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2. Epigenetic memory in induced pluripotent stem cells

Author

Kim, K, Doi, A, Wen, B, Ng, K, Zhao, R, Cahan, P, Kim, J, Aryee, MJ, Ji, H, Ehrlich, LIR, Yabuuchi, A, Takeuchi, A, Cunniff, KC, Hongguang, H, Mckinney-Freeman, S, Naveiras, O, Yoon, TJ, Irizarry, RA, Jung, N, Seita, J, Hanna, J, Murakami, P, Jaenisch, R, Weissleder, R, Orkin, SH, Weissman, IL, Feinberg, AP, and Daley, GQ

Subjects
Stem Cell Research - Nonembryonic - Human, Stem Cell Research, Human Genome, Regenerative Medicine, Stem Cell Research - Induced Pluripotent Stem Cell, Genetics, Stem Cell Research - Induced Pluripotent Stem Cell - Human, Stem Cell Research - Embryonic - Non-Human, Stem Cell Research - Induced Pluripotent Stem Cell - Non-Human, Stem Cell Research - Embryonic - Human, 5.2 Cellular and gene therapies, Underpinning research, 1.1 Normal biological development and functioning, Development of treatments and therapeutic interventions, Generic health relevance, Animals, Cell Differentiation, Cell Lineage, Cellular Reprogramming, DNA Methylation, Embryonic Stem Cells, Epigenesis, Genetic, Genome, Hematopoietic Stem Cells, Induced Pluripotent Stem Cells, Mice, Mice, Inbred C57BL, Mice, Inbred CBA, Nuclear Transfer Techniques, Transcription Factors, General Science & Technology
Abstract

Somatic cell nuclear transfer and transcription-factor-based reprogramming revert adult cells to an embryonic state, and yield pluripotent stem cells that can generate all tissues. Through different mechanisms and kinetics, these two reprogramming methods reset genomic methylation, an epigenetic modification of DNA that influences gene expression, leading us to hypothesize that the resulting pluripotent stem cells might have different properties. Here we observe that low-passage induced pluripotent stem cells (iPSCs) derived by factor-based reprogramming of adult murine tissues harbour residual DNA methylation signatures characteristic of their somatic tissue of origin, which favours their differentiation along lineages related to the donor cell, while restricting alternative cell fates. Such an 'epigenetic memory' of the donor tissue could be reset by differentiation and serial reprogramming, or by treatment of iPSCs with chromatin-modifying drugs. In contrast, the differentiation and methylation of nuclear-transfer-derived pluripotent stem cells were more similar to classical embryonic stem cells than were iPSCs. Our data indicate that nuclear transfer is more effective at establishing the ground state of pluripotency than factor-based reprogramming, which can leave an epigenetic memory of the tissue of origin that may influence efforts at directed differentiation for applications in disease modelling or treatment.

Published
2010

3. Type I collagen-deficient Mov-13 mice do not retain SPARC in the extracellular matrix: implications for fibroblast function.

Author

Iruela-Arispe, ML, Vernon, RB, Wu, H, Jaenisch, R, and Sage, EH

Subjects
Cells, Cultured, Extracellular Matrix, Fibroblasts, Animals, Mice, Collagen, Osteonectin, RNA, Messenger, Female, Male, Cells, Cultured, RNA, Messenger, Genetics, Medical And Health Sciences, Biological Sciences, Developmental Biology, Medical and Health Sciences
Abstract

The Mov-13 strain of mice was created by the insertion of the murine Moloney leukemia virus into the first intron of the alpha 1 (I) collagen gene. Consequently, Mov-13 embryos do not transcribe alpha 1 (I) collagen mRNA and lack type I collagen protein in the extracellular matrix (ECM). Homozygotes die within 12-14 days of embryonic development, in part from the rupture of large blood vessels, and also exhibit deficiencies in hematopoesis and assembly of the ECM (Lohler et al. [1984] Cell 38:597-607). Several matricellular proteins, proteoglycans, and growth factors bind to type I collagen, e.g., fibronectin, secreted protein acidic and rich in cysteine (SPARC), decorin, and transforming growth factor-beta. Here we investigate the expression and function of SPARC in the absence of type I collagen. We show that fibroblasts isolated from Mov-13 homozygous, heterozygous, and wild-type embryos transcribed and translated SPARC mRNA in vitro. However, accumulation of extracellular SPARC was severely affected in the tissues of Mov-13 homozygotes, whereas extracellular deposition of the secreted glycoproteins fibronectin and type III collagen was not altered. Since SPARC has been shown to be a regulator of cell shape, the functional consequences of the absence of extracellular SPARC were evaluated in collagen gel contraction assays. Fibroblasts isolated from homozygous Mov-13 mice did not contract native type I collagen gels as efficiently as fibroblasts from heterozygous littermates; however, addition of exogenous SPARC enhanced the contraction of collagen by homozygous Mov-13 fibroblasts. The stimulatory effect of SPARC was blocked by antibodies specific for the amino terminus of the protein. These results provide evidence that type I collagen is one of the major extracellular proteins that binds SPARC in vivo. Furthermore, the capacity of fibroblasts to contract ECM in vitro is enhanced by extracellular SPARC. We therefore propose that the remodeling of ECM by cells in vivo is regulated in part by a specific interaction between SPARC and type I collagen.

Published
1996

4. Modelling of Radiographic Inspections

Author

Schumm, A., Duvauchelle, P., Kaftandjian, V., Jaenisch, R., Bellon, C., Tabary, J., Mathy, F., Legoupil, S., Büyüköztürk, Oral, Taşdemir, Mehmet Ali, Güneş, Oğuz, editor, and Akkaya, Yılmaz, editor

Published
2013
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15. Modelling of Radiographic Inspections

Author

Schumm, A., primary, Duvauchelle, P., additional, Kaftandjian, V., additional, Jaenisch, R., additional, Bellon, C., additional, Tabary, J., additional, Mathy, F., additional, and Legoupil, S., additional

Published
2011
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26. Expression of Retroviruses During Early Mouse Embryogenesis

Author

Jaenisch, R., Harbers, K., Jähner, D., Stewart, C., Stuhlmann, H., Heimpel, H., editor, Huhn, D., editor, Mueller-Eckhardt, C., editor, Ruhenstroth-Bauer, G., editor, Neth, Rolf, editor, Gallo, Robert C., editor, Greaves, Melvyn F., editor, Moore, Malcolm A. S., editor, and Winkler, Kurt, editor

Published
1983
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28. MeCP2-regulated miRNAs control early human neurogenesis through differential effects on ERK and AKT signaling

Author

Mellios, N, primary, Feldman, D A, additional, Sheridan, S D, additional, Ip, J P K, additional, Kwok, S, additional, Amoah, S K, additional, Rosen, B, additional, Rodriguez, B A, additional, Crawford, B, additional, Swaminathan, R, additional, Chou, S, additional, Li, Y, additional, Ziats, M, additional, Ernst, C, additional, Jaenisch, R, additional, Haggarty, S J, additional, and Sur, M, additional

Published
2017
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29. Failure to replicate the STAP cell phenomenon

Author

De Los Angeles, A, Ferrari, F, Fujiwara, Y, Mathieu, R, Lee, Shirley, Tu, H C, Ross, S, Chou, S, Nguyen, M, Wu, Z T, Theunissen, T W, Powell, B E, Imsoonthornruksa, S, Chen, J K, Borkent, Marti, Krupalnik, V, Lujan, E, Wernig, M, Hanna, J H, Hochedlinger, K, Pei, D Q, Jaenisch, R, Deng, H K, Orkin, SH, Park, P J, Daley, GQ, Medical Microbiology & Infectious Diseases, and Developmental Biology

Published
2015

30. Mitochondrial Proteins Possess Antigenicity and Can Cause Rejection

Author

Deuse, T., primary, Hu, X., additional, Wang, D., additional, Stubbendorff, M., additional, Itagaki, R., additional, Grabosch, A., additional, Graeves, L., additional, Alawi, M., additional, Gruenewald, A., additional, Hua, X., additional, Velden, J., additional, Reichenspurner, H., additional, Robbins, R.C., additional, Jaenisch, R., additional, Weissman, I., additional, and Schrepfer, S., additional

