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Article ; Online: A novel long non-coding RNA, Leat1, causes reduced anogenital distance and fertility in female mice.

Mattiske, Deidre / Behringer, Richard R / Overbeek, Paul A / Pask, Andrew J

Differentiation; research in biological diversity

2019 Volume 112, Page(s) 1–6

Abstract: Defective anorectal and urogenital malformations are some of the most severe congenital anomalies encountered in children. Only a few molecular cues have been identified in early formation of the female urogenital system. Here we describe a novel long ... ...

Abstract	Defective anorectal and urogenital malformations are some of the most severe congenital anomalies encountered in children. Only a few molecular cues have been identified in early formation of the female urogenital system. Here we describe a novel long non-coding RNA molecule known as Leat1 (long non-coding RNA, EphrinB2 associated transcript 1). This lncRNA is syntenic with EfnB2 (which encodes EphrinB2) and expressed during embryonic development of the genital tubercle. While lncRNAs have varied functions, many are known to regulate their neighbouring genes. Eph/Ephrin bidirectional signaling molecules mediate many patterning pathways in early embryonic development, including cloacal septation and urethral development. Here we investigate the role of Leat1 and its possible regulation of EphrinB2 during development of the female reproductive tract. We show that a loss of Leat1 leads to reduced EfnB2 expression in the developing female genital tubercle, reduced anogenital distance and decreased fertility.
Language	English
Publishing date	2019-12-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	184540-8
ISSN	1432-0436 ; 0301-4681
ISSN (online)	1432-0436
ISSN	0301-4681
DOI	10.1016/j.diff.2019.10.007
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Article: A long non-coding RNA

Mattiske, Deidre / Bernard, Pascal / Gradie, Paul E / Behringer, Richard R / Overbeek, Paul A / O'Neill, Rachel J / Phillips, Tiffany / Tarulli, Gerard / Pask, Andrew J

Research square

2023

Abstract: The novel long non-coding RNA (lncRNA) ...

Abstract	The novel long non-coding RNA (lncRNA)
Language	English
Publishing date	2023-07-03
Publishing country	United States
Document type	Preprint
DOI	10.21203/rs.3.rs-3098271/v1
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Article ; Online: Primary Ovarian Insufficiency Induced by Fanconi Anemia E Mutation in a Mouse Model.

Fu, Chun / Begum, Khurshida / Overbeek, Paul A

PloS one

2016 Volume 11, Issue 3, Page(s) e0144285

Abstract: In most cases of primary ovarian insufficiency (POI), the cause of the depletion of ovarian follicles is unknown. Fanconi anemia (FA) proteins are known to play important roles in follicular development. Using random insertional mutagenesis with a ... ...

Abstract	In most cases of primary ovarian insufficiency (POI), the cause of the depletion of ovarian follicles is unknown. Fanconi anemia (FA) proteins are known to play important roles in follicular development. Using random insertional mutagenesis with a lentiviral transgene, we identified a family with reduced fertility in the homozygous transgenic mice. We identified the integration site and found that the lentivirus had integrated into intron 8 of the Fanconi E gene (Fance). By RT-PCR and in situ hybridization, we found that Fance transcript levels were significantly reduced. The Fance homozygous mutant mice were assayed for changes in ovarian development, follicle numbers and estrous cycle. Ovarian dysplasias and a severe lack of follicles were seen in the mutant mice. In addition, the estrous cycle was disrupted in adult females. Our results suggest that POI has been induced by the Fance mutation in this new mouse model.
MeSH term(s)	Animals ; Disease Models, Animal ; Estrous Cycle/genetics ; Fanconi Anemia/complications ; Fanconi Anemia/genetics ; Fanconi Anemia/metabolism ; Fanconi Anemia/pathology ; Fanconi Anemia Complementation Group E Protein/deficiency ; Fanconi Anemia Complementation Group E Protein/genetics ; Female ; Genetic Vectors ; Homozygote ; Humans ; In Situ Hybridization ; Introns ; Lentivirus/genetics ; Mice ; Mutagenesis, Insertional ; Mutation ; Ovarian Follicle/metabolism ; Ovarian Follicle/pathology ; Primary Ovarian Insufficiency/complications ; Primary Ovarian Insufficiency/genetics ; Primary Ovarian Insufficiency/metabolism ; Primary Ovarian Insufficiency/pathology ; Reverse Transcriptase Polymerase Chain Reaction ; Transcription, Genetic ; Transgenes
Chemical Substances	Fanconi Anemia Complementation Group E Protein
Language	English
Publishing date	2016-03-03
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0144285
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Article ; Online: PGC1α is required for the renoprotective effect of lncRNA Tug1 in vivo and links Tug1 with urea cycle metabolites.

Li, Li / Long, Jianyin / Mise, Koki / Galvan, Daniel L / Overbeek, Paul A / Tan, Lin / Kumar, Shwetha V / Chan, Wai Kin / Lorenzi, Phillip L / Chang, Benny H / Danesh, Farhad R

Cell reports

2021 Volume 36, Issue 6, Page(s) 109510

Abstract: lncRNA taurine-upregulated gene 1 (Tug1) is a promising therapeutic target in the progression of diabetic nephropathy (DN), but the molecular basis of its protection remains poorly understood. Here, we generate a triple-mutant diabetic mouse model ... ...

Abstract	lncRNA taurine-upregulated gene 1 (Tug1) is a promising therapeutic target in the progression of diabetic nephropathy (DN), but the molecular basis of its protection remains poorly understood. Here, we generate a triple-mutant diabetic mouse model coupled with metabolomic profiling data to interrogate whether Tug1 interaction with peroxisome proliferator-activated receptor gamma coactivator 1α (PGC1α) is required for mitochondrial remodeling and progression of DN in vivo. We find that, compared with diabetic conditional deletion of Pgc1α in podocytes alone (db/db; Pgc1α
MeSH term(s)	Animals ; Arginase/metabolism ; Diabetic Nephropathies/genetics ; Diabetic Nephropathies/pathology ; Disease Progression ; Gene Deletion ; Kidney/metabolism ; Metabolome ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondria/metabolism ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/deficiency ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism ; Podocytes/metabolism ; Protective Agents/metabolism ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; Urea/metabolism ; Mice
Chemical Substances	Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Protective Agents ; RNA, Long Noncoding ; long non-coding RNA TUG1, mouse ; Urea (8W8T17847W) ; Arginase (EC 3.5.3.1)
Language	English
Publishing date	2021-08-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2021.109510
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Article ; Online: FGF9 can induce endochondral ossification in cranial mesenchyme

Overbeek Paul A / Govindarajan Venkatesh

BMC Developmental Biology, Vol 6, Iss 1, p

2006 Volume 7

Abstract: Abstract Background The flat bones of the skull (i.e., the frontal and parietal bones) normally form through intramembranous ossification. At these sites cranial mesenchymal cells directly differentiate into osteoblasts without the formation of a ... ...

Abstract	Abstract Background The flat bones of the skull (i.e., the frontal and parietal bones) normally form through intramembranous ossification. At these sites cranial mesenchymal cells directly differentiate into osteoblasts without the formation of a cartilage intermediate. This type of ossification is distinct from endochondral ossification, a process that involves initial formation of cartilage and later replacement by bone. Results We have analyzed a line of transgenic mice that expresses FGF9, a member of the fibroblast growth factor family (FGF), in cranial mesenchymal cells. The parietal bones in these mice show a switch from intramembranous to endochondral ossification. Cranial cartilage precursors are induced to proliferate, then hypertrophy and are later replaced by bone. These changes are accompanied by upregulation of Sox9 , Ihh , Col2a1 , Col10a1 and downregulation of CbfaI and Osteocalcin . Fate mapping studies show that the cranial mesenchymal cells in the parietal region that show a switch in cell fate are likely to be derived from the mesoderm. Conclusion These results demonstrate that FGF9 expression is sufficient to convert the differentiation program of (at least a subset of) mesoderm-derived cranial mesenchyme cells from intramembranous to endochondral ossification.
Keywords	Biology (General) ; QH301-705.5
Subject code	616
Language	English
Publishing date	2006-02-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Dearth and Delayed Maturation of Testicular Germ Cells in Fanconi Anemia E Mutant Male Mice.

Fu, Chun / Begum, Khurshida / Jordan, Philip W / He, Yan / Overbeek, Paul A

PloS one

2016 Volume 11, Issue 8, Page(s) e0159800

Abstract: After using a self-inactivating lentivirus for non-targeted insertional mutagenesis in mice, we identified a transgenic family with a recessive mutation that resulted in reduced fertility in homozygous transgenic mice. The lentiviral integration site was ...

