demonstrate that JUNB and NR5A1 are being recruited to DNA regulatory elements in the proximal region of the Axl promoter. The fourth intronic region of Axl also participates in the recruitment of JUNB. Conclusion Thus, Axl expression is regulated by a cooperation between the transcription factors JUNB and NR5A1 and influences the morphology of TM4 Sertoli cells.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>39271559</pmid><doi>10.1007/s11033-024-09934-3</doi><tpages>1</tpages></addata></record>
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subjects Animal Anatomy
Animal Biochemistry
Animals
Apoptosis
Axl protein
Axl Receptor Tyrosine Kinase
Biomedical and Life Sciences
Brief Report
Cell Line
Cell lines
Cell morphology
cell structures
Chromatin
chromatin immunoprecipitation
Cooperation
family
Fertility
Gene Expression Regulation
Gene regulation
Histology
Immunoprecipitation
introns
JunB protein
Kinases
Life Sciences
luciferase
Male
male fertility
Mice
Morphology
Plasmids
Promoter Regions, Genetic - genetics
Protein-tyrosine kinase receptors
Proto-Oncogene Proteins - genetics
Proto-Oncogene Proteins - metabolism
receptor protein-tyrosine kinase
Receptor Protein-Tyrosine Kinases - genetics
Receptor Protein-Tyrosine Kinases - metabolism
Regulatory sequences
Sertoli cells
Sertoli Cells - metabolism
Steroidogenesis
Steroidogenic Factor 1 - genetics
Steroidogenic Factor 1 - metabolism
Transcription factors
Transcription Factors - genetics
Transcription Factors - metabolism
Tubules
title The transcription factors NR5A1 and JUNB cooperate to activate the Axl promoter in mouse Sertoli cell lines
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