Now showing 1 - 6 of 6
  • 2012Journal Article
    [["dc.bibliographiccitation.firstpage","216"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Molecular and Cellular Biology"],["dc.bibliographiccitation.lastpage","225"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Yang, Kefei"],["dc.contributor.author","Meinhardt, Andreas"],["dc.contributor.author","Zhang, B."],["dc.contributor.author","Grzmil, Pawel"],["dc.contributor.author","Adham, Ibrahim M."],["dc.contributor.author","Hoyer-Fender, Sigrid"],["dc.date.accessioned","2018-11-07T09:16:11Z"],["dc.date.available","2018-11-07T09:16:11Z"],["dc.date.issued","2012"],["dc.description.abstract","Sperm motility and hence male fertility strictly depends on proper development of the sperm tail and its tight anchorage to the head. The main protein of sperm tail outer dense fibers, ODF1/HSPB10, belongs to the family of small heat shock proteins that function as molecular chaperones. However, the impact of ODF1 on sperm tail formation and motility and on male fecundity is unknown. We therefore generated mutant mice in which the Odf1 gene was disrupted. Heterozygous mutant male mice are fertile while sperm motility is reduced, but Odf1-deficient male mice are infertile due to the detachment of the sperm head. Although headless tails are somehow motile, transmission electron microscopy revealed disturbed organization of the mitochondrial sheath, as well as of the outer dense fibers. Our results thus suggest that ODF1, besides being involved in the correct arrangement of mitochondrial sheath and outer dense fibers, is essential for rigid junction of sperm head and tail. Loss of function of ODF1, therefore, might account for some of the cases of human infertility with decapitated sperm heads. In addition, since sperm motility is already affected in heterozygous mice, impairment of ODF1 might even account for some cases of reduced fertility in male patients."],["dc.identifier.doi","10.1128/MCB.06158-11"],["dc.identifier.isi","000298366000019"],["dc.identifier.pmid","22037768"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27875"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Microbiology"],["dc.relation.issn","1098-5549"],["dc.relation.issn","0270-7306"],["dc.title","The Small Heat Shock Protein ODF1/HSPB10 Is Essential for Tight Linkage of Sperm Head to Tail and Male Fertility in Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2018Journal Article
    [["dc.bibliographiccitation.firstpage","49"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Histochemistry and Cell Biology"],["dc.bibliographiccitation.lastpage","59"],["dc.bibliographiccitation.volume","150"],["dc.contributor.author","Yang, Kefei"],["dc.contributor.author","Adham, Ibrahim M."],["dc.contributor.author","Meinhardt, Andreas"],["dc.contributor.author","Hoyer-Fender, Sigrid"],["dc.date.accessioned","2020-12-10T14:10:35Z"],["dc.date.available","2020-12-10T14:10:35Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1007/s00418-018-1668-7"],["dc.identifier.eissn","1432-119X"],["dc.identifier.issn","0948-6143"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70808"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Ultra-structure of the sperm head-to-tail linkage complex in the absence of the spermatid-specific LINC component SPAG4"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]
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  • 2015Journal Article
    [["dc.bibliographiccitation.firstpage","1795"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Cellular and Molecular Life Sciences"],["dc.bibliographiccitation.lastpage","1809"],["dc.bibliographiccitation.volume","72"],["dc.contributor.author","Tylkowski, Marco Andreas"],["dc.contributor.author","Yang, Kefei"],["dc.contributor.author","Hoyer-Fender, Sigrid"],["dc.contributor.author","Stoykova, Anastassia"],["dc.date.accessioned","2018-11-07T09:58:04Z"],["dc.date.available","2018-11-07T09:58:04Z"],["dc.date.issued","2015"],["dc.description.abstract","Cortical glutamatergic neurons are generated by radial glial cells (RGCs), specified by the expression of transcription factor (TF) Pax6, in the germinative zones of the dorsal telencephalon. Here, we demonstrate that Pax6 regulates the structural assembly of the interphase centrosomes. In the cortex of the Pax6-deficient Small eye (Sey/Sey) mutant, we find a defect of the appendages of the mother centrioles, indicating incomplete centrosome maturation. Consequently, RGCs fail to generate primary cilia, and instead of staying in the germinative zone for renewal, RGCs detach from the ventricular surface thus affecting the interkinetic nuclear migration and they exit prematurely from mitosis. Mechanistically, we show that TF Pax6 directly regulates the activity of the Odf2 gene encoding for the appendage-specific protein Odf2 with a role for the assembly of mother centriole. Our findings demonstrate a molecular mechanism that explains important characteristics of the centrosome disassembly and malfunctioning in developing cortex lacking Pax6."],["dc.identifier.doi","10.1007/s00018-014-1766-1"],["dc.identifier.isi","000352791200011"],["dc.identifier.pmid","25352170"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37296"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Basel"],["dc.relation.issn","1420-9071"],["dc.relation.issn","1420-682X"],["dc.title","Pax6 controls centriole maturation in cortical progenitors through Odf2"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2014Journal Article