Abstract	After using a self-inactivating lentivirus for non-targeted insertional mutagenesis in mice, we identified a transgenic family with a recessive mutation that resulted in reduced fertility in homozygous transgenic mice. The lentiviral integration site was amplified by inverse PCR. Sequencing revealed that integration had occurred in intron 8 of the mouse Fance gene, which encodes the Fanconi anemia E (Fance) protein. Fanconi anemia (FA) proteins play pivotal roles in cellular responses to DNA damage and Fance acts as a molecular bridge between the FA core complex and Fancd2. To investigate the reduced fertility in the mutant males, we analyzed postnatal development of testicular germ cells. At one week after birth, most tubules in the mutant testes contained few or no germ cells. Over the next 2-3 weeks, germ cells accumulated in a limited number of tubules, so that some tubules contained germ cells around the full periphery of the tubule. Once sufficient numbers of germ cells had accumulated, they began to undergo the later stages of spermatogenesis. Immunoassays revealed that the Fancd2 protein accumulated around the periphery of the nucleus in normal developing spermatocytes, but we did not detect a similar localization of Fancd2 in the Fance mutant testes. Our assays indicate that although Fance mutant males are germ cell deficient at birth, the extant germ cells can proliferate and, if they reach a threshold density, can differentiate into mature sperm. Analogous to previous studies of FA genes in mice, our results show that the Fance protein plays an important, but not absolutely essential, role in the initial developmental expansion of the male germ line.
MeSH term(s)	Animals ; Animals, Newborn ; Cell Differentiation ; Cell Proliferation ; Fanconi Anemia Complementation Group D2 Protein/metabolism ; Fanconi Anemia Complementation Group E Protein/genetics ; Infertility, Male/genetics ; Infertility, Male/metabolism ; Introns ; Male ; Mice ; Mice, Transgenic ; Mutagenesis, Insertional ; Seminiferous Tubules/ultrastructure ; Sperm Maturation ; Spermatogenesis ; Spermatozoa/cytology ; Spermatozoa/metabolism ; Spermatozoa/physiology
Chemical Substances	Fancd2 protein, mouse ; Fance protein, mouse ; Fanconi Anemia Complementation Group D2 Protein ; Fanconi Anemia Complementation Group E Protein
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0159800
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Article ; Online: Activation of unfolded protein response in transgenic mouse lenses.

Reneker, Lixing W / Chen, Huiyi / Overbeek, Paul A

Investigative ophthalmology & visual science

2011 Volume 52, Issue 5, Page(s) 2100–2108

Abstract: Purpose: Overloading of unfolded or misfolded proteins in the endoplasmic reticulum (ER) can cause ER stress and activate the unfolded protein response (UPR) in the cell. The authors tested whether transgene overexpression in the mouse lens would ... ...

Abstract	Purpose: Overloading of unfolded or misfolded proteins in the endoplasmic reticulum (ER) can cause ER stress and activate the unfolded protein response (UPR) in the cell. The authors tested whether transgene overexpression in the mouse lens would activate the UPR. Methods: Transgenic mice expressing proteins that either enter the ER secretory pathway or are synthesized in cytosol were selected. Activation of the UPR was assessed by determining the expression levels of the ER chaperone protein BiP, the spliced form of X-box binding protein-1 (Xbp-1) mRNA, and the transcription factor CHOP. Changes in the ubiquitin-proteasome system in the mouse lens were detected by ubiquitin immunofluorescence. Results: BiP expression was upregulated in the fiber cells of transgenic mouse lenses expressing platelet-derived growth factor-A (PDGF-A), dominant-negative fibroblast growth factor receptor (DN-FGFR), or DN-Sprouty2 (DN-Spy2). BiP upregulation occurred around embryonic day 16.5, primarily in the fiber cells adjacent to the organelle free zone. Fiber cell differentiation was disrupted in the PDGF-A and DN-Spry2 lenses, whereas the fiber cells were degenerating in the DN-FGFR lens. High levels of UPR activation and ubiquitin-labeled protein aggregates were found in the DN-FGFR lens, indicating inefficient disposal of unfolded/misfolded proteins in the fiber cells. Conclusions: This study implies that overexpression of some transgenes in the lens can induce ER or overall cell stress in fiber cells, resulting in the activation of UPR signaling pathways. Therefore, investigators should assess the levels of UPR activation when they analyze the downstream effects of transgene expression in the lens.
MeSH term(s)	Adaptor Proteins, Signal Transducing ; Animals ; Animals, Newborn ; Cell Differentiation ; DNA-Binding Proteins/genetics ; Endoplasmic Reticulum/metabolism ; Fluorescent Antibody Technique, Indirect ; Gene Expression Regulation/physiology ; Heat-Shock Proteins/genetics ; In Situ Nick-End Labeling ; Intracellular Signaling Peptides and Proteins ; Lens, Crystalline/metabolism ; Membrane Proteins ; Mice ; Mice, Transgenic ; Protein-Serine-Threonine Kinases ; RNA, Messenger/metabolism ; Regulatory Factor X Transcription Factors ; Reverse Transcriptase Polymerase Chain Reaction ; Transcription Factor CHOP/genetics ; Transcription Factors/genetics ; Ubiquitin-Protein Ligases ; Unfolded Protein Response/physiology ; Up-Regulation ; X-Box Binding Protein 1
Chemical Substances	Adaptor Proteins, Signal Transducing ; DNA-Binding Proteins ; Ddit3 protein, mouse ; Heat-Shock Proteins ; Intracellular Signaling Peptides and Proteins ; Membrane Proteins ; RNA, Messenger ; Regulatory Factor X Transcription Factors ; Transcription Factors ; X-Box Binding Protein 1 ; Xbp1 protein, mouse ; Transcription Factor CHOP (147336-12-7) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Spry2 protein, mouse (EC 2.7.11.1) ; molecular chaperone GRP78 (YCYIS6GADR)
Language	English
Publishing date	2011-04-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	391794-0
ISSN	1552-5783 ; 0146-0404
ISSN (online)	1552-5783
ISSN	0146-0404
DOI	10.1167/iovs.10-5650
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Article ; Online: Role for carbohydrate response element-binding protein (ChREBP) in high glucose-mediated repression of long noncoding RNA Tug1.

