Study of stem cell function using microarray experiments

Perez‐Iratxeta, Carolina; Palidwor, Gareth; Porter, Christopher J.; Sanche, Neal A.; Huska, Matthew R.; Suomela, Brian P; Muro, Enrique M.; Krzyzanowski, Paul M.; Hughes, E.J.; Campbell, Pearl A.; Rudnicki, Michael A.; Andrade, Miguel Ángel Gutiérrez

doi:10.1016/j.febslet.2005.02.020

Cited by 69 publications

(53 citation statements)

References 31 publications

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“…The tRNase Z S gene could also function as a reservoir for the evolution of other His domain (metal binding) proteins. Interestingly, tRNase ZL and tRNase ZS exhibit complementary patterns of expression in mouse stem cells; tRNase ZL is expressed most heavily in embryonic stem cells, and tRNase ZS is most heavily expressed in adult stem cells (57).…”

Section: Discussionmentioning

confidence: 99%

Naturally Occurring Mutations in Human Mitochondrial Pre-tRNASer(UCN) Can Affect the Transfer Ribonuclease Z Cleavage Site, Processing Kinetics, and Substrate Secondary Structure

Yan¹,

Zareen²,

Levinger

2006

Journal of Biological Chemistry

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tRNAs are transcribed as precursors with a 5 end leader and a 3 end trailer. The 5 end leader is processed by RNase P, and in most organisms in all three kingdoms, transfer ribonuclease (tRNase) Z can endonucleolytically remove the 3 end trailer. Long ( L ) and short ( S ) forms of the tRNase Z gene are present in the human genome. tRNase Z L processes a nuclear-encoded pre-tRNA ϳ1600-fold more efficiently than tRNase Z S and is predicted to have a strong mitochondrial transport signal. tRNase Z L could, thus, process both nuclear-and mitochondrially encoded pre-tRNAs. More than 150 pathogenesis-associated mutations have been found in the mitochondrial genome, most of them in the 22 mitochondrially encoded tRNAs. All the mutations investigated in human mitochondrial tRNA Ser(UCN) affect processing efficiency, and some affect the cleavage site and secondary structure. These changes could affect tRNase Z processing of mutant pre-tRNAs, perhaps contributing to mitochondrial disease.Mitochondria, the intracellular organelles responsible for most of a eukaryotic cell energy production, possess their own maternally inherited genome. The circular 16,568-base pair human mitochondrial genome (1) is bidirectionally transcribed into long polycistronic heavy (H) 4 -and light (L)-strand precursor RNAs. Two rRNAs and 11 mRNAs encoding 13 polypeptides (all of them subunits of complexes in the respiratory transport chain) are punctuated by 22 tRNAs (1 tRNA for each of 18 amino acids and 2 each for leucine and serine with different anticodons) with very little intergenic RNA (2, 3). Several thousand additional polypeptides required for mitochondrial metabolism are nuclear-encoded, cytoplasmically translated and imported.Precursor tRNA transcripts have a 5Ј end leader and a 3Ј end trailer. Eukaryotic nuclear-encoded tRNAs are transcribed from RNA polymerase III promoters with short 5Ј end leaders and 3Ј end trailers ending with a U 3 tail. The characteristic length and sequence of mitochondrial pre-tRNA leaders and trailers, on the other hand, depend on the setting of individual tRNAs among the neighboring functional RNA units (other tRNAs, mRNAs, rRNAs) on the long polycistronic H-and L-strand transcripts (4).The 5Ј end leader is removed from pre-tRNAs by RNase P in a largely conserved, well characterized reaction (5). On the other hand, there are different paths to a mature tRNA 3Ј end (6). In the tRNAs of some prokaryotes, CCA is transcriptionally encoded, and the 3Ј end trailer is removed by the sequential activity of an endonuclease (RNase E) and exonucleases (7,8). In contrast, in most organisms in all three kingdoms and in extranuclear organelles, CCA is not transcriptionally encoded and can be added to the discriminator (the unpaired nucleotide after the 3Ј end of the acceptor stem, which is retained in mature tRNA) after precise endonucleolytic removal of the 3Ј end trailer by tRNase Z (9 -14).Intriguingly, CCA is a tRNase Z anti-determinant that prevents mature tRNA from recycling through tRNase Z, thus ensuring that ...

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Section: Discussionmentioning

confidence: 99%

Naturally Occurring Mutations in Human Mitochondrial Pre-tRNASer(UCN) Can Affect the Transfer Ribonuclease Z Cleavage Site, Processing Kinetics, and Substrate Secondary Structure

Yan¹,

Zareen²,

Levinger

2006

Journal of Biological Chemistry

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“…cDNA was submitted to the Microarray Facility of the Ontario Genomics Innovation Centre, Ontario Health Research Institute for labeling and hybridization to Affymetrix MOE 430 A and B chips, using a protocol described in Iscove et al, 2002. Microarray data have been deposited with NCBI GEO, accession number GSE8163. The experiment (Stembase experiment 235) is part of a large collection of microarray experiments aimed at analyzing stem cell function (Perez-Iratxeta, et al, 2005). Microarray data were analysed with ArrayAssist 2.0 (Stratagene).…”

