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Article ; Online: Transposable elements as genetic regulatory substrates in early development.

Gifford, Wesley D / Pfaff, Samuel L / Macfarlan, Todd S

2013 Volume 23, Issue 5, Page(s) 218–226

Abstract: The abundance and ancient origins of transposable elements (TEs) in eukaryotic genomes has spawned research into the potential symbiotic relationship between these elements and their hosts. In this review, we introduce the diversity of TEs, discuss how ... ...

Abstract	The abundance and ancient origins of transposable elements (TEs) in eukaryotic genomes has spawned research into the potential symbiotic relationship between these elements and their hosts. In this review, we introduce the diversity of TEs, discuss how distinct classes are uniquely regulated in development, and describe how they appear to have been coopted for the purposes of gene regulation and the orchestration of a number of processes during early embryonic development. Although young, active TEs play an important role in somatic tissues and evolution, we focus mostly on the contributions of the older, fixed elements in mammalian genomes. We also discuss major challenges inherent in the study of TEs and contemplate future experimental approaches to further investigate how they coordinate developmental processes.
MeSH term(s)	Animals ; DNA Transposable Elements ; Embryonic Development/physiology ; Endogenous Retroviruses/genetics ; Endogenous Retroviruses/physiology ; Epigenesis, Genetic/physiology ; Female ; Gene Expression Regulation, Developmental ; Genes, Viral/physiology ; Humans ; Long Interspersed Nucleotide Elements/physiology ; Mammals/genetics ; Mice ; Placenta/physiology ; Pregnancy ; Retroelements/physiology
Chemical Substances	DNA Transposable Elements ; Retroelements
Language	English
Publishing date	2013-02-12
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	30122-x
ISSN	1879-3088 ; 0962-8924
ISSN (online)	1879-3088
ISSN	0962-8924
DOI	10.1016/j.tcb.2013.01.001
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Article: Transposable elements as genetic regulatory substrates in early development

Gifford, Wesley D / Pfaff, Samuel L / Macfarlan, Todd S

Trends in cell biology. 2013 May, v. 23, no. 5

2013

Abstract	The abundance and ancient origins of transposable elements (TEs) in eukaryotic genomes has spawned research into the potential symbiotic relationship between these elements and their hosts. In this review, we introduce the diversity of TEs, discuss how distinct classes are uniquely regulated in development, and describe how they appear to have been coopted for the purposes of gene regulation and the orchestration of a number of processes during early embryonic development. Although young, active TEs play an important role in somatic tissues and evolution, we focus mostly on the contributions of the older, fixed elements in mammalian genomes. We also discuss major challenges inherent in the study of TEs and contemplate future experimental approaches to further investigate how they coordinate developmental processes.
Keywords	early development ; embryogenesis ; genes ; hosts ; mammals ; somatic cells ; symbiosis ; transposons
Language	English
Dates of publication	2013-05
Size	p. 218-226.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	30122-x
ISSN	1879-3088 ; 0962-8924
ISSN (online)	1879-3088
ISSN	0962-8924
DOI	10.1016/j.tcb.2013.01.001
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Article ; Online: A scalable solution for isolating human multipotent clinical-grade neural stem cells from ES precursors.

Bohaciakova, Dasa / Hruska-Plochan, Marian / Tsunemoto, Rachel / Gifford, Wesley D / Driscoll, Shawn P / Glenn, Thomas D / Wu, Stephanie / Marsala, Silvia / Navarro, Michael / Tadokoro, Takahiro / Juhas, Stefan / Juhasova, Jana / Platoshyn, Oleksandr / Piper, David / Sheckler, Vickie / Ditsworth, Dara / Pfaff, Samuel L / Marsala, Martin

Stem cell research & therapy

2019 Volume 10, Issue 1, Page(s) 83

Abstract: Background: A well-characterized method has not yet been established to reproducibly, efficiently, and safely isolate large numbers of clinical-grade multipotent human neural stem cells (hNSCs) from embryonic stem cells (hESCs). Consequently, the ... ...

