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Mitochondrial movement during the ascidian sperm reaction (1983)

Lambert, Charles C. ; Lambert, Gretchen

New York, NY : Wiley-Blackwell

Gamete Research 8 (1983), S. 295-307

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ISSN: 0148-7280

Keywords: sprem ; mitochondrion ; calcium ; calmodulin ; actin ; Life and Medical Sciences ; Cell & Developmental Biology

Source: Wiley InterScience Backfile Collection 1832-2000

Topics: Biology

Notes: The ascidian sperm reaction, Which involves swelling, migration, and loss of the single large mitochondrion, can be triggered in vitro by raising the seawater pH to 9.3 or lowering Na+ to 20 mM, but only if the sperm are allowed to attach to a suitable Substate. Mitochondrial translocation does not usually occur in the absence of sperm attachment. Extracellular Ca2+ is necessary for triggering the reaction with low Na+ but not high pH; however, the intrecellular Ca2+ blocker, TMB-8, inhibits high pH-induced mitochondrial movement in the absence of extracellular Ca2+. After swelling, the mitochondrion fluoresces in the presence of chlortetracycline, suggesting that Ca2+ becomes membranebound after activation. Elevated cAMP and theophylline both inhibit mitochondrial move ment but not sperm motility. The antiactin drug cytochalasin B(10μM) and the calmodulinblocking drugs TFP (1 μM) and W-13 (10 μM) block mitochondrial movement, suggesting roles for actin and calmodulin in mitochondrial movement. A model is proposed relating intracellular alkalinization, Ca2+ influx, actin, myosin, and calmodulin in mitochondrial translocation.

Additional Material: 3 Ill.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1002/mrd.1120080309

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Volume-induced increase of K+ and Cl− permeabilities in Ehrlich ascites tumor cells. Role of internal Ca2+ (1984)

Hoffmann, Else K. ; Simonsen, Lars Ole ; Lambert, Ian H.

Springer

The journal of membrane biology 78 (1984), S. 211-222

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ISSN: 1432-1424

Keywords: volume regulation ; regulatory volume decrease ; Ca2+-dependent K+ channel ; Cl− channel ; Ca2+ ionophore A23187 ; quinine ; calmodulin ; Ehrlich mouse ascites tumor cells

Source: Springer Online Journal Archives 1860-2000

Topics: Biology , Chemistry and Pharmacology

Notes: Summary Ehrlich ascites tumor cells resuspended in hypotonic medium initially swell as nearly perfect osmometers, but subsequently recover their volume within 5 to 10 min with an associated KCl loss. 1. The regulatory volume decrease was unaffected when nitrate was substituted for Cl−, and was insensitive to bumetanide and DIDS. 2. Quinine, an inhibitor of the Ca2+-activated K+ pathway, blocked the volume recovery. 3. The hypotonic response was augmented by addition of the Ca2+ ionophore A23187 in the presence of external Ca2+, and also by a sudden increase in external Ca2+. The volume response was accelerated at alkaline pH. 4. The anti-calmodulin drugs trifluoperazine, pimozide, flupentixol, and chlorpromazine blocked the volume response. 5. Depletion of intracellular Ca2+ stores inhibited the regulatory volume decrease. 6. Consistent with the low conductive Cl− permeability of the cell membrane there was no change in cell volume or Cl− content when the K+ permeability was increased with valinomycin in isotonic medium. In contrast, addition of the Ca2+ ionophore A23187 in isotonic medium promoted Cl− loss and cell shrinkage. During regulatory volume decrease valinomycin accelerated the net loss of KCl, indicating that the conductive Cl− permeability was increased in parallel with and even more than the K+ permeability. It is proposed that separate conductive K+ and Cl− channels are activated during regulatory volume decrease by release of Ca2+ from internal stores, and that the effect is mediated by calmodulin.