Gene Expression 15(4) Abstracts

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Gene Expression, Vol. 15, pp. 153–162, 2012
1052-2166/12 $90.00 + .00
DOI: http://dx.doi.org/10.3727/105221612X13372578119571
E-ISSN 1555-3884
Copyright © 2012 Cognizant Comm. Corp.
Printed in the USA. All rights reserved

Stable Expression of FoxA1 Promotes Pluripotent P19 Embryonal Carcinoma Cells to Be Neural Stem-Like Cells

Difei Dong,1 Lei Meng,1 Qiqi Yu, Guixiang Tan, Miao Ding, and Yongjun Tan

State Key Laboratory of Chemo/Biosensing and Chemometrics, College of Biology, Hunan University, Changsha, Hunan, China

FoxA1 belongs to the fork head/winged-helix transcription factor family and participates in stimulating neuronal differentiation of pluripotent stem cells at early stages. To explore the biological roles of FoxA1 during this process, the stable expression of a GFP-FoxA1 fusion protein was established in P19 pluripotent embryonal carcinoma cells. Although they still express pluripotency-related transcription factors such as Oct4, Nanog, and Sox2, the generated P19 GFPFoxA1 cells exhibited a decreased activity of alkaline phosphatase and an increased expression of SSEA-3 compared with P19 cells. Elevated levels of nestin expression and prominin-1+ populations were observed in P19 GFPFoxA1 cells, implicating that the stable expression of FoxA1 promoted P19 cells to gain partial characteristics of neural stem cells. Furthermore, the promoter of nestin was confirmed to be bound and activated by FoxA1 directly. The expression of neuron-specific marker tubulin βIII also existed in P19 GFPFoxA1 cells. P19 GFPFoxA1 cells showed an earlier onset of differentiation during RA-induced neuronal differentiation, evidenced by a more rapid change on the Nanog decrease and the tubulin βIII increase. Thus, overexpression of FoxA1 alone may promote pluripotent P19 cells to become neural stem-like cells.

Key words: FoxA1 transcription factor; Pluripotent P19 embryonal carcinoma (EC) cells; Nestin; Retinoic acid-induced neuronal differentiation; Stable cell line

1These authors provided equal contribution to this study.
Address correspondence to Yongjun Tan, State Key Laboratory of Chemo/Biosensing and Chemometrics, College of Biology, Hunan University, Changsha, Hunan 410082, China. Tel/Fax: (86) 731-8882-3211; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Gene Expression, Vol. 15, pp. 163–170, 2012
1052-2166/12 $90.00 + .00
DOI: http://dx.doi.org/10.3727/105221612X13372578119616
E-ISSN 1555-3884
Copyright © 2012 Cognizant Comm. Corp.
Printed in the USA. All rights reserved

Expression Patterns of Ubiquitin Conjugating Enzyme UbcM2 During Mouse Embryonic Development

Xing Yanjiang,* He Hongjuan,* Gu Tiantian,* Zhang Yan,† Huang Zhijun,* and Wu Qiong*

*School of Life Science and Technology, State Key Laboratory of Urban Water Resource and Environment,Harbin Institute of Technology, Heilongjiang, China
†College of Bioinformatics Science and Technology, Harbin Medical University, Heilongjiang, China

Ubiquitin conjugating enzyme UbcM2 (Ubiquitin-conjugating enzymes from mice, the number reveals the identification order) has been implicated in many critical processes, such like growth-inhibiting, mediating cell proliferation and regulation of some transcription factor, but the expression profile during mouse embryo development remains unclear. Hereby, during mid-later embryonic stage, the expression patterns of UbcM2 were examined using in situ hybridization and quantitative real-time PCR (qRT-PCR). The signals were significantly intense in central nervous system and skeletal system, weak in tongue, heart, lung, liver, and kidney. In the central nervous system, UbcM2 was principally expressed in thalamus, external germinal layer of cerebellum (EGL), mitral cell layer of olfactory bulb, hippocampus, marginal zone and ventricular zone of cerebral cortex, and spinal cord. In the skeletal system, UbcM2 was primarily expressed in proliferating cartilage. Furthermore, qRT-PCR analysis displayed that the expression of UbcM2 was ubiquitous at E15.5, most prominent in brain, weaker in lung liver and kidney, accompanied by the lowest level in tongue and heart. During brain development, the expression level of UbcM2 first ascended and then decreased from E12.5 to E18.5, the peak of which sustained starting at E14.5 until E16.5. Together, these results suggest that UbcM2 may play potential roles in the development of mouse diverse tissues and organs, particularly in the development of brain and skeleton.

