Turgor regulation in the salt-tolerant alga Chara longifolia

Authors

  • N. A. Stento,

    1. Department of Biological Sciences, State University of New York at Buffalo, Cooke Hall 109, Buffalo NY 14260–1300, USA
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    • *Present address: 316 Maple Street, Vestal, NY13850, USA.

  • N. Gerber Ryba,

    1. Department of Biological Sciences, State University of New York at Buffalo, Cooke Hall 109, Buffalo NY 14260–1300, USA
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  • E. A. Kiegle,

    1. Department of Biological Sciences, State University of New York at Buffalo, Cooke Hall 109, Buffalo NY 14260–1300, USA
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    • Present address: Ceres, Inc., 3007 