    [["dc.bibliographiccitation.firstpage","499"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Reproduction"],["dc.bibliographiccitation.lastpage","506"],["dc.bibliographiccitation.volume","148"],["dc.contributor.author","Yang, Kefei"],["dc.contributor.author","Grzmil, Pawel"],["dc.contributor.author","Meinhardt, Andreas"],["dc.contributor.author","Hoyer-Fender, Sigrid"],["dc.date.accessioned","2018-11-07T09:33:05Z"],["dc.date.available","2018-11-07T09:33:05Z"],["dc.date.issued","2014"],["dc.description.abstract","The small heat shock protein ODF1/HSPB10 is essential for male fertility in mice. Targeted deletion of Odf1 resulted in acephalic sperm in homozygous mice of mixed background (C57BL/6J//129/Sv), whereas heterozygous animals are fully fertile. To further elucidate the function of ODF1, we generated incipient congenic mice with targeted deletion of Odf1 by successive backcrossing on the 129/Sv background. We observed that fecundity of heterozygous Odf1(+/-) male mice was severely reduced over backcross generations. However, neither aberrant sperm parameters nor sperm anomalies could be observed. Ultra-structural analyses of sperm from incipient congenic heterozygous Odf1(+/-) males of backcross generation N7 revealed no obvious pathological findings. However, we observed an enlargement of the distance between nuclear membrane and capitulum, indicating a weakening of the sperm head-to-tail coupling. Severe male subfertility provoked by haplo-deficiency of ODF1 is therefore most probably caused by impaired head-to-tail coupling that eventually might induce sperm decapitation on the specific conditions of in vivo fertilisation. As subfertility in haplo-deficient ODF1 male mice could not be diagnosed by semen analysis, it seems to be a paradigm for unexplained infertility that is a frequent diagnosis for male fertility impairment in humans."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [HO 1440/13-1, 13-2]"],["dc.identifier.doi","10.1530/REP-14-0370"],["dc.identifier.isi","000345131400007"],["dc.identifier.pmid","25118300"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31892"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Bioscientifica Ltd"],["dc.relation.issn","1470-1626"],["dc.title","Haplo-deficiency of ODF1/HSPB10 in mouse sperm causes relaxation of head-to-tail linkage"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2018Journal Article
    [["dc.bibliographiccitation.firstpage","jcs220954"],["dc.bibliographiccitation.issue","20"],["dc.bibliographiccitation.journal","Journal of Cell Science"],["dc.bibliographiccitation.volume","131"],["dc.contributor.author","Yang, Kefei"],["dc.contributor.author","Tylkowski, Marco Andreas"],["dc.contributor.author","Hüber, Daniela"],["dc.contributor.author","Contreras, Constanza Tapia"],["dc.contributor.author","Hoyer-Fender, Sigrid"],["dc.date.accessioned","2020-12-10T18:41:52Z"],["dc.date.available","2020-12-10T18:41:52Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1242/jcs.220954"],["dc.identifier.eissn","1477-9137"],["dc.identifier.issn","0021-9533"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77712"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","ODF2 maintains centrosome cohesion by restricting β-catenin accumulation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]
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  • 2013Journal Article
    [["dc.bibliographiccitation.firstpage","1338"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Biochimica et Biophysica Acta (BBA) - Molecular Cell Research"],["dc.bibliographiccitation.lastpage","1346"],["dc.bibliographiccitation.volume","1833"],["dc.contributor.author","Pletz, Nadin"],["dc.contributor.author","Medack, Anja"],["dc.contributor.author","Riess, Eva Maria"],["dc.contributor.author","Yang, Kefei"],["dc.contributor.author","Kazerouni, Zahra Basir"],["dc.contributor.author","Hueber, Daniela"],["dc.contributor.author","Hoyer-Fender, Sigrid"],["dc.date.accessioned","2018-11-07T09:24:28Z"],["dc.date.available","2018-11-07T09:24:28Z"],["dc.date.issued","2013"],["dc.description.abstract","The centrosome/basal body protein ODF2/Cenexin is necessary for the formation of the primary cilium. Primary cilia are essential organelles that sense and transduce environmental signals. Primary cilia are therefore critical for embryonic and postnatal development as well as for tissue homeostasis in adulthood. Impaired function of primary cilia causes severe human diseases. ODF2 deficiency prevents formation of the primary cilium and is embryonically lethal. To explore the regulation of primary cilia formation we analyzed the promoter region of Odf2 and its transcriptional activity. In cycling cells, Odf2 transcription is depressed but becomes up-regulated in quiescent cells. Low transcriptional activity is mediated by sequences located upstream from the basal promoter, and neither transcription factors with predicted binding sites in the Odf2 promoter nor Rfx3 or Foxj, which are known to control ciliary gene expression, could activate Odf2 transcription. However, co-expression of either C/EBP alpha, c-Jun or c-Jun and its regulator MEKK1 enhances Odf2 transcription in cycling cells. Our results provide the first analysis of transcriptional regulation of a ciliary gene. Furthermore, we suggest that transcription of even more ciliary genes is largely inhibited in cycling cells but could be activated by cell cycle arrest and by the stress signaling JNK pathway. (c) 2013 Elsevier B.V. All rights reserved."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [Ho 1440/8-1]"],["dc.identifier.doi","10.1016/j.bbamcr.2013.02.023"],["dc.identifier.isi","000318390900006"],["dc.identifier.pmid","23458833"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29827"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0167-4889"],["dc.title","Transcriptional activation of Odf2/Cenexin by cell cycle arrest and the stress activated signaling pathway (JNK pathway)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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