Key words: UbcM2; In situ hybridization; Mouse embryo development

Address correspondence to Wu Qiong, School of Life Science and Technology, State Key Laboratory of Urban Water Resource and Environment, Harbin Institute of Technology, 150001, Heilongjiang, China. Tel/Fax: 86-451-86403181; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Gene Expression, Vol. 15, pp. 171–181, 2012
1052-2166/12 $90.00 + .00
DOI: http://dx.doi.org/10.3727/105221612X13372578119652
E-ISSN 1555-3884
Copyright © 2012 Cognizant Comm. Corp.
Printed in the USA. All rights reserved

Genome-Wide Gene Expression Profiling of Human Narcolepsy

Camilla Bernardini,*1 Wanda Lattanzi,*1 Paolo Bosco,† Christian Franceschini,‡ Giuseppe Plazzi,‡ Fabrizio Michetti,* and Raffaele Ferri†

*Institute of Anatomy and Cell Biology, Catholic University, Rome, Italy
†Department of Neurology I.C, Sleep Research Center, Oasi Institute for Research on Mental Retardation and Brain Aging (IRCCS), Troina, Italy
‡Sleep Disorders Center, Department of Neurological Sciences, University of Bologna, Bologna, Italy

The objective of this study was to perform global gene expression profiling of patients affected by narcolepsy with cataplexy (NRLCP). This enabled identifying new potential biomarkers and relevant molecules possibly involved in the disease pathogenesis. In this study 10 NRLCP patients and 10 healthy controls were compared. Total RNA isolated from blood specimens was analyzed using microarray technology followed by statistical data analysis to detect genome-wide differential gene expression between patients and controls. Functional analysis of the gene list was performed in order to interpret the biological significance of the data. One hundred and seventy-three genes showed significant (p < 0.01) differential expression between the two tested conditions. The biological interpretation allowed categorizing differentially expressed genes involved in neurite outgrowth/extension and brain development, which could be possibly regarded as peripheral markers of the disease. Moreover, the NRLCP-related gene expression profiles indicated a dysregulation of metabolic and immune-related mechanisms. In conclusion, the gene expression profile associated to NRLCP suggested that molecular markers of neurological impairment, dysmetabolic and immune-related mechanisms, can be detected in blood of NRLCP patients.

Key words: Microarray; Narcolepsy; Cataplexy; Gene expression

1These authors provided equal contribution.
Address correspondence to Camilla Bernardini, Institute of Anatomy and Cell Biology, Universita` Cattolica del Sacro Cuore, Largo F. Vito, 1, 00168 Rome, Italy. Tel: +39 06 30154711; Fax: +39 0630154813; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Gene Expression, Vol. 15, pp. 183–198, 2012
1052-2166/12 $90.00 + .00
DOI: http://dx.doi.org/10.3727/105221612X13372578119698
E-ISSN 1555-3884
Copyright © 2012 Cognizant Comm. Corp.
Printed in the USA. All rights reserved

Distribution of Histone3 Lysine 4 Trimethylation at T3-Responsive Loci in the Heart During Reversible Changes in Gene Expression

Kumar Pandya,*1 Takahide Kohro,†1 Imari Mimura,† Mika Kobayashi,† Youichiro Wada,† Tatsuhiko Kodama,† and Oliver Smithies*

*Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
†Department of Molecular Biology and Medicine, The Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan

Expression in the adult heart of a number of cardiac genes, including the two genes comprising the cardiac myosin heavy chain locus (Myh), is controlled by thyroid hormone (T3) levels, but there is minimal information concerning the epigenetic status of the genes when their expressions change. We fed mice normal chow or a propyl thio uracil (PTU, an inhibitor of T3 production) diet for 6 weeks, or the PTU diet for 6 weeks followed by normal chow for a further 2 weeks. Heart ventricles from these groups were then used for ChIP-seq analyses with an antibody to H3K4me3, a well-documented epigenetic marker of gene activation. The resulting data show that, at the Myh7 locus, H3K4me3 modifications are induced primarily at 5′ transcribed region in parallel with increased expression of beta myosin heavy chain (MHC). At the Myh6 locus, decreases in H3K4me3 modifications occurred at the promoter and 5′ transcribed region. Extensive H3K4me3 modifications also occurred at the intergenic region between the two Myh genes, which extended into the 3′ transcribed region of Myh7. The PTU-induced changes in H3K4me3 levels are, for the most part, reversible but are not invariably complete. We found full restoration of Myh6 gene expression upon PTU withdrawal; however, the H3K4me3 pattern was only partially restored at Myh6, suggesting that full reexpression of Myh6 does not require that the H3K4me3 modifications return fully to the untreated conditions. Together, our data show that the H3K4me3 modification is an epigenetic marker closely associated with changes in Myh gene expression.

Key words: Myosin heavy chain; Epigenetic; ChIP-seq; Thyroid hormone; Heart; Histone methylation

1Co-first authors.
Address correspondence to Oliver Smithies, D.Phil., Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, 701 Brinkhous Bullit Building, Chapel Hill, NC 27599-7525, USA. Tel: +1-919-966-6912; Fax: +1-919-966-8800; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it or Youichiro Wada, M.D., Ph.D., Laboratory of Systems Biology and Medicine, Research Center for Advanced Science and Technology, University of Tokyo, 4th building Room 310, 4-6-1 Komaba, Meguro-ku, Tokyo 153-8904, Japan. Tel: +81-3-5452-5117; Fax: +81-3-5452-5117; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it