Abstract	Background: A well-characterized method has not yet been established to reproducibly, efficiently, and safely isolate large numbers of clinical-grade multipotent human neural stem cells (hNSCs) from embryonic stem cells (hESCs). Consequently, the transplantation of neurogenic/gliogenic precursors into the CNS for the purpose of cell replacement or neuroprotection in humans with injury or disease has not achieved widespread testing and implementation. Methods: Here, we establish an approach for the in vitro isolation of a highly expandable population of hNSCs using the manual selection of neural precursors based on their colony morphology (CoMo-NSC). The purity and NSC properties of established and extensively expanded CoMo-NSC were validated by expression of NSC markers (flow cytometry, mRNA sequencing), lack of pluripotent markers and by their tumorigenic/differentiation profile after in vivo spinal grafting in three different animal models, including (i) immunodeficient rats, (ii) immunosuppressed ALS rats (SOD1 Results: In vitro analysis of established CoMo-NSCs showed a consistent expression of NSC markers (Sox1, Sox2, Nestin, CD24) with lack of pluripotent markers (Nanog) and stable karyotype for more than 15 passages. Gene profiling and histology revealed that spinally grafted CoMo-NSCs differentiate into neurons, astrocytes, and oligodendrocytes over a 2-6-month period in vivo without forming neoplastic derivatives or abnormal structures. Moreover, transplanted CoMo-NSCs formed neurons with synaptic contacts and glia in a variety of host environments including immunodeficient rats, immunosuppressed ALS rats (SOD1G93A), or spinally injured minipigs, indicating these cells have favorable safety and differentiation characteristics. Conclusions: These data demonstrate that manually selected CoMo-NSCs represent a safe and expandable NSC population which can effectively be used in prospective human clinical cell replacement trials for the treatment of a variety of neurodegenerative disorders, including ALS, stroke, spinal traumatic, or spinal ischemic injury.
MeSH term(s)	Cell Line ; Flow Cytometry ; Humans ; Multipotent Stem Cells/cytology ; Neural Stem Cells/cytology
Language	English
Publishing date	2019-03-12
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2548671-8
ISSN	1757-6512 ; 1757-6512
ISSN (online)	1757-6512
ISSN	1757-6512
DOI	10.1186/s13287-019-1163-7
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Article ; Online: Speed and segmentation control mechanisms characterized in rhythmically-active circuits created from spinal neurons produced from genetically-tagged embryonic stem cells.

Sternfeld, Matthew J / Hinckley, Christopher A / Moore, Niall J / Pankratz, Matthew T / Hilde, Kathryn L / Driscoll, Shawn P / Hayashi, Marito / Amin, Neal D / Bonanomi, Dario / Gifford, Wesley D / Sharma, Kamal / Goulding, Martyn / Pfaff, Samuel L

eLife

2017 Volume 6

Abstract: Flexible neural networks, such as the interconnected spinal neurons that control distinct motor actions, can switch their activity to produce different behaviors. Both excitatory (E) and inhibitory (I) spinal neurons are necessary for motor behavior, but ...

Abstract	Flexible neural networks, such as the interconnected spinal neurons that control distinct motor actions, can switch their activity to produce different behaviors. Both excitatory (E) and inhibitory (I) spinal neurons are necessary for motor behavior, but the influence of recruiting different ratios of E-to-I cells remains unclear. We constructed synthetic microphysical neural networks, called circuitoids, using precise combinations of spinal neuron subtypes derived from mouse stem cells. Circuitoids of purified excitatory interneurons were sufficient to generate oscillatory bursts with properties similar to in vivo central pattern generators. Inhibitory V1 neurons provided dual layers of regulation within excitatory rhythmogenic networks - they increased the rhythmic burst frequency of excitatory V3 neurons, and segmented excitatory motor neuron activity into sub-networks. Accordingly, the speed and pattern of spinal circuits that underlie complex motor behaviors may be regulated by quantitatively gating the intra-network cellular activity ratio of E-to-I neurons.
MeSH term(s)	Animals ; Cells, Cultured ; Embryonic Stem Cells/physiology ; Interneurons/physiology ; Mice ; Motor Activity ; Motor Neurons/physiology ; Nerve Net/physiology ; Spinal Cord/physiology
Language	English
Publishing date	2017--14
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.21540
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Article ; Online: Loss of motoneuron-specific microRNA-218 causes systemic neuromuscular failure.

