Pantakani, Dasaradha Venkata Krishna

[["dc.bibliographiccitation.artnumber","e22413"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Xu, X."],["dc.contributor.author","Pantakani, Dasaradha Venkata Krishna"],["dc.contributor.author","Luehrig, Sandra"],["dc.contributor.author","Tan, Xiaoying"],["dc.contributor.author","Khromov, Tatjana"],["dc.contributor.author","Nolte, Jessica"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Zechner, Ulrich"],["dc.contributor.author","Engel, Wolfgang"],["dc.date.accessioned","2018-11-07T08:54:13Z"],["dc.date.available","2018-11-07T08:54:13Z"],["dc.date.issued","2011"],["dc.description.abstract","Embryonic stem cells (ESCs) generated from the in-vitro culture of blastocyst stage embryos are known as equivalent to blastocyst inner cell mass (ICM) in-vivo. Though several reports have shown the expression of germ cell/pre-meiotic (GC/PrM) markers in ESCs, their functional relevance for the pluripotency and germ line commitment are largely unknown. In the present study, we used mouse as a model system and systematically analyzed the RNA and protein expression of GC/PrM markers in ESCs and found them to be comparable to the expression of cultured pluripotent cells originated from the germ line. Further, siRNA knockdown experiments have demonstrated the parallel maintenance and independence of pluripotent and GC/PrM networks in ESCs. Through chromatin immunoprecipitation experiments, we observed that pluripotent cells exhibit active chromatin states at GC marker genes and a bivalent chromatin structure at PrM marker genes. Moreover, gene expression analysis during the time course of iPS cells generation revealed that the expression of GC markers precedes pluripotency markers. Collectively, through our observations we hypothesize that the chromatin state and the expression of GC/PrM markers might indicate molecular parallels between in-vivo germ cell specification and pluripotent stem cell generation."],["dc.identifier.doi","10.1371/journal.pone.0022413"],["dc.identifier.isi","000293172900028"],["dc.identifier.pmid","21799849"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8198"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22620"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Stage-Specific Germ-Cell Marker Genes Are Expressed in All Mouse Pluripotent Cell Types and Emerge Early during Induced Pluripotency"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","6008"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.lastpage","11"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Xu, Xingbo"],["dc.contributor.author","Smorag, Lukasz"],["dc.contributor.author","Nakamura, Toshinobu"],["dc.contributor.author","Kimura, Tohru"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Fitzner, Antje"],["dc.contributor.author","Tan, Xiaoying"],["dc.contributor.author","Linke, Matthias"],["dc.contributor.author","Zechner, Ulrich"],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Pantakani, D.V. Krishna"],["dc.date.accessioned","2018-11-07T10:03:46Z"],["dc.date.available","2018-11-07T10:03:46Z"],["dc.date.issued","2015"],["dc.description.abstract","Reprogramming of mouse somatic cells into induced pluripotent stem cells (iPSCs) often generates partially reprogrammed iPSCs (pre-iPSCs), low-grade chimera forming iPSCs (lg-iPSCs) and fully reprogrammed, high-grade chimera production competent iPSCs (hg-iPSCs). Lg-iPSC transcriptome analysis revealed misregulated Dlk1-Dio3 cluster gene expression and subsequently the imprinting defect at the Dlk1-Dio3 locus. Here, we show that germ-cell marker Dppa3 is present only in lg-iPSCs and hg-iPSCs, and that induction with exogenous Dppa3 enhances reprogramming kinetics, generating all hg-iPSCs, similar to vitamin C (Vc). Conversely, Dppa3-null fibroblasts show reprogramming block at pre-iPSCs state and Dlk1-Dio3 imprinting defect. At the molecular level, we show that Dppa3 is associated with Dlk1-Dio3 locus and identify that Dppa3 maintains imprinting by antagonizing Dnmt3a binding. Our results further show molecular parallels between Dppa3 and Vc in Dlk1-Dio3 imprinting maintenance and suggest that early activation of Dppa3 is one of the cascades through which Vc facilitates the generation of fully reprogrammed iPSCs."],["dc.identifier.doi","10.1038/ncomms7008"],["dc.identifier.isi","000348812400009"],["dc.identifier.pmid","25613421"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11863"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38545"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/130"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","Najko"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C05: Bedeutung von zellulären Immunreaktionen für das kardiale Remodeling und die Therapie der Herzinsuffizienz durch Stammzelltransplantation"],["dc.relation.issn","2041-1723"],["dc.relation.workinggroup","RG Dressel"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Dppa3 expression is critical for generation of fully reprogrammed iPS cells and maintenance of Dlk1-Dio3 imprinting"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","166"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","MHR Basic science of reproductive medicine"],["dc.bibliographiccitation.lastpage","174"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Khromov, Tatjana"],["dc.contributor.author","Pantakani, Dasaradha Venkata Krishna"],["dc.contributor.author","Nolte, Jessica"],["dc.contributor.author","Wolf, Marieke"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Zechner, Ulrich"],["dc.date.accessioned","2018-11-07T08:58:57Z"],["dc.date.available","2018-11-07T08:58:57Z"],["dc.date.issued","2011"],["dc.description.abstract","We