Published
2016
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33. Modelling of Radiographic inspections: State of the art, Challenges, Applications

Author

Schumm, Andreas, Duvauchelle, Philippe, Kaftandjian, Valerie, Jaenisch, R., Bellon, Carsten, Tabary, Joachim, Mathy, Francoise, Legoupil, Samuel, Simulation Neutronique, Technologies de l’Information et Calcul Scientifique (EDF R&D SINETICS), EDF R&D (EDF R&D), EDF (EDF)-EDF (EDF), Controle Non Destructif par Rayonnements Ionisants (CNDRI), Institut National des Sciences Appliquées de Lyon (INSA Lyon), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Université de Lyon-Institut National des Sciences Appliquées (INSA), BAM Bundesanstalt für Materialforschung u. -prüfung, Commissariat à l'énergie atomique et aux énergies alternatives - Laboratoire d'Electronique et de Technologie de l'Information (CEA-LETI), Direction de Recherche Technologique (CEA) (DRT (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Laboratoire d'Intégration des Systèmes et des Technologies (LIST), ANR-07-TLOG-0026,RADIOLA,PROJET RADIOLA – Simulation numérique de la radiographie industrielle pour le contrôle non-destructif(2007), and Laboratoire d'Intégration des Systèmes et des Technologies (LIST (CEA))

Subjects
[SPI]Engineering Sciences [physics]
Abstract

International audience; Computer modelling of non-destructive testing methods has come a long way from the beginnings in the mid 90s to today. In this article we review radiographic modelling from the perspective of two important application domains with very different requirements, nuclear and aerospace. Radiographic modelling for components with higher wall thicknesses, as they are typical for nuclear applications, must include precise predictions of scattered radiation and its impact in terms of contrast reduction. Dedicated or general purpose Monte Carlo methods with the ability to calculate higher order scattering events are the state of the art for these applications. The challenge here is to obtain the simulation results in reasonable computation time, and a number of acceleration schemes have been devised to that end. Aerospace applications, on the other hand, have stronger requirements on the modelling code's capabilities to import complex CAD geometries, and can benefit from faster analytical scatter models, limited to first or second order scattering events. Similar distinctions can be made for the various approaches proposed to accurately model geometrical and film unsharpness, film granularity, film responses, film/foil cartridges and photon noise. With the advent of digital radiography, computer modelling faces new challenges to take physical effects into account which could be neglected with traditional silver films.

Published
2011

36. MeCP2-regulated miRNAs control early human neurogenesis through differential effects on ERK and AKT signaling

Author

Mellios, N, Feldman, D A, Sheridan, S D, Ip, J P K, Kwok, S, Amoah, S K, Rosen, B, Rodriguez, B A, Crawford, B, Swaminathan, R, Chou, S, Li, Y, Ziats, M, Ernst, C, Jaenisch, R, Haggarty, S J, and Sur, M

Abstract

Rett syndrome (RTT) is an X-linked, neurodevelopmental disorder caused primarily by mutations in the methyl-CpG-binding protein 2 (MECP2) gene, which encodes a multifunctional epigenetic regulator with known links to a wide spectrum of neuropsychiatric disorders. Although postnatal functions of MeCP2 have been thoroughly investigated, its role in prenatal brain development remains poorly understood. Given the well-established importance of microRNAs (miRNAs) in neurogenesis, we employed isogenic human RTT patient-derived induced pluripotent stem cell (iPSC) and MeCP2 short hairpin RNA knockdown approaches to identify novel MeCP2-regulated miRNAs enriched during early human neuronal development. Focusing on the most dysregulated miRNAs, we found miR-199 and miR-214 to be increased during early brain development and to differentially regulate extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase and protein kinase B (PKB/AKT) signaling. In parallel, we characterized the effects on human neurogenesis and neuronal differentiation brought about by MeCP2 deficiency using both monolayer and three-dimensional (cerebral organoid) patient-derived and MeCP2-deficient neuronal culture models. Inhibiting miR-199 or miR-214 expression in iPSC-derived neural progenitors deficient in MeCP2 restored AKT and ERK activation, respectively, and ameliorated the observed alterations in neuronal differentiation. Moreover, overexpression of miR-199 or miR-214 in the wild-type mouse embryonic brains was sufficient to disturb neurogenesis and neuronal migration in a similar manner to Mecp2 knockdown. Taken together, our data support a novel miRNA-mediated pathway downstream of MeCP2 that influences neurogenesis via interactions with central molecular hubs linked to autism spectrum disorders.