Amin, Neal D / Bai, Ge / Klug, Jason R / Bonanomi, Dario / Pankratz, Matthew T / Gifford, Wesley D / Hinckley, Christopher A / Sternfeld, Matthew J / Driscoll, Shawn P / Dominguez, Bertha / Lee, Kuo-Fen / Jin, Xin / Pfaff, Samuel L

Science (New York, N.Y.)

2015 Volume 350, Issue 6267, Page(s) 1525–1529

Abstract: Dysfunction of microRNA (miRNA) metabolism is thought to underlie diseases affecting motoneurons. One miRNA, miR-218, is abundantly and selectively expressed by developing and mature motoneurons. Here we show that mutant mice lacking miR-218 die ... ...

Abstract	Dysfunction of microRNA (miRNA) metabolism is thought to underlie diseases affecting motoneurons. One miRNA, miR-218, is abundantly and selectively expressed by developing and mature motoneurons. Here we show that mutant mice lacking miR-218 die neonatally and exhibit neuromuscular junction defects, motoneuron hyperexcitability, and progressive motoneuron cell loss, all of which are hallmarks of motoneuron diseases such as amyotrophic lateral sclerosis and spinal muscular atrophy. Gene profiling reveals that miR-218 modestly represses a cohort of hundreds of genes that are neuronally enriched but are not specific to a single neuron subpopulation. Thus, the set of messenger RNAs targeted by miR-218, designated TARGET(218), defines a neuronal gene network that is selectively tuned down in motoneurons to prevent neuromuscular failure and neurodegeneration.
MeSH term(s)	Animals ; Gene Expression Regulation ; Gene Regulatory Networks ; Mice ; Mice, Knockout ; MicroRNAs/genetics ; MicroRNAs/physiology ; Motor Neuron Disease/genetics ; Motor Neuron Disease/physiopathology ; Motor Neurons/metabolism ; Motor Neurons/pathology ; Motor Neurons/physiology ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/pathology ; Spinal Cord/metabolism ; Spinal Cord/physiopathology
Chemical Substances	MIRN218 microRNA, mouse ; MicroRNAs
Language	English
Publishing date	2015-10-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	128410-1
ISSN	1095-9203 ; 0036-8075
ISSN (online)	1095-9203
ISSN	0036-8075
DOI	10.1126/science.aad2509
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Article ; Online: Local compartment changes and regulatory landscape alterations in histone H1-depleted cells.

Geeven, Geert / Zhu, Yun / Kim, Byung Ju / Bartholdy, Boris A / Yang, Seung-Min / Macfarlan, Todd S / Gifford, Wesley D / Pfaff, Samuel L / Verstegen, Marjon J A M / Pinto, Hugo / Vermunt, Marit W / Creyghton, Menno P / Wijchers, Patrick J / Stamatoyannopoulos, John A / Skoultchi, Arthur I / de Laat, Wouter

Genome biology

2015 Volume 16, Page(s) 289

Abstract: Background: Linker histone H1 is a core chromatin component that binds to nucleosome core particles and the linker DNA between nucleosomes. It has been implicated in chromatin compaction and gene regulation and is anticipated to play a role in higher- ... ...

Abstract	Background: Linker histone H1 is a core chromatin component that binds to nucleosome core particles and the linker DNA between nucleosomes. It has been implicated in chromatin compaction and gene regulation and is anticipated to play a role in higher-order genome structure. Here we have used a combination of genome-wide approaches including DNA methylation, histone modification and DNase I hypersensitivity profiling as well as Hi-C to investigate the impact of reduced cellular levels of histone H1 in embryonic stem cells on chromatin folding and function. Results: We find that depletion of histone H1 changes the epigenetic signature of thousands of potential regulatory sites across the genome. Many of them show cooperative loss or gain of multiple chromatin marks. Epigenetic alterations cluster to gene-dense topologically associating domains (TADs) that already showed a high density of corresponding chromatin features. Genome organization at the three-dimensional level is largely intact, but we find changes in the structural segmentation of chromosomes specifically for the epigenetically most modified TADs. Conclusions: Our data show that cells require normal histone H1 levels to expose their proper regulatory landscape. Reducing the levels of histone H1 results in massive epigenetic changes and altered topological organization particularly at the most active chromosomal domains. Changes in TAD configuration coincide with epigenetic landscape changes but not with transcriptional output changes, supporting the emerging concept that transcriptional control and nuclear positioning of TADs are not causally related but independently controlled by the locally associated trans-acting factors.
MeSH term(s)	Animals ; Cell Line ; Chromatin/genetics ; Chromatin/metabolism ; Chromatin Assembly and Disassembly ; Epigenesis, Genetic ; Histones/genetics ; Histones/metabolism ; Mice
Chemical Substances	Chromatin ; Histones
Language	English
Publishing date	2015-12-23
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2040529-7
ISSN	1474-760X ; 1465-6914 ; 1465-6906
ISSN (online)	1474-760X ; 1465-6914
ISSN	1465-6906
DOI	10.1186/s13059-015-0857-0
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Article ; Online: Embryonic stem cell potency fluctuates with endogenous retrovirus activity.

