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A postmitotic role for Isl-class LIM homeodomain proteins in the assignment of visceral spinal motor neuron identity 总被引:5,自引:0,他引:5
LIM homeobox genes have a prominent role in the regulation of neuronal subtype identity and distinguish motor neuron subclasses in the embryonic spinal cord. We have investigated the role of Isl-class LIM homeodomain proteins in motor neuron diversification using mouse genetic methods. All spinal motor neuron subtypes initially express both Isl1 and Isl2, but Isl2 is rapidly downregulated by visceral motor neurons. Mouse embryos lacking Isl2 function exhibit defects in the migration and axonal projections of thoracic level motor neurons that appear to reflect a cell-autonomous switch from visceral to somatic motor neuron character. Additional genetic mutations that reduce or eliminate both Isl1 and Isl2 activity result in more pronounced defects in visceral motor neuron generation and erode somatic motor neuron character. Thus, an early phase of high Isl expression and activity in newly generated motor neurons permits the diversification of visceral and somatic motor neuron subtypes in the developing spinal cord. 相似文献
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J Frasor U Barkai L Zhong A T Fazleabas G Gibori 《Molecular endocrinology (Baltimore, Md.)》2001,15(11):1941-1952
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LIM homeodomain codes regulate the development of many cell types, though it is poorly understood how these factors control gene expression in a cell-specific manner. Lhx3 is involved in the generation of two adjacent, but distinct, cell types for locomotion, motor neurons and V2 interneurons. Using in vivo function and protein interaction assays, we found that Lhx3 binds directly to the LIM cofactor NLI to trigger V2 interneuron differentiation. In motor neurons, however, Isl1 is available to compete for binding to NLI, displacing Lhx3 to a high-affinity binding site on the C-terminal region of Isl1 and thereby transforming Lhx3 from an interneuron-promoting factor to a motor neuron-promoting factor. This switching mechanism enables specific LIM complexes to form in each cell type and ensures that neuronal fates are tightly segregated. 相似文献
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Requirement for Ras/Rac1-mediated p38 and c-Jun N-terminal kinase signaling in Stat3 transcriptional activity induced by the Src oncoprotein. 总被引:9,自引:0,他引:9
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James Turkson Tammy Bowman Jalila Adnane Yi Zhang Julie Y. Djeu Madhavi Sekharam David A. Frank Lawrence B. Holzman Jie Wu Said Sebti Richard Jove 《Molecular and cellular biology》1999,19(11):7519-7528
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Neilson LM Zhu J Xie J Malabarba MG Sakamoto K Wagner KU Kirken RA Rui H 《Molecular endocrinology (Baltimore, Md.)》2007,21(9):2218-2232
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Progestins induce transcriptional activation of signal transducer and activator of transcription 3 (Stat3) via a Jak- and Src-dependent mechanism in breast cancer cells
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Proietti C Salatino M Rosemblit C Carnevale R Pecci A Kornblihtt AR Molinolo AA Frahm I Charreau EH Schillaci R Elizalde PV 《Molecular and cellular biology》2005,25(12):4826-4840
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Regulation of Stat3 activation by MEK kinase 1 总被引:6,自引:0,他引:6
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