previously reported the generation of multipotent adult germline stem cells (maGSCs) from spermatogonial stem cells (SSCs) isolated from adult mouse testis. In a later study, we substantiated the pluripotency of maGSCs by demonstrating their close similarity to pluripotent male embryonic stem cells (ESCs) at the epigenetic level of global and gene-specific DNA methylation. Here, we extended the comparative epigenetic analysis of maGSCs and male ESCs by investigating the second main epigenetic modification in mammals, i.e. global and gene-specific modifications of histones (H3K4 trimethylation, H3K9 acetylation, H3K9 trimethylation and H3K27 trimethylation). Using immunofluorescence staining, flow cytometry and western blot analysis, we show that maGSCs are very similar to male ESCs with regard to global levels and nuclear distribution patterns of these modifications. Chromatin immunoprecipitation real-time PCR analysis of these modifications at the gene-specific level further revealed modification patterns of the pluripotency marker genes Oct4, Sox2 and Nanog in maGSCs that are nearly identical to those of male ESCs. These genes were enriched for activating histone modifications including H3K4me3 and H3K9ac and depleted of repressive histone modifications including H3K27me3 and H3K9me3. In addition, Hoxa11, a key regulator of early embryonic development showed the ESC-typical bivalent chromatin conformation with enrichment of both the activating H3K4me3 and the repressive H3K27me3 modification also in maGSCs. Collectively, our results demonstrate that maGSCs also closely resemble ESCs with regard to their chromatin state and further evidence their pluripotent nature."],["dc.identifier.doi","10.1093/molehr/gaq085"],["dc.identifier.isi","000287257000003"],["dc.identifier.pmid","20935159"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23771"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1360-9947"],["dc.title","Global and gene-specific histone modification profiles of mouse multipotent adult germline stem cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","61"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Stem Cell Research"],["dc.bibliographiccitation.lastpage","74"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Nyamsuren, Gunsmaa"],["dc.contributor.author","Kata, Aleksandra"],["dc.contributor.author","Xu, X."],["dc.contributor.author","Raju, Priyadharsini"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Pantakani, Dasaradha Venkata Krishna"],["dc.contributor.author","Adham, Ibrahim M."],["dc.date.accessioned","2018-11-07T09:37:55Z"],["dc.date.available","2018-11-07T09:37:55Z"],["dc.date.issued","2014"],["dc.description.abstract","Pelota (Pelo) is ubiquitously expressed, and its genetic deletion in mice leads to embryonic lethality at an early post-implantation stage. In the present study, we conditionally deleted Pelo and showed that PELO deficiency did not markedly affect the self-renewal of embryonic stem cells (ESCs) or their capacity to differentiate in teratoma assays. However, their differentiation into extraembryonic endoderm (ExEn) in embryoid bodies (EBs) was severely compromised. Conversely, forced expression of Pelo in ESCs resulted in spontaneous differentiation toward the ExEn lineage. Failure of Pelo-deficient ESCs to differentiate into ExEn was accompanied by the retained expression of pluripotency-related genes and alterations in expression of components of the bone morphogenetic protein (BMP) signaling pathway. Further experiments have also revealed that attenuated activity of BMP signaling is responsible for the impaired development of ExEn. The recovery of ExEn and down-regulation of pluripotent genes in BMP4-treated Pelo-null EBs indicate that the failure of mutant cells to down-regulate pluripotency-related genes in EBs is not a result of autonomous defect, but rather to failed signals from surrounding ExEn lineage that induce the differentiation program. In vivo studies showed the presence of ExEn in Pelo-null embryos at E6.5, yet embryonic lethality at E7.5, suggesting that PELO is not required for the induction of ExEn development, but rather for ExEn maintenance or for terminal differentiation toward functional visceral endoderm which provides the embryos with growth factors required for further development. Moreover, Pelo-null fibroblasts failed to reprogram toward induced pluripotent stem cells (iPSCs) due to inactivation of BMP signaling and impaired mesenchymal-to-epithelial transition. Thus, our results indicate that PELO plays an important role in the establishment of pluripotency and differentiation of ESCs into ExEn lineage through activation of BMP signaling. (C) 2014 The Authors. Published by Elsevier B.V."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2014"],["dc.identifier.doi","10.1016/j.scr.2014.04.011"],["dc.identifier.isi","000342287000006"],["dc.identifier.pmid","24835669"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10452"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32951"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1876-7753"],["dc.relation.issn","1873-5061"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","Pelota regulates the development of extraembryonic endoderm through activation of bone morphogenetic protein (BMP) signaling"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1664"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Journal of Investigative Dermatology"],["dc.bibliographiccitation.lastpage","1671"],["dc.bibliographiccitation.volume","136"],["dc.contributor.author","Elkenani, Manar"],["dc.contributor.author","Nyamsuren, Gunsmaa"],["dc.contributor.author","Raju, Priyadharsini"],["dc.contributor.author","Liakath-Ali, Kifayathullah"],["dc.contributor.author","Hamdaoui, Aicha"],["dc.contributor.author","Kata, Aleksandra"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Klonisch, Thomas"],["dc.contributor.author","Watt, Fiona M."],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Thliveris, James A."],["dc.contributor.author","Pantakani, Dasaradha Venkata Krishna"],["dc.contributor.author","Adham, Ibrahim M."],["dc.date.accessioned","2018-11-07T10:11:05Z"],["dc.date.available","2018-11-07T10:11:05Z"],["dc.date.issued","2016"],["dc.description.abstract","The depletion of evolutionarily conserved pelota protein causes impaired differentiation of embryonic and spermatogonial stem cells. In this study, we show that temporal deletion of pelota protein before epidermal barrier acquisition leads to neonatal lethality due to perturbations in permeability barrier formation. Further analysis indicated that this phenotype is a result of failed processing of profilaggrin into filaggrin monomers, which promotes the formation of a protective epidermal layer. Molecular analyses showed that pelota protein negatively regulates the activities of bone morphogenetic protein and phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathways in the epidermis. To address whether elevated activities of bone morphogenetic protein and PI3K/AKT signaling pathways were the cause for the perturbed epidermal barrier in Pelo-deficient mice, we made use of organotypic cultures of skin explants from control and mutant embryos at embryonic day 15.5. Inhibition of PI3K/AKT signaling did not significantly affect the bone morphogenetic protein activity. However, inhibition of bone morphogenetic protein signaling caused a significant attenuation of PI3K/AKT activity in mutant skin and, more interestingly, the restoration of profilaggrin processing and normal epidermal barrier function. Therefore, increased activity of the PI3K/AKT signaling pathway in Pelo-deficient skin might conflict with the dephosphorylation of profilaggrin and thereby affect its proper processing into filaggrin monomers and ultimately the epidermal differentiation."],["dc.description.sponsorship","Medical Research Council [G1100073, MR/L022699/1]"],["dc.identifier.doi","10.1016/j.jid.2016.04.020"],["dc.identifier.isi","000380585200092"],["dc.identifier.pmid","27164299"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39976"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","1523-1747"],["dc.relation.issn","0022-202X"],["dc.title","Pelota Regulates Epidermal Differentiation by Modulating BMP and PI3K/AKT Signaling Pathways"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e48869"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Khromov, Tatjana"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Siamishi, Iliana"],["dc.contributor.author","Nolte, Jessica"],["dc.contributor.author","Opitz, Lennart"],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Pantakani, Dasaradha Venkata Krishna"],["dc.date.accessioned","2018-11-07T09:03:34Z"],["dc.date.available","2018-11-07T09:03:34Z"],["dc.date.issued","2012"],["dc.description.abstract","Stem cells in the developing embryo proliferate and differentiate while maintaining genomic integrity, failure of which may lead to accumulation of mutations and subsequent damage to the embryo. Embryonic stem cells (ESCs), the in vitro counterpart of embryo stem cells are highly sensitive to genotoxic stress. Defective ESCs undergo either efficient DNA damage repair or apoptosis, thus maintaining genomic integrity. However, the genotoxicity- and apoptosis-related processes in germ-line derived pluripotent cells, multipotent adult germ-line stem cells (maGSCs), are currently unknown. Here, we analyzed the expression of apoptosis-related genes using OligoGEArray in undifferentiated maGSCs and ESCs and identified a similar set of genes expressed in both cell types. We detected the expression of intrinsic, but not extrinsic, apoptotic pathway genes in both cell types. Further, we found that apoptosis-related gene expression patterns of differentiated ESCs and maGSCs are identical to each other. Comparative analysis revealed that several pro-and antiapoptotic genes are expressed specifically in pluripotent cells, but markedly downregulated in the differentiated counterparts of these cells. Activation of the intrinsic apoptotic pathway cause approximately similar to 35% of both ESCs and maGSCs to adopt an early-apoptotic phenotype. Moreover, we performed transcriptome studies using early-apoptotic cells to identify novel pluripotency- and apoptosis-related genes. From these transcriptome studies, we selected Fgf4 (Fibroblast growth factor 4) and Mnda (Myeloid cell nuclear differentiating antigen), which are highly downregulated in early-apoptotic cells, as novel candidates and analyzed their roles in apoptosis and genotoxicity responses in ESCs. Collectively, our results show the existence of common molecular mechanisms for maintaining the pristine stem cell pool of both ESCs and maGSCs."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2012"],["dc.identifier.doi","10.1371/journal.pone.0048869"],["dc.identifier.isi","000311935800158"],["dc.identifier.pmid","23145002"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8319"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24921"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Apoptosis-Related Gene Expression Profiles of Mouse ESCs and maGSCs: Role of Fgf4 and Mnda in Pluripotent Cell Responses to Genotoxicity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]