Published
2018
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41. Targeted mutagenesis of Timp-1 reveals that lung tumor invasion is influenced by Timp-1 genotype of the tumor but not by that of the host

Author

Paul Soloway, Cm, Alexander, Werb Z, and Jaenisch R

Subjects
Mice, Lung Neoplasms, Genotype, Mutagenesis, Site-Directed, Tumor Cells, Cultured, Animals, Neoplasm Invasiveness, Tissue Inhibitor of Metalloproteinases, Glycoproteins
Abstract

Timp-1 has been implicated as a suppressor of tumor metastasis. To study the relative importance of Timp-1 expression by tumor vs host during tumor invasion, three pairs of co-isogenic, tumorigenic cells containing wild-type or mutant Timp-1 alleles were generated. These were used in experimental metastasis assays in wild-type or Timp-1-deficient mice. Timp-1 expression in tumorigenic cells could either increase or decrease tumor invasion of lungs in a tumor cell-specific manner. This suggests that depending on the tumor, Timp-1 can either suppress or potentiate metastasis. Mice deficient for Timp-1 were indistinguishable from wild-type mice in metastasis assays with all tumorigenic cells tested. Although Timp-1 is a secreted protein, and lung produces other Timps, the influence of Timp-1 on lung invasion by the tumorigenic cells tested is cell-autonomous, depending only on Timp-1 genotype of tumor and not that of host.

Published
1996

44. Folate Deficiency Induces Neurodegeneration and Brain Dysfunction in Mice Lacking Uracil DNA Glycosylase

Author

Kronenberg, G., primary, Harms, C., additional, Sobol, R. W., additional, Cardozo-Pelaez, F., additional, Linhart, H., additional, Winter, B., additional, Balkaya, M., additional, Gertz, K., additional, Gay, S. B., additional, Cox, D., additional, Eckart, S., additional, Ahmadi, M., additional, Juckel, G., additional, Kempermann, G., additional, Hellweg, R., additional, Sohr, R., additional, Hortnagl, H., additional, Wilson, S. H., additional, Jaenisch, R., additional, and Endres, M., additional

Published
2008
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48. Phenotypic rescue of mutant brown melanocytes by a retrovirus carrying a wild-type tyrosinase-related protein gene

Author

Dc, Bennett, Huszar D, Pj, Laipis, Jaenisch R, and Ian Jackson

Subjects
Melanins, Membrane Glycoproteins, Genetic Vectors, Proteins, Transfection, Mice, Phenotype, Phorbol Esters, Animals, Melanocytes, Moloney murine leukemia virus, Oxidoreductases, Molecular Biology, Cells, Cultured, Developmental Biology
Abstract

A mouse cDNA for the developmentally controlled, melanocyte-specific protein, tyrosinase-related protein 1 (TRP-1), was previously cloned and reported to show genetic linkage with the coat-colour locus brown (b) on mouse chromosome 4. The cDNA has been inserted into a retroviral vector derived from Moloney murine leukaemia virus, under the control of the human histone H4 promoter. This vector was used to infect melanocytes of the immortal line melan-b, which are homozygous for the b mutation and which display light brown pigmentation in culture. Infected cultures containing between 0.2 and 2 copies of provirus per cell displayed an altered phenotype: 20-50 % of cells now had the black to dark brown colour characteristic of cultured wild-type (Black, B/B) mouse melanocytes. Thus the TRP-1 gene complements the brown mutation. We conclude that TRP-1 is the product of the wild-type-b-locus.

Published
1990

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