Mmot1, a New Helix-Loop-Helix Transcription Factor Gene Displaying a Sharp Expression Boundary in the Embryonic Mouse Brain*
- Nicoletta Malgaretti‡§,
- Ombretta Pozzoli‡§,
- Alessandro Bosetti‡,
- Anna Corradi‡,
- Sonia Ciarmatori‡,
- Maddalena Panigada‡,
- Marco E. Bianchi‡¶,
- Salvador Martinez‖ and
- G. Giacomo Consalez‡**
- From the ‡Department of Biological and Technological Research (DIBIT), San Raffaele Scientific Institute (HSR) and¶Department of Genetics and Microbiology, University of Milan School of Biology, I-20132 Milan, Italy and ‖Institute of Morphological Sciences, University of Murcia School of Medicine, E-30071 Murcia, Spain
Abstract
Several genetic factors have been proven to contribute to the specification of the metencephalic-mesencephalic territory, a process that sets the developmental foundation for prospective morphogenesis of the cerebellum and mesencephalon. However, evidence stemming from genetic and developmental studies performed in man and various model organisms suggests the contribution of many additional factors in determining the fine subdivision and differentiation of these central nervous system regions. In man, the cerebellar ataxias/aplasias represent a large and heterogeneous family of genetic disorders.
Here, we describe the identification by differential screening and the characterization of Mmot1, a new gene encoding a DNA-binding protein strikingly similar to the helix-loop-helix factor Ebf/Olf1. Throughout midgestation embryogenesis, Mmot1is expressed at high levels in the metencephalon, mesencephalon, and sensory neurons of the nasal cavity. In vitro DNA binding data suggest some functional equivalence of Mmot1 and Ebf/Olf1, possibly accounting for the reported lack of olfactory or neural defects in Ebf −/− knockout mutants. The isolation of Mmot1 and of an additional homolog in the mouse genome defines a novel, phylogenetically conserved mammalian family of transcription factor genes of potential relevance in studies of neural development and its aberrations.
Footnotes
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↵* This work was supported by Italian Telethon Grant B14 and European Union Grant BMH4-CT96-0777.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
The nucleotide sequence(s) reported in this paper has been submitted to the GenBank™/EMBL Data Bank with accession number(s) U71189.
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↵§ These two authors contributed equally to this work.
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↵** To whom correspondence should be addressed: DIBIT-HSR, via Olgettina 58, I-20132 Milano, Italy. Fax: 39-2-26434855; E-mail:consaleg{at}dibit.hsr.it.
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↵1 G. G. Consalez, A. Cabibbo, A. Corradi, C. Alli, M. Sardella, R. Sitia, and R. Fesce, submitted for publication.
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↵2 The abbreviations used are: PCR, polymerase chain reaction; HLH, helix-loop-helix; RT, reverse transcription; PCNA, proliferating cell nuclear antigen; contig, group of overlapping clones; BSS, (C57BL/6j × SPRET/Ei)F1 × SPRET/Ei; nt, nucleotide(s); EST, expressed sequence tag.
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↵3 R. Turner and J. Nadeau, unpublished data.
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↵4 A. Corradi and G. G. Consalez, unpublished data.
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- Received January 24, 1997.
- Revision received April 14, 1997.
