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

Authors

  • Olga Britanova,

    1. Department of Molecular Biology of Neuronal Signals, Max-Planck Institute for Experimental Medicine, 37075 Goettingen, Germany
    2. Shemiakin and Ovchinnikov Institute of Bioorganic Chemistry RAS, Miklukho-Maklaya 16/10, 117871 Moscow, Russia
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  • Sergey Akopov,

    1. Shemiakin and Ovchinnikov Institute of Bioorganic Chemistry RAS, Miklukho-Maklaya 16/10, 117871 Moscow, Russia
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  • Sergey Lukyanov,

    1. Shemiakin and Ovchinnikov Institute of Bioorganic Chemistry RAS, Miklukho-Maklaya 16/10, 117871 Moscow, Russia
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  • Peter Gruss,

    1. Department of Molecular Cell Biology, Max-Planck Institute for Biophysical Chemistry, 37077 Goettingen, Germany
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  • Victor Tarabykin

    1. Department of Molecular Biology of Neuronal Signals, Max-Planck Institute for Experimental Medicine, 37075 Goettingen, Germany
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Dr V. Tarabykin, as above.
E.mail: vtaraby@gwdg.de

Abstract

Satb1 is a first cell-type-specific transcription factor of a novel type that functions as a regulator of the transcription of large chromatin domains. We identified a close homologue of Satb1, Satb2, in a cDNA subtraction screening in a search for genes controlling neural differentiation. Satb2 showed 61% amino-acid homology to Satb1. Satb2 and Satb1 expression was detected in different cell subpopulations of developing mouse CNS in a mutually exclusive manner. In the electrophoretic mobility shift assay we demonstrate that nuclear extracts from the embryonic day 18.5 mouse developing neocortex, in contrast to basal ganglia, contain a protein complex interacting with matrix attachment region DNA elements (MARs) with high affinity. Endogenous Satb2 protein is a part of this complex. In the developing neocortex Satb2 was detected largely in the superficial layers. In the developing spinal cord Satb2 expression marks a subpopulation of Lbx1-positive neurons dorsally and a subgroup of Isl1-positive neurons ventrally. In the Lbx1 mutants Satb2 expression is greatly reduced. We suggest that Satb2 may regulate differentiation of subsets of neurons at the level of higher order chromatin structure via binding to MARs.

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