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Differential activation of transcription factors induced by Ca2+ response amplitude and duration

Author

Listed:
  • Ricardo E. Dolmetsch

    (Department of Molecular and Cellular Physiology and Neurosciences Program)

  • Richard S. Lewis

    (Department of Molecular and Cellular Physiology and Neurosciences Program
    Stanford University School of Medicine)

  • Christopher C. Goodnow

    (Stanford University School of Medicine
    Stanford University School of Medicine)

  • James I. Healy

    (Stanford University School of Medicine
    Stanford University School of Medicine)

Abstract

An increase in the intracellular calcium ion concentration ([Ca2+]i) controls a diverse range of cell functions, including adhesion, motility, gene expression and proliferation1,2. Calcium signalling patterns can occur as single transients, repetitive oscillations or sustained plateaux2,3, but it is not known whether these patterns are responsible for encoding the specificity of cellular responses. We report here that the amplitude and duration of calcium signals in B lymphocytes controls differential activation of the pro–inflammatory transcriptional regulators NF-κB, c-Jun N-terminal kinase (JNK) and NFAT. NF-κB and JNK are selectively activated by a large transient [Ca2+]i rise, whereas NFAT is activated by a low, sustained Ca2+ plateau. Differential activation results from differences in the Ca2+ sensitivities and kinetic behaviour of the three pathways. Our results show how downstream effectors can decode information contained in the amplitude and duration of Ca2+ signals, revealing a mechanism by which a multifunctional second messenger such as Ca2+ can achieve specificity in signalling to the nucleus.

Suggested Citation

  • Ricardo E. Dolmetsch & Richard S. Lewis & Christopher C. Goodnow & James I. Healy, 1997. "Differential activation of transcription factors induced by Ca2+ response amplitude and duration," Nature, Nature, vol. 386(6627), pages 855-858, April.
    • Handle: RePEc:nat:nature:v:386:y:1997:i:6627:d:10.1038_386855a0
    DOI: 10.1038/386855a0
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    Cited by:

    1. Jason W Locasale & Arup K Chakraborty, 2008. "Regulation of Signal Duration and the Statistical Dynamics of Kinase Activation by Scaffold Proteins," PLOS Computational Biology, Public Library of Science, vol. 4(6), pages 1-12, June.
    2. Agne Tilūnaitė & Wayne Croft & Noah Russell & Tomas C Bellamy & Rüdiger Thul, 2017. "A Bayesian approach to modelling heterogeneous calcium responses in cell populations," PLOS Computational Biology, Public Library of Science, vol. 13(10), pages 1-25, October.
    3. Manasi Iyer & Husniye Kantarci & Madeline H. Cooper & Nicholas Ambiel & Sammy Weiser Novak & Leonardo R. Andrade & Mable Lam & Graham Jones & Alexandra E. Münch & Xinzhu Yu & Baljit S. Khakh & Uri Man, 2024. "Oligodendrocyte calcium signaling promotes actin-dependent myelin sheath extension," Nature Communications, Nature, vol. 15(1), pages 1-20, December.
    4. Andreja Jovic & Bryan Howell & Michelle Cote & Susan M Wade & Khamir Mehta & Atsushi Miyawaki & Richard R Neubig & Jennifer J Linderman & Shuichi Takayama, 2010. "Phase-Locked Signals Elucidate Circuit Architecture of an Oscillatory Pathway," PLOS Computational Biology, Public Library of Science, vol. 6(12), pages 1-8, December.
    5. Hyung Chul Lee & Nidia M. M. Oliveira & Cato Hastings & Peter Baillie-Benson & Adam A. Moverley & Hui-Chun Lu & Yi Zheng & Elise L. Wilby & Timothy T. Weil & Karen M. Page & Jianping Fu & Naomi Moris , 2024. "Regulation of long-range BMP gradients and embryonic polarity by propagation of local calcium-firing activity," Nature Communications, Nature, vol. 15(1), pages 1-13, December.

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