Long, Jianyin / Galvan, Daniel L / Mise, Koki / Kanwar, Yashpal S / Li, Li / Poungavrin, Naravat / Overbeek, Paul A / Chang, Benny H / Danesh, Farhad R

The Journal of biological chemistry

2020 Volume 295, Issue 47, Page(s) 15840–15852

Abstract: Long noncoding RNAs (lncRNAs) have been shown to play key roles in a variety of biological activities of the cell. However, less is known about how lncRNAs respond to environmental cues and what transcriptional mechanisms regulate their expression. ... ...

Abstract	Long noncoding RNAs (lncRNAs) have been shown to play key roles in a variety of biological activities of the cell. However, less is known about how lncRNAs respond to environmental cues and what transcriptional mechanisms regulate their expression. Studies from our laboratory have shown that the lncRNA Tug1 (taurine upregulated gene 1) is crucial for the progression of diabetic kidney disease, a major microvascular complication of diabetes. Using a combination of proximity labeling with the engineered soybean ascorbate peroxidase (APEX2), ChIP-qPCR, biotin-labeled oligonucleotide pulldown, and classical promoter luciferase assays in kidney podocytes, we extend our initial observations in the current study and now provide a detailed analysis on a how high-glucose milieu downregulates Tug1 expression in podocytes. Our results revealed an essential role for the transcription factor carbohydrate response element binding protein (ChREBP) in controlling Tug1 transcription in the podocytes in response to increased glucose levels. Along with ChREBP, other coregulators, including MAX dimerization protein (MLX), MAX dimerization protein 1 (MXD1), and histone deacetylase 1 (HDAC1), were enriched at the
MeSH term(s)	Animals ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/genetics ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/metabolism ; Cell Line, Tumor ; Gene Expression Regulation ; Glucose/genetics ; Glucose/metabolism ; Histone Deacetylase 1/genetics ; Histone Deacetylase 1/metabolism ; Humans ; Mice ; Podocytes/metabolism ; RNA, Long Noncoding/biosynthesis ; RNA, Long Noncoding/genetics ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Transcription, Genetic
Chemical Substances	Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; Mad protein, mouse ; Mlxipl protein, mouse ; RNA, Long Noncoding ; Repressor Proteins ; long non-coding RNA TUG1, mouse ; Hdac1 protein, mouse (EC 3.5.1.98) ; Histone Deacetylase 1 (EC 3.5.1.98) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2020-05-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.RA120.013228
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Article ; Online: FGF9 can induce endochondral ossification in cranial mesenchyme.

Govindarajan, Venkatesh / Overbeek, Paul A

BMC developmental biology

2006 Volume 6, Page(s) 7

Abstract: Background: The flat bones of the skull (i.e., the frontal and parietal bones) normally form through intramembranous ossification. At these sites cranial mesenchymal cells directly differentiate into osteoblasts without the formation of a cartilage ... ...

Abstract	Background: The flat bones of the skull (i.e., the frontal and parietal bones) normally form through intramembranous ossification. At these sites cranial mesenchymal cells directly differentiate into osteoblasts without the formation of a cartilage intermediate. This type of ossification is distinct from endochondral ossification, a process that involves initial formation of cartilage and later replacement by bone. Results: We have analyzed a line of transgenic mice that expresses FGF9, a member of the fibroblast growth factor family (FGF), in cranial mesenchymal cells. The parietal bones in these mice show a switch from intramembranous to endochondral ossification. Cranial cartilage precursors are induced to proliferate, then hypertrophy and are later replaced by bone. These changes are accompanied by upregulation of Sox9, Ihh, Col2a1, Col10a1 and downregulation of CbfaI and Osteocalcin. Fate mapping studies show that the cranial mesenchymal cells in the parietal region that show a switch in cell fate are likely to be derived from the mesoderm. Conclusion: These results demonstrate that FGF9 expression is sufficient to convert the differentiation program of (at least a subset of) mesoderm-derived cranial mesenchyme cells from intramembranous to endochondral ossification.
MeSH term(s)	Animals ; Biomarkers/metabolism ; Cell Differentiation ; Cell Proliferation ; Chondrocytes/cytology ; Chondrocytes/metabolism ; Fibroblast Growth Factor 9/genetics ; Fibroblast Growth Factor 9/metabolism ; Mesoderm/cytology ; Mice ; Mice, Transgenic ; Osteogenesis ; Parietal Bone/cytology ; Parietal Bone/embryology ; Receptor, Fibroblast Growth Factor, Type 2/metabolism ; Receptor, Fibroblast Growth Factor, Type 3/metabolism ; Skull/abnormalities ; Skull/embryology ; Skull/growth & development
Chemical Substances	Biomarkers ; Fgf9 protein, mouse ; Fibroblast Growth Factor 9 ; Fgfr3 protein, mouse (EC 2.7.10.1) ; Receptor, Fibroblast Growth Factor, Type 2 (EC 2.7.10.1) ; Receptor, Fibroblast Growth Factor, Type 3 (EC 2.7.10.1)
Language	English
Publishing date	2006-02-20
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1471-213X
ISSN (online)	1471-213X
DOI	10.1186/1471-213X-6-7
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Article ; Online: Live four-dimensional optical coherence tomography reveals embryonic cardiac phenotype in mouse mutant.

Lopez, Andrew L / Wang, Shang / Larin, Kirill V / Overbeek, Paul A / Larina, Irina V

Journal of biomedical optics

2015 Volume 20, Issue 9, Page(s) 90501

Abstract: Efficient phenotyping of developmental defects in model organisms is critical for understanding the genetic specification of normal development and congenital abnormalities in humans. We previously reported that optical coherence tomography (OCT) ... ...

Abstract	Efficient phenotyping of developmental defects in model organisms is critical for understanding the genetic specification of normal development and congenital abnormalities in humans. We previously reported that optical coherence tomography (OCT) combined with live embryo culture is a valuable tool for mouse embryo imaging and four-dimensional (4-D) cardiodynamic analysis; however, its capability for analysis of mouse mutants with cardiac phenotypes has not been previously explored. Here, we report 4-D (three-dimensional+time) OCT imaging and analysis of the embryonic heart in a Wdr19 mouse mutant, revealing a heart looping defect. Quantitative analysis of cardiac looping revealed a statistically significant difference between mutant and control embryos. Our results indicate that live 4-D OCT imaging provides a powerful phenotyping approach to characterize embryonic cardiac function in mouse models.
MeSH term(s)	Animals ; Cardiac-Gated Imaging Techniques/methods ; Embryo, Mammalian/pathology ; Fetal Diseases ; Heart Defects, Congenital/embryology ; Heart Defects, Congenital/pathology ; Image Interpretation, Computer-Assisted/methods ; Imaging, Three-Dimensional/methods ; Mice ; Mice, Mutant Strains ; Prenatal Diagnosis/methods ; Reproducibility of Results ; Sensitivity and Specificity ; Subtraction Technique
Language	English
Publishing date	2015-09-18
Publishing country	United States
Document type	Letter ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1309154-2
ISSN	1560-2281 ; 1083-3668
ISSN (online)	1560-2281
ISSN	1083-3668
DOI	10.1117/1.JBO.20.9.090501
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