Section: Preparation Of Cdna From Uniparental Blastocystsmentioning

confidence: 99%

The PcG gene Sfmbt2 is paternally expressed in extraembryonic tissues

Kuzmin

Han

Golding

et al. 2008

Gene Expression Patterns

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Genomic imprinting has dramatic effects on placental development, as has been clearly observed in interspecific hybrid, somatic cell nuclear transfer, and uniparental embryos. In fact, the earliest defects in uniparental embryos are evident first in the extraembryonic trophoblast. We performed a microarray comparison of gynogenetic and androgenetic mouse blastocysts, which are predisposed to placental pathologies, to identify imprinted genes. In addition to identifying a large number of known imprinted genes, we discovered that the Polycomb group (PcG) gene Sfmbt2 is imprinted. Sfmbt2 is expressed preferentially from the paternal allele in early embryos, and in later stage extraembryonic tissues. A CpG island spanning the transcriptional start site is differentially methylated on the maternal allele in e14.5 placenta. Sfmbt2 is located on proximal chromosome 2, in a region known to be imprinted, but for which no genes had been identified until now. This possibly identifies a new imprinted domain within the murine genome. We further demonstrate that murine SFMBT2 protein interacts with the transcription factor YY1, similar to the Drosophila PHO-RC. KeywordsGenomic Imprinting; Sfmbt2; PcG gene; Extraembryonic tissues; placenta; MMU2; YY1; microarrays; uniparental embryos Results and DiscusssionThe role played by imprinted genes in placental development is gaining wider attention as the impact of imprinting disruptions on placental pathology is explored. Both hyper-and hypoplastic placentation are linked to imprinted gene function (Kanayama et al., 2002;Murdoch et al., 2006; reviewed in Kaneko-Ishino et al., 2003). The most dramatic example of this is diploid, uniparental embryos. Gynogenetic embryos (two maternal/no paternal genomes) and androgenetic embryos (two paternal/no maternal genomes) both exhibit defects in the earliest differentiated tissue in mammals, the extraembryonic trophoblast (Barton et al., 1984;McGrath and Solter, 1984;Mann, 2005). At mid-gestation, gynogenetic embryos possess only a few residual trophoblast giant cells while androgenetic embryos are characterized by a mass of hypertrophic trophoblast. These observations indicate that a suite of genes required * Corresponding author. s.varmuza@utoronto.ca; tel. 1-416-978-2759; FAX 1-416-978-8532. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptGene Expr Patterns. Author manuscript; available in PMC 2009 January 1. Published in final edited form as:Gene Expr Patterns. 2008 January ; 8(2): 107-116. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manu...

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“…Since the identity of stem cells is still an issue [32] cells were also screened for other markers, though not in every individual patient. Cells were also positive for CD29, 99.8 ± 0.2% (4 patients); CD44, 99.4 ± 0.5% (3 patients); CD73, 98.8 ± 1.3% (6 patients); CD90, 92.3 ± 5.6% (3 patients); whereas they were negative for CD14, 0.81 ± 0.43% (7 patients) and CD34, 0.41 ± 0.30% (6 patients).…”

Section: Expression Of Surface Markersmentioning

confidence: 99%

5-Azacytidine induces changes in electrophysiological properties of human mesenchymal stem cells

et al. 2006

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Previously, mouse bone marrow-derived stem cells (MSC) treated with the unspecific DNA methyltransferase inhibitor 5-azacytidine were reported to differentiate into cardiomyocytes. The aim of the present study was to investigate the efficiency of a similar differentiation strategy in human mononuclear cells obtained from healthy bone marrow donors. After 1-3 passages, cultures were exposed for 24 h to 5-azacytidine (3 µM) followed by 6 weeks of further culture. Drug treatment did not induce expression of myogenic marker MyoD or cardiac markers Nkx2.5 and GATA-4 and did not yield beating cells during follow-up. In patch clamp experiments, approximately 10-15% of treated and untreated cells exhibited L-type Ca 2+ currents. Almost all cells showed outwardly rectifying K + currents of rapid or slow activation kinetics. Mean current amplitude at +60 mV doubled after 6 weeks of treatment compared with time-matched controls. Membrane capacitance of treated cells was significantly larger than in controls 2 weeks after treatment and remained high after 6 weeks. Expression levels of mRNAs for the K + channels Kv1.1, Kv1.5, Kv2.1, Kv4.3 and KCNMA1 and for the Ca 2+ channel Ca v 1.2 were not affected by 5-azacytidine. Treatment with potassium channel blockers tetraethylammonium and clofilium at concentrations shown previously to inhibit rapid or slowly activating K + currents of hMSC inhibited proliferation of these cells. Our results suggest that despite the absence of differentiation of hMSC into cardiomyocytes, treatment with 5-azacytidine caused profound changes in current density.Cell Research (2006) 16:949-960.

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Study of stem cell function using microarray experiments

Cited by 69 publications

References 31 publications

Naturally Occurring Mutations in Human Mitochondrial Pre-tRNASer(UCN) Can Affect the Transfer Ribonuclease Z Cleavage Site, Processing Kinetics, and Substrate Secondary Structure

Naturally Occurring Mutations in Human Mitochondrial Pre-tRNASer(UCN) Can Affect the Transfer Ribonuclease Z Cleavage Site, Processing Kinetics, and Substrate Secondary Structure

The PcG gene Sfmbt2 is paternally expressed in extraembryonic tissues

5-Azacytidine induces changes in electrophysiological properties of human mesenchymal stem cells

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