Notch and MAML Signaling Drives Scl-Dependent Interneuron Diversity in the Spinal Cord

Chian Yu Peng; Hiroshi Yajima; Caroline Erter Burns; Leonard I. Zon; Sangram S. Sisodia; Samuel L. Pfaff; Kamal Sharma

doi:10.1016/j.neuron.2007.02.019

Notch and MAML Signaling Drives Scl-Dependent Interneuron Diversity in the Spinal Cord

Chian Yu Peng, Hiroshi Yajima, Caroline Erter Burns, Leonard I. Zon, Sangram S. Sisodia, Samuel L. Pfaff, Kamal Sharma^*

^*Corresponding author for this work

Neurology

Research output: Contribution to journal › Article › peer-review

131 Scopus citations

Abstract

The ventral spinal cord generates multiple inhibitory and excitatory interneuron subtypes from four cardinal progenitor domains (p0, p1, p2, p3). Here we show that cell-cell interactions mediated by the Notch receptor play a critical evolutionarily conserved role in the generation of excitatory v2aIN and inhibitory v2bIN interneurons. Lineage-tracing experiments show that the v2aIN and v2bIN develop from genetically identical p2 progenitors. The p2 daughter cell fate is controlled by Delta4 activation of Notch receptors together with MAML factors. Cells receiving Notch signals activate a transcription factor code that specifies the v2bIN fate, whereas cells deprived of Notch signaling express another code for v2aIN formation. Thus, our study provides insight into the cell-extrinsic signaling that controls combinatorial transcription factor profiles involved in regulating the process of interneuron subtype diversification.

Original language	English (US)
Pages (from-to)	813-827
Number of pages	15
Journal	Neuron
Volume	53
Issue number	6
DOIs	https://doi.org/10.1016/j.neuron.2007.02.019
State	Published - Mar 15 2007

Keywords

DEVBIO
MOLNEURO

ASJC Scopus subject areas

Neuroscience(all)

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10.1016/j.neuron.2007.02.019

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@article{95bde726da6447febe00b395ef05211f,

title = "Notch and MAML Signaling Drives Scl-Dependent Interneuron Diversity in the Spinal Cord",

abstract = "The ventral spinal cord generates multiple inhibitory and excitatory interneuron subtypes from four cardinal progenitor domains (p0, p1, p2, p3). Here we show that cell-cell interactions mediated by the Notch receptor play a critical evolutionarily conserved role in the generation of excitatory v2aIN and inhibitory v2bIN interneurons. Lineage-tracing experiments show that the v2aIN and v2bIN develop from genetically identical p2 progenitors. The p2 daughter cell fate is controlled by Delta4 activation of Notch receptors together with MAML factors. Cells receiving Notch signals activate a transcription factor code that specifies the v2bIN fate, whereas cells deprived of Notch signaling express another code for v2aIN formation. Thus, our study provides insight into the cell-extrinsic signaling that controls combinatorial transcription factor profiles involved in regulating the process of interneuron subtype diversification.",

keywords = "DEVBIO, MOLNEURO",

author = "Peng, {Chian Yu} and Hiroshi Yajima and Burns, {Caroline Erter} and Zon, {Leonard I.} and Sisodia, {Sangram S.} and Pfaff, {Samuel L.} and Kamal Sharma",

note = "Funding Information: We thank Drs. Thomas Jessell and Martyn Goulding for numerous discussions and comments on previous versions of this manuscript. We thank Dr. David Rowitch for many discussions during the course of these studies and Dr. William Richardson for sharing data prior to publication. We also thank Drs. Bruce Appel, John Crispino, Chris Kintner, Kathy Millen, and Warren Pear for providing various cDNA constructs. Special thanks to Drs. Catherine Porcher and Paresh Vyas for the generous gift of affinity-purified anti-Scl antibody. Special thanks to Ms. Charity Goodman, Aida Pourbovali, and Jennifer Setlak for technical help. This work was supported by grants from Brain Research foundation, Basil O'Connor grant from March of Dimes, and NIH-RO1 NS045106 to K.S. ",

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AU - Peng, Chian Yu

AU - Yajima, Hiroshi

AU - Burns, Caroline Erter

AU - Zon, Leonard I.

AU - Sisodia, Sangram S.

AU - Pfaff, Samuel L.

AU - Sharma, Kamal

N1 - Funding Information: We thank Drs. Thomas Jessell and Martyn Goulding for numerous discussions and comments on previous versions of this manuscript. We thank Dr. David Rowitch for many discussions during the course of these studies and Dr. William Richardson for sharing data prior to publication. We also thank Drs. Bruce Appel, John Crispino, Chris Kintner, Kathy Millen, and Warren Pear for providing various cDNA constructs. Special thanks to Drs. Catherine Porcher and Paresh Vyas for the generous gift of affinity-purified anti-Scl antibody. Special thanks to Ms. Charity Goodman, Aida Pourbovali, and Jennifer Setlak for technical help. This work was supported by grants from Brain Research foundation, Basil O'Connor grant from March of Dimes, and NIH-RO1 NS045106 to K.S.

PY - 2007/3/15

Y1 - 2007/3/15

N2 - The ventral spinal cord generates multiple inhibitory and excitatory interneuron subtypes from four cardinal progenitor domains (p0, p1, p2, p3). Here we show that cell-cell interactions mediated by the Notch receptor play a critical evolutionarily conserved role in the generation of excitatory v2aIN and inhibitory v2bIN interneurons. Lineage-tracing experiments show that the v2aIN and v2bIN develop from genetically identical p2 progenitors. The p2 daughter cell fate is controlled by Delta4 activation of Notch receptors together with MAML factors. Cells receiving Notch signals activate a transcription factor code that specifies the v2bIN fate, whereas cells deprived of Notch signaling express another code for v2aIN formation. Thus, our study provides insight into the cell-extrinsic signaling that controls combinatorial transcription factor profiles involved in regulating the process of interneuron subtype diversification.

AB - The ventral spinal cord generates multiple inhibitory and excitatory interneuron subtypes from four cardinal progenitor domains (p0, p1, p2, p3). Here we show that cell-cell interactions mediated by the Notch receptor play a critical evolutionarily conserved role in the generation of excitatory v2aIN and inhibitory v2bIN interneurons. Lineage-tracing experiments show that the v2aIN and v2bIN develop from genetically identical p2 progenitors. The p2 daughter cell fate is controlled by Delta4 activation of Notch receptors together with MAML factors. Cells receiving Notch signals activate a transcription factor code that specifies the v2bIN fate, whereas cells deprived of Notch signaling express another code for v2aIN formation. Thus, our study provides insight into the cell-extrinsic signaling that controls combinatorial transcription factor profiles involved in regulating the process of interneuron subtype diversification.

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Notch and MAML Signaling Drives Scl-Dependent Interneuron Diversity in the Spinal Cord

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