Novel transcription factor <i>Satb2</i> interacts with matrix attachment region DNA elements in a tissue‐specific manner and demonstrates cell‐type‐dependent expression in the developing mouse CNS

Britanova, Olga V.; Akopov, S. B.; Lukyanov, Sergey; Gruß, Peter; Tarabykin, Victor

doi:10.1111/j.1460-9568.2005.03897.x

Cited by 212 publications

(250 citation statements)

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“…Cortical neurons can be identified by immunostaining with antibodies recognizing neuronal markers such as Brn2, Satb2, Ctip2, Foxp2, and Tbr2 (Bulfone et al, 1999;McEvilly et al, 2002;Ferland et al, 2003;Arlotta et al, 2005;Britanova et al, 2005). We detected expression of all of these markers in Mkk7 flox/flox Nestin-Cre cortex (Fig.…”

Section: Impaired Axon Formationmentioning

confidence: 99%

Stress-Activated Protein Kinase MKK7 Regulates Axon Elongation in the Developing Cerebral Cortex

et al. 2011

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The c-Jun NH 2 -terminal protein kinase (JNK), which belongs to the mitogen-activated protein kinase family, plays important roles in a broad range of physiological processes. JNK is controlled by two upstream regulators, mitogen-activated protein kinase kinase (MKK) 7 and MKK4. To elucidate the physiological functions of MKK7, we used Nestin-Cre to generate a novel mouse model in which the mkk7 gene was specifically deleted in the nervous system (Mkk7 flox/flox Nestin-Cre mice). These mice were indistinguishable from their control littermates in gross appearance during embryogenesis but died immediately after birth without breathing. Histological examination showed that the mutants had severe defects in brain development, including enlarged ventricles, reduced striatum, and minimal axon tracts. Electron microscopy revealed abnormal accumulations of filamentous structures and autophagic vacuoles in Mkk7 flox/flox NestinCre brain. Further analysis showed that MKK7 deletion decreased numbers of TAG-1-expressing axons and delayed neuronal migration in the cerebrum. Neuronal differentiation was not altered. In utero electroporation studies showed that contralateral projection of axons by layer 2/3 neurons was impaired in the absence of MKK7. Moreover, MKK7 regulated axon elongation in a cell-autonomous manner in vivo, a finding confirmed in vitro. Finally, phosphorylation levels of JNK substrates, including c-Jun, neurofilament heavy chain, microtubule-associated protein 1B, and doublecortin, were reduced in Mkk7 flox/flox Nestin-Cre brain. Our findings demonstrate that the phenotype of Mkk7 flox/flox Nestin-Cre mice differs substantially from that of Mkk4 flox/flox Nestin-Cre mice, and establish that MKK7-mediated regulation of JNK is uniquely critical for both axon elongation and radial migration in the developing brain.

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Section: Impaired Axon Formationmentioning

confidence: 99%

Stress-Activated Protein Kinase MKK7 Regulates Axon Elongation in the Developing Cerebral Cortex

et al. 2011

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“…SATB2 belongs to the family of special AT-rich sequence-binding proteins, members of which are present in the nuclear matrix and can bind to AT-rich sequences, activating the transcription of particular genes (Britanova et al 2005). In vivo studies have shown that Satb2 physically interacts with and enhances the activity of Runx2 and Atf4 (Dobreva et al 2006, Conner & Hornick 2013.…”

Section: Mirnas and Osteoblast Differentiationmentioning

confidence: 99%

MicroRNAs and post-transcriptional regulation of skeletal development

Gámez¹,

Rodríguez-Carballo²,

Ventura³

2014

Journal of Molecular Endocrinology

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MicroRNAs (miRNAs) have become integral nodes of post-transcriptional control of genes that confer cellular identity and regulate differentiation. Cell-specific signaling and transcriptional regulation in skeletal biology are extremely dynamic processes that are highly reliant on dose-dependent responses. As such, skeletal cell-determining genes are ideal targets for quantitative regulation by miRNAs. So far, large amounts of evidence have revealed a characteristic temporal miRNA signature in skeletal cell differentiation and confirmed the essential roles that numerous miRNAs play in bone development and homeostasis. In addition, microarray expression data have provided evidence for their role in several skeletal pathologies. Mouse models in which their expression is altered have provided evidence of causal links between miRNAs and bone abnormalities. Thus, a detailed understanding of the function of miRNAs and their tight relationship with bone diseases would constitute a powerful tool for early diagnosis and future therapeutic approaches.

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“…Basal progenitors differ from apical progenitors in terms of gene expression: they do not express astroglial markers, nor the transcription factors Pax6 and Hes (Cappello et al 2006;Englund et al 2005), while they can be positively identified by the expression of Tbr2 (Englund et al 2005), Cux1 and 2 (Conti et al 2005), VGlut2 (Schuurmans et al 2004), Satb2 (Britanova et al 2005) and the non-coding RNA Svet1 (Tarabykin et al 2001).…”

Section: Basal Progenitorsmentioning

confidence: 99%

Radial glia and neural stem cells

2007

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During the last decade, the role of radial glia has been radically revisited. Rather than being considered a mere structural component serving to guide newborn neurons towards their final destinations, radial glia is now known to be the main source of neurons in several regions of the central nervous system, notably in the cerebral cortex. Radial glial cells differentiate from neuroepithelial progenitors at the beginning of neurogenesis and share with their ancestors the bipolar shape and the expression of some molecular markers. Radial glia, however, can be distinguished from neuroepithelial progenitors by the expression of astroglial markers. Clonal analyses showed that radial glia is a heterogeneous population, comprising both pluripotent and different lineage-restricted neural progenitors. At late-embryonic and postnatal stages, radial glial cells give rise to the neural stem cells responsible for adult neurogenesis. Embryonic pluripotent radial glia and adult neural stem cells may be clonally linked, thus representing a lineage displaying stem cell features in both the developing and mature central nervous system.

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Novel transcription factor Satb2 interacts with matrix attachment region DNA elements in a tissue‐specific manner and demonstrates cell‐type‐dependent expression in the developing mouse CNS

Cited by 212 publications

References 23 publications

Stress-Activated Protein Kinase MKK7 Regulates Axon Elongation in the Developing Cerebral Cortex

Stress-Activated Protein Kinase MKK7 Regulates Axon Elongation in the Developing Cerebral Cortex

MicroRNAs and post-transcriptional regulation of skeletal development

Radial glia and neural stem cells

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