Wolf, Katrin

[["dc.bibliographiccitation.firstpage","1973"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Biology of Reproduction"],["dc.bibliographiccitation.lastpage","1978"],["dc.bibliographiccitation.volume","69"],["dc.contributor.author","Nayernia, K."],["dc.contributor.author","Drabent, B."],["dc.contributor.author","Adham, Ibrahim M."],["dc.contributor.author","Moschner, M."],["dc.contributor.author","Wolf, S."],["dc.contributor.author","Meinhardt, Andreas"],["dc.contributor.author","Engel, Wolfgang"],["dc.date.accessioned","2018-11-07T10:34:15Z"],["dc.date.available","2018-11-07T10:34:15Z"],["dc.date.issued","2003"],["dc.description.abstract","In recent years, much knowledge about the functions of defined genes in spermatogenesis has been gained by making use of mouse transgenic and gene knockout models. Single null mutations in mouse genes encoding four male germ cell proteins, transition protein 2 (Tnp-2), proacrosin (Acr), histone H1.1 (H1.1), and histone H1t (H1t), have been generated and analyzed. Tnp-2 is believed to participate in the removal of the nuclear histones and initial condensation of the spermatid nucleus. Proacrosin is an acrosomal protease synthesized as a proenzyme and activated into acrosin during the acrosome reaction. The linker histone subtype H1.1 belongs to the group of main-type histones and is synthesized in somatic tissues and germ cells during the S-phase of the cell cycle. The histone gene H1t is expressed exclusively in spermatocytes and may have a function in establishing an open chromatin structure for the replacement of histones by transition proteins and protamines. Male mutant mice lacking any of these proteins show no apparent defects in spermatogenesis or fertility. To examine the synergistic effects of these proteins in spermatogenesis and during fertilization, two lines of triple null mice (Tnp-2(-/-)/Acr(-/-)/H1.1(-/-) and Tnp-2(-/-)/Acr(-1-)/H1t(-/-)) were established. Both lines are fertile and show normal sperm parameters, which clearly demonstrate the functional redundancy of these proteins in male mouse fertility. However, sperm only deficient for Acr (Acr(-/-)) are able to compete significantly with sperm from triple knockout mice Tnp-2(-/-)/Acr(-/-)/H1.1(-/-) (70.7% vs. 29.3%) but not with sperm from triple knockout mice Tnp-2(-/-)/Acr(-/-)/H1t(-/-) (53.6% vs. 46.4%). These results are consistent with a model that suggests that some sperm proteins play a role during sperm competition."],["dc.identifier.doi","10.1095/biolreprod.103.018564"],["dc.identifier.isi","000186772300028"],["dc.identifier.pmid","12930723"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44819"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Soc Study Reproduction"],["dc.relation.issn","0006-3363"],["dc.title","Male mice lacking three germ cell expressed genes are fertile"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","155"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","MHR Basic science of reproductive medicine"],["dc.bibliographiccitation.lastpage","163"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Jaroszynski, L."],["dc.contributor.author","Dev, A."],["dc.contributor.author","Li, M."],["dc.contributor.author","Meinhardt, Andreas"],["dc.contributor.author","de Rooij, D. G."],["dc.contributor.author","Mueller, Christian"],["dc.contributor.author","Boehm, Detlef"],["dc.contributor.author","Wolf, S."],["dc.contributor.author","Adham, Ibrahim M."],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Nayernia, K."],["dc.date.accessioned","2018-11-07T11:04:40Z"],["dc.date.available","2018-11-07T11:04:40Z"],["dc.date.issued","2007"],["dc.description.abstract","Testis expressed gene 18 (Tex18) is a small gene with one exon of 240 bp, which is specifically expressed in male germ cells. The gene encodes for a protein of 80 amino acids with unknown domain. To investigate the function of (Tex18) gene, we generated mice with targeted disruption of the (Tex18) gene by homologous recombination. Homozygous mutant males on a mixed genetic background (C57BL/6J x 129/Sv) are fertile, while they are subfertile on the 129/Sv background, although mating is normal. We showed that Tex18(-/-) males are subfertile because of abnormal sperm morphology and reduced motility, which is called asthenoteratozoospermia, suggesting that (Tex18) affects sperm characteristics. Maturation of spermatids is unsynchronized and partially impaired in seminiferous tubules of Tex18(-/-) mice. Electron microscopical examination demonstrated abnormal structures of sperm head. In vivo experiments with sperm of Tex18(-/-) 129/Sv mice revealed that the migration of spermatozoa from the uterus into the oviduct is reduced. This result is supported by the observation that sperm motility, as determined by the computer-assisted semen analysis system, is significantly affected, compared to wild-type spermatozoa. Generation of transgenic mice containing Tex18-EGFP fusion construct revealed a high transcriptional activity