Macfarlan, Todd S / Gifford, Wesley D / Driscoll, Shawn / Lettieri, Karen / Rowe, Helen M / Bonanomi, Dario / Firth, Amy / Singer, Oded / Trono, Didier / Pfaff, Samuel L

Nature

2012 Volume 487, Issue 7405, Page(s) 57–63

Abstract: Embryonic stem (ES) cells are derived from blastocyst-stage embryos and are thought to be functionally equivalent to the inner cell mass, which lacks the ability to produce all extraembryonic tissues. Here we identify a rare transient cell population ... ...

Abstract	Embryonic stem (ES) cells are derived from blastocyst-stage embryos and are thought to be functionally equivalent to the inner cell mass, which lacks the ability to produce all extraembryonic tissues. Here we identify a rare transient cell population within mouse ES and induced pluripotent stem (iPS) cell cultures that expresses high levels of transcripts found in two-cell (2C) embryos in which the blastomeres are totipotent. We genetically tagged these 2C-like ES cells and show that they lack the inner cell mass pluripotency proteins Oct4 (also known as Pou5f1), Sox2 and Nanog, and have acquired the ability to contribute to both embryonic and extraembryonic tissues. We show that nearly all ES cells cycle in and out of this privileged state, which is partially controlled by histone-modifying enzymes. Transcriptome sequencing and bioinformatic analyses showed that many 2C transcripts are initiated from long terminal repeats derived from endogenous retroviruses, suggesting this foreign sequence has helped to drive cell-fate regulation in placental mammals.
MeSH term(s)	Animals ; Cell Dedifferentiation/genetics ; Cell Dedifferentiation/physiology ; Cell Lineage/genetics ; Chimera/embryology ; Chromatin/genetics ; Chromatin/metabolism ; Embryo, Mammalian/cytology ; Embryo, Mammalian/metabolism ; Embryo, Mammalian/virology ; Embryonic Stem Cells/cytology ; Embryonic Stem Cells/metabolism ; Embryonic Stem Cells/virology ; Endogenous Retroviruses/genetics ; Epigenesis, Genetic ; Female ; Gene Expression Regulation, Developmental ; Genes, Reporter/genetics ; Histones/chemistry ; Histones/metabolism ; Induced Pluripotent Stem Cells/cytology ; Induced Pluripotent Stem Cells/metabolism ; Lysine/chemistry ; Lysine/metabolism ; Methylation ; Mice ; Phenotype ; Pluripotent Stem Cells/cytology ; Pluripotent Stem Cells/metabolism ; Pluripotent Stem Cells/virology ; Terminal Repeat Sequences/genetics ; Totipotent Stem Cells/cytology ; Totipotent Stem Cells/metabolism ; Totipotent Stem Cells/virology ; Transcriptome/genetics
Chemical Substances	Chromatin ; Histones ; Lysine (K3Z4F929H6)
Language	English
Publishing date	2012-06-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/nature11244
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Article: Local compartment changes and regulatory landscape alterations in histone H1-depleted cells

Geeven, Geert / Zhu, Yun / Kim, Byung Ju / Bartholdy, Boris A / Yang, Seung-Min / Macfarlan, Todd S / Gifford, Wesley D / Pfaff, Samuel L / Verstegen, Marjon J. A. M / Pinto, Hugo / Vermunt, Marit W / Creyghton, Menno P / Wijchers, Patrick J / Stamatoyannopoulos, John A / Skoultchi, Arthur I / de Laat, Wouter

Genome biology. 2015 Dec., v. 16, no. 1

2015

Abstract: BACKGROUND: Linker histone H1 is a core chromatin component that binds to nucleosome core particles and the linker DNA between nucleosomes. It has been implicated in chromatin compaction and gene regulation and is anticipated to play a role in higher- ... ...

