scholarly journals Calmodulin Binds to Extracellular Sites on the Plasma Membrane of Plant Cells and Elicits a Rise in Intracellular Calcium Concentration

2009 ◽  
Vol 284 (18) ◽  
pp. 12000-12007 ◽  
Author(s):  
Qinli Wang ◽  
Bo Chen ◽  
Peng Liu ◽  
Maozhong Zheng ◽  
Yuqing Wang ◽  
...  
Development ◽  
1993 ◽  
Vol 117 (1) ◽  
pp. 1-12 ◽  
Author(s):  
M. Whitaker ◽  
K. Swann

In most deuterostome eggs, fertilization is marked by an abrupt and transient increase in intracellular calcium concentration. The transient takes the form of a propagating wave and is the signal for the onset of development. For those interested in cell signalling, the two obvious questions to ask are how the wave is initiated and how it propagates through the egg cytoplasm. Answers have come largely from experiments in frog, hamster, mouse and sea urchin eggs. One explanation of signal transduction at fertilization makes an analogy with transmembrane signalling in somatic cells, where a family of G-protein-linked receptors pass activating signals across the plasma membrane. Another, older idea is that it is the fusion of sperm and egg that is responsible for detonating the calcium explosion at fertilization. We discuss the relative merits of the two ideas. Both are plausible; the creative tension between them has led to experiments that broaden our view of signal transduction at fertilization.


2002 ◽  
Vol 58 (2) ◽  
pp. 203-205 ◽  
Author(s):  
András Palotás ◽  
János Kálmán ◽  
Miklós Palotás ◽  
Anna Juhász ◽  
Zoltán Janka ◽  
...  

1995 ◽  
Vol 74 (6) ◽  
pp. 2625-2637 ◽  
Author(s):  
N. E. Ziv ◽  
M. E. Spira

1. Axonal transection triggers a cascade of pathological processes that frequently lead to the degeneration of the injured neuron. It is generally believed that the degenerative process is triggered by an overwhelming influx of calcium through the cut end of the axon. 2. Theoretical considerations and indirect observations suggest that axotomy is followed by an increase in the free intracellular calcium concentration ([Ca2+]i) to the millimolar level. In contrast, only relatively modest and transient elevation in [Ca2+]i to the micromolar level was revealed by recent fura-2 studies. 3. In the current study we used the low-affinity Ca2+ indicator mag-fura-2 to reexamine the spatiotemporal distribution pattern of Ca2+ after axotomy and to map the free intracellular Mg2+ concentration gradients. 4. We report that axotomy elevates [Ca2+]i well beyond the "physiological" range of calcium concentrations, to levels > 1 mM near the tip of the cut axon and to hundreds of micromolars along the axon further away from the cut end. Nevertheless, [Ca2+]i recovers to the control levels within 2-3 min after the resealing of the cut end. 5. A comparison of the behavior of fura-2 and mag-fura-2 in the cytosol of the axotomized neurons reveals that the determination of [Ca2+]i by fura-2 largely underestimates the actual intracellular Ca2+ concentrations. 6. Experiments in which one branch of a bifurcated axon was transected revealed that the elevation in [Ca2+]i is confined to the transected axonal branch and does not spread beyond the bifurcation point. 7. After axotomy, the intracellular Mg2+ concentration equilibrates rapidly with the external concentration and then recovers at a rate somewhat slower than that of [Ca2+]i. 8. To the best of our knowledge, this study is the first direct demonstration that axotomy elevates [Ca2+]i to the millimolar range and that neurons are able to recover from these extreme calcium concentrations.


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