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A terminal selector prevents a Hox transcriptional switch to safeguard motor neuron identity throughout life.
Feng, Weidong; Li, Yinan; Dao, Pauline; Aburas, Jihad; Islam, Priota; Elbaz, Benayahu; Kolarzyk, Anna; Brown, André Ex; Kratsios, Paschalis.
Afiliación
  • Feng W; Department of Neurobiology, University of Chicago, Chicago, United States.
  • Li Y; Committee on Development, Regeneration and Stem Cell Biology, University of Chicago, Chicago, United States.
  • Dao P; Department of Neurobiology, University of Chicago, Chicago, United States.
  • Aburas J; Committee on Neurobiology, University of Chicago, Chicago, United States.
  • Islam P; Department of Neurobiology, University of Chicago, Chicago, United States.
  • Elbaz B; Department of Neurobiology, University of Chicago, Chicago, United States.
  • Kolarzyk A; MRC London Institute of Medical Sciences, London, United Kingdom.
  • Brown AE; Institute of Clinical Sciences, Imperial College London, London, United Kingdom.
  • Kratsios P; Department of Neurology, Center for Peripheral Neuropathy, University of Chicago, Chicago, United States.
Elife ; 92020 01 03.
Article en En | MEDLINE | ID: mdl-31902393
To become and remain functional, individual neuron types must select during development and maintain throughout life their distinct terminal identity features, such as expression of specific neurotransmitter receptors, ion channels and neuropeptides. Here, we report a molecular mechanism that enables cholinergic motor neurons (MNs) in the C. elegans ventral nerve cord to select and maintain their unique terminal identity. This mechanism relies on the dual function of the conserved terminal selector UNC-3 (Collier/Ebf). UNC-3 synergizes with LIN-39 (Scr/Dfd/Hox4-5) to directly co-activate multiple terminal identity traits specific to cholinergic MNs, but also antagonizes LIN-39's ability to activate terminal features of alternative neuronal identities. Loss of unc-3 causes a switch in the transcriptional targets of LIN-39, thereby alternative, not cholinergic MN-specific, terminal features become activated and locomotion defects occur. The strategy of a terminal selector preventing a transcriptional switch may constitute a general principle for safeguarding neuronal identity throughout life.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Factores de Transcripción / Caenorhabditis elegans / Proteínas de Homeodominio / Regulación del Desarrollo de la Expresión Génica / Proteínas de Caenorhabditis elegans / Neuronas Colinérgicas / Neuronas Motoras Límite: Animals Idioma: En Revista: Elife Año: 2020 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Factores de Transcripción / Caenorhabditis elegans / Proteínas de Homeodominio / Regulación del Desarrollo de la Expresión Génica / Proteínas de Caenorhabditis elegans / Neuronas Colinérgicas / Neuronas Motoras Límite: Animals Idioma: En Revista: Elife Año: 2020 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido