Hoyer-Fender, Sigrid

[["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"]]

[["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"]]

[["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"]]

[["dc.bibliographiccitation.firstpage","1647"],["dc.bibliographiccitation.issue","14"],["dc.bibliographiccitation.journal","Human Molecular Genetics"],["dc.bibliographiccitation.lastpage","1658"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Mendoza-Lujambio, I."],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Dixkens, C."],["dc.contributor.author","Meinhardt, Andreas"],["dc.contributor.author","Hoyer-Fender, Sigrid"],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Neesen, J."],["dc.date.accessioned","2018-11-07T10:21:12Z"],["dc.date.available","2018-11-07T10:21:12Z"],["dc.date.issued","2002"],["dc.description.abstract","In mice carrying the autosomal recessive mutation 'abnormal spermatozoon head shape' (azh) all spermatozoa display a highly abnormal head morphology that differs drastically from the compact and hook-shaped head of the normal murine sperm. Moreover, the azh mutation causes tail abnormalities often resulting in coiled sperm tails or in the decapitation of the sperm head from the flagellum. We have isolated and characterized murine Hook1 cDNA and analyzed the corresponding genomic structure. Furthermore, the Hook1 gene was mapped to the same region on chromosome 4 to which the azh locus was previously linked. The Hook1 gene is predominantly expressed in haploid male germ cells, and immunohistochemical analysis revealed that Hook1 is responsible for the linkage of the microtubular manchette and the flagellum to cellular structures. Here, we report that the azh mutation is due to a deletion of exons 10 and 11 in the murine Hook1 gene leading to a non-functional protein. Our results indicate that loss of Hook1 function results in ectopic positioning of microtubular structures within the spermatid and causes the azh phenotype. Therefore, the human HOOK1 gene could serve as a candidate gene for male infertility due to teratozoospermia or decapitation defects."],["dc.identifier.doi","10.1093/hmg/11.14.1647"],["dc.identifier.isi","000176606300007"],["dc.identifier.pmid","12075009"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42045"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0964-6906"],["dc.title","The Hook1 gene is non-functional in the abnormal spermatozoon head shape (azh) mutant mouse"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]