Abstract	BACKGROUND: Linker histone H1 is a core chromatin component that binds to nucleosome core particles and the linker DNA between nucleosomes. It has been implicated in chromatin compaction and gene regulation and is anticipated to play a role in higher-order genome structure. Here we have used a combination of genome-wide approaches including DNA methylation, histone modification and DNase I hypersensitivity profiling as well as Hi-C to investigate the impact of reduced cellular levels of histone H1 in embryonic stem cells on chromatin folding and function. RESULTS: We find that depletion of histone H1 changes the epigenetic signature of thousands of potential regulatory sites across the genome. Many of them show cooperative loss or gain of multiple chromatin marks. Epigenetic alterations cluster to gene-dense topologically associating domains (TADs) that already showed a high density of corresponding chromatin features. Genome organization at the three-dimensional level is largely intact, but we find changes in the structural segmentation of chromosomes specifically for the epigenetically most modified TADs. CONCLUSIONS: Our data show that cells require normal histone H1 levels to expose their proper regulatory landscape. Reducing the levels of histone H1 results in massive epigenetic changes and altered topological organization particularly at the most active chromosomal domains. Changes in TAD configuration coincide with epigenetic landscape changes but not with transcriptional output changes, supporting the emerging concept that transcriptional control and nuclear positioning of TADs are not causally related but independently controlled by the locally associated trans-acting factors.
Keywords	DNA ; DNA methylation ; deoxyribonuclease I ; embryonic stem cells ; epigenetics ; genes ; histones ; hypersensitivity ; nucleosomes ; topology ; transactivators ; transcription (genetics)
Language	English
Dates of publication	2015-12
Size	p. 289.
Publishing place	BioMed Central
Document type	Article
ZDB-ID	2040529-7
ISSN	1474-760X ; 1465-6906
ISSN (online)	1474-760X
ISSN	1465-6906
DOI	10.1186/s13059-015-0857-0
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Article ; Online: Endogenous retroviruses and neighboring genes are coordinately repressed by LSD1/KDM1A.

Macfarlan, Todd S / Gifford, Wesley D / Agarwal, Saurabh / Driscoll, Shawn / Lettieri, Karen / Wang, Jianxun / Andrews, Shane E / Franco, Laura / Rosenfeld, Michael G / Ren, Bing / Pfaff, Samuel L

Genes & development

2011 Volume 25, Issue 6, Page(s) 594–607

Abstract: Endogenous retroviruses (ERVs) constitute a substantial portion of mammalian genomes, and their retrotransposition activity helped to drive genetic variation, yet their expression is tightly regulated to prevent unchecked amplification. We generated a ... ...