of (Tex18) during spermiogenesis, a process with morphological changes of haploid germ cells and development to mature spermatozoa. These results indicate that (Tex18) is expressed predominantly during spermatid differentiation and subfertility of the male Tex18(-/-) mice on the 129/Sv background is due to the differentiation arrest, abnormal sperm morphology and reduced sperm motility."],["dc.identifier.doi","10.1093/molehr/gal107"],["dc.identifier.isi","000244662300003"],["dc.identifier.pmid","17208930"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51894"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1360-9947"],["dc.title","Asthenoteratozoospermia in mice lacking testis expressed gene 18 (Tex18)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","The Journal of Urology"],["dc.bibliographiccitation.volume","182"],["dc.contributor.author","Shirneshan, Katayoon"],["dc.contributor.author","Binder, S."],["dc.contributor.author","Bohm, D."],["dc.contributor.author","Wolf, S."],["dc.contributor.author","Sancken, Ulrich"],["dc.contributor.author","Meinhardt, Andreas"],["dc.contributor.author","Schmid, M."],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Adham, Ibrahim M."],["dc.date.accessioned","2018-11-07T08:28:19Z"],["dc.date.available","2018-11-07T08:28:19Z"],["dc.date.issued","2009"],["dc.format.extent","391"],["dc.identifier.doi","10.1016/j.juro.2009.03.040"],["dc.identifier.isi","000266949800151"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16391"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0022-5347"],["dc.title","Directed Overexpression of Insulin in Leydig Cells Causes a Progressive Loss of Germ Cells Editorial Comment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","editorial_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3046"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Molecular and Cellular Biology"],["dc.bibliographiccitation.lastpage","3052"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Nayernia, K."],["dc.contributor.author","Adham, Ibrahim M."],["dc.contributor.author","Burkhardt-Gottges, E."],["dc.contributor.author","Neesen, J."],["dc.contributor.author","Rieche, M."],["dc.contributor.author","Wolf, S."],["dc.contributor.author","Sancken, Ulrich"],["dc.contributor.author","Kleene, K."],["dc.contributor.author","Engel, Wolfgang"],["dc.date.accessioned","2018-11-07T10:30:22Z"],["dc.date.available","2018-11-07T10:30:22Z"],["dc.date.issued","2002"],["dc.description.abstract","The sperm mitochondria-associated cysteine-rich protein (SMCP) is a cysteine- and proline-rich structural protein that is closely associated with the keratinous capsules of sperm mitochondria in the mitochondrial sheath surrounding the outer dense fibers and axoneme. To investigate the function of SMCP, we generated mice with a targeted disruption of the gene Smcp by homologous recombination. Homozygous mutant males on a mixed genetic background (C57BL/6J x 129/Sv) are fully fertile, while they are infertile on the 129/Sv background, although spermatogenesis and mating are normal. Homozygous Smcp(-/-) female mice are fertile on both genetic backgrounds. Electron microscopical examination demonstrated normal structures of sperm head, mitochondria, and tail. In vivo experiments with sperm of Smcp(-/-) 129/Sv mice revealed that the migration of spermatozoa from the uterus into the oviduct is reduced. This result is supported by the observation that sperm motility as determined by the computer-assisted semen analysis system (CASA) is significantly affected as compared to wild-type spermatozoa. In vitro fertilization assays showed that Smcp-deficient spermatozoa are able to bind to the oocyte but that the number of fertilized eggs is reduced by more than threefold relative to the wild-type control. However, removal of the zona pellucida resulted in an unaffected sperm-egg fusion which was monitored by the presence of pronuclei and generation of blastocyts. These results indicate that the infertility of the male Smep(-/-) mice on the 129/Sv background is due to reduced motility of the spermatozoa and decreased capability of the spermatozoa to penetrate oocytes."],["dc.identifier.doi","10.1128/MCB.22.9.3046-3052.2002"],["dc.identifier.isi","000174972600016"],["dc.identifier.pmid","11940662"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43852"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Microbiology"],["dc.relation.issn","0270-7306"],["dc.title","Asthenozoospermia in mice with targeted deletion of the sperm mitochondrion-associated cysteine-rich protein (Smcp) gene"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Reproduction in Domestic Animals"],["dc.bibliographiccitation.volume","47"],["dc.contributor.author","Grzmil, Pawel"],["dc.contributor.author","Altman, M. E."],["dc.contributor.author","Adham, Ibrahim M."],["dc.contributor.author","Engel, Ulrike"],["dc.contributor.author","Jarry, Hubertus"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Wolf, S."],["dc.contributor.author","Maenz, Johanna"],["dc.contributor.author","Engel, Wolfgang"],["dc.date.accessioned","2018-11-07T09:13:11Z"],["dc.date.available","2018-11-07T09:13:11Z"],["dc.date.issued","2012"],["dc.format.extent","25"],["dc.identifier.isi","000300500500075"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27115"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Malden"],["dc.relation.eventlocation","Berlin, GERMANY"],["dc.relation.issn","0936-6768"],["dc.title","The targeted disruption of Ube2q1 gene leads to pleiotropic reproductive defects in female mutant mice"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1249"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Human Molecular Genetics"],["dc.bibliographiccitation.lastpage","1255"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Schwarz, Guenter"],["dc.contributor.author","Santamaria-Araujo, Jose Angel"],["dc.contributor.author","Wolf, S."],["dc.contributor.author","Lee, H. J."],["dc.contributor.author","Adham, Ibrahim M."],["dc.contributor.author","Grone, H. J."],["dc.contributor.author","Schwegler, H."],["dc.contributor.author","Sass, Joern Oliver"],["dc.contributor.author","Otte, T."],["dc.contributor.author","Hanzelmann, P."],["dc.contributor.author","Mendel, R. R."],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Reiss, Jochen"],["dc.date.accessioned","2018-11-07T10:48:04Z"],["dc.date.available","2018-11-07T10:48:04Z"],["dc.date.issued","2004"],["dc.description.abstract","Substitution therapies for orphan genetic diseases, including enzyme replacement methods, are frequently hampered by the limited availability of the required therapeutic substance. We describe the isolation of a pterin intermediate from bacteria that was successfully used for the therapy of a hitherto incurable and lethal disease. Molybdenum cofactor (Moco) deficiency is a pleiotropic genetic disorder characterized by the loss of the molybdenum-dependent enzymes sulphite oxidase, xanthine oxidoreductase and aldehyde oxidase due to mutations in Moco biosynthesis genes. An intermediate of this pathway-'precursor Z'-is more stable than the cofactor itself and has an identical structure in all phyla. Thus, it was overproduced in the bacterium Escherichia coli, purified and used to inject precursor Z-deficient knockout mice that display a phenotype which resembles that of the human deficiency state. Precursor Z-substituted mice reach adulthood and fertility. Biochemical analyses further suggest that the described treatment can lead to the alleviation of most symptoms associated with human Moco deficiency."],["dc.identifier.doi","10.1093/hmg/ddh136"],["dc.identifier.isi","000221748400006"],["dc.identifier.pmid","15115759"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48113"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0964-6906"],["dc.title","Rescue of lethal molybdenum cofactor deficiency by a biosynthetic precursor from Escherichia coli"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","74"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Cytogenetic and Genome Research"],["dc.bibliographiccitation.lastpage","82"],["dc.bibliographiccitation.volume","119"],["dc.contributor.author","Grzmil, Pawel"],["dc.contributor.author","Burfeind, C."],["dc.contributor.author","Preuss, Thomas"],["dc.contributor.author","Dixkens, C."],["dc.contributor.author","Wolf, S."],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Burfeind, Peter"],["dc.date.accessioned","2018-11-07T11:06:22Z"],["dc.date.available","2018-11-07T11:06:22Z"],["dc.date.issued","2007"],["dc.description.abstract","Genes reported to be crucial for spermatogenesis are often exclusively expressed in the testis. We have identified a novel male germ cell-specific expressed gene named peroxisomal testis specific 1 (Pxt1) with expression starting at the spermatocyte stage during mouse spermatogenesis. The putative amino acid sequence encoded by the cDNA of the Pxt1 gene contains a conserved Asn-His-Leu (NHL)-motif at its C-terminal end, which is characteristic for peroxisomal proteins. Pxt1-EGFP fusion protein is co-localized with known peroxisomal marker proteins in transfected NIH3T3 cells. In addition, we could demonstrate that the peroxisomal targeting signal NHL is functional and responsible for the correct subcellular localization of the Pxt1-EGFP fusion protein. In male germ cells peroxisomes were reported only in spermatogonia. The Pxt1 gene is so far the first gene coding for a putative peroxisomal protein which is expressed in later steps of spermatogenesis, namely in pachytene spermatocytes. Copyright (C) 2007 S. Karger AG, Basel."],["dc.identifier.doi","10.1159/000109622"],["dc.identifier.isi","000251909600013"],["dc.identifier.pmid","18160785"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52294"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1424-8581"],["dc.title","The putative peroxisomal gene Pxt1 is exclusively expressed in the testis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]