Abstract	Endogenous retroviruses (ERVs) constitute a substantial portion of mammalian genomes, and their retrotransposition activity helped to drive genetic variation, yet their expression is tightly regulated to prevent unchecked amplification. We generated a series of mouse mutants and embryonic stem (ES) cell lines carrying "deletable" and "rescuable" alleles of the lysine-specific demethylase LSD1/KDM1A. In the absence of KDM1A, the murine endogenous retrovirus MuERV-L/MERVL becomes overexpressed and embryonic development arrests at gastrulation. A number of cellular genes normally restricted to the zygotic genome activation (ZGA) period also become up-regulated in Kdm1a mutants. Strikingly, many of these cellular genes are flanked by MERVL sequences or have cryptic LTRs as promoters that are targets of KDM1A repression. Using genome-wide epigenetic profiling of Kdm1a mutant ES cells, we demonstrate that this subset of ZGA genes and MERVL elements displays increased methylation of histone H3K4, increased acetylation of H3K27, and decreased methylation of H3K9. As a consequence, Kdm1a mutant ES cells exhibit an unusual propensity to generate extraembryonic tissues. Our findings suggest that ancient retroviral insertions were used to co-opt regulatory sequences targeted by KDM1A for epigenetic silencing of cell fate genes during early mammalian embryonic development.
MeSH term(s)	Animals ; Cell Line ; Cells, Cultured ; Embryonic Stem Cells/metabolism ; Embryonic Stem Cells/virology ; Gene Expression Regulation, Developmental ; Histone Deacetylases/metabolism ; Histone Demethylases ; Histones/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Nude ; Mutation ; Nuclear Proteins/metabolism ; Oxidoreductases, N-Demethylating/genetics ; Oxidoreductases, N-Demethylating/metabolism ; Promoter Regions, Genetic/genetics ; Repressor Proteins/metabolism ; Retroviridae ; Tripartite Motif-Containing Protein 28 ; Virus Activation/genetics
Chemical Substances	Histones ; Nuclear Proteins ; Repressor Proteins ; Histone Demethylases (EC 1.14.11.-) ; KDM1a protein, mouse (EC 1.14.11.-) ; Oxidoreductases, N-Demethylating (EC 1.5.-) ; Trim28 protein, mouse (EC 2.3.2.27) ; Tripartite Motif-Containing Protein 28 (EC 2.3.2.27) ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2011-02-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	806684-x
ISSN	1549-5477 ; 0890-9369
ISSN (online)	1549-5477
ISSN	0890-9369
DOI	10.1101/gad.2008511
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Article ; Online: Identification of a microRNA that activates gene expression by repressing nonsense-mediated RNA decay.

Bruno, Ivone G / Karam, Rachid / Huang, Lulu / Bhardwaj, Anjana / Lou, Chih H / Shum, Eleen Y / Song, Hye-Won / Corbett, Mark A / Gifford, Wesley D / Gecz, Jozef / Pfaff, Samuel L / Wilkinson, Miles F

Molecular cell

2011 Volume 42, Issue 4, Page(s) 500–510

Abstract: Nonsense-mediated decay (NMD) degrades both normal and aberrant transcripts harboring stop codons in particular contexts. Mutations that perturb NMD cause neurological disorders in humans, suggesting that NMD has roles in the brain. Here, we identify a ... ...

Abstract	Nonsense-mediated decay (NMD) degrades both normal and aberrant transcripts harboring stop codons in particular contexts. Mutations that perturb NMD cause neurological disorders in humans, suggesting that NMD has roles in the brain. Here, we identify a brain-specific microRNA-miR-128-that represses NMD and thereby controls batteries of transcripts in neural cells. miR-128 represses NMD by targeting the RNA helicase UPF1 and the exon-junction complex core component MLN51. The ability of miR-128 to regulate NMD is a conserved response occurring in frogs, chickens, and mammals. miR-128 levels are dramatically increased in differentiating neuronal cells and during brain development, leading to repressed NMD and upregulation of mRNAs normally targeted for decay by NMD; overrepresented are those encoding proteins controlling neuron development and function. Together, these results suggest the existence of a conserved RNA circuit linking the microRNA and NMD pathways that induces cell type-specific transcripts during development.
MeSH term(s)	Animals ; Brain/growth & development ; Brain/metabolism ; Chick Embryo ; Exons ; Gene Expression Regulation, Developmental ; HEK293 Cells ; HeLa Cells ; Humans ; Mice ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Neurogenesis/genetics ; Neurons/metabolism ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Oligonucleotide Array Sequence Analysis ; RNA Helicases ; RNA Stability ; RNA-Binding Proteins ; Rats ; Trans-Activators/genetics ; Trans-Activators/metabolism ; Transcriptional Activation ; Xenopus laevis
Chemical Substances	CASC3 protein, human ; MIRN128 microRNA, human ; MicroRNAs ; Neoplasm Proteins ; Nuclear Proteins ; RNA-Binding Proteins ; Rent1 protein, mouse ; Trans-Activators ; RNA Helicases (EC 3.6.4.13) ; UPF1 protein, human (EC 3.6.4.13)
Language	English
Publishing date	2011-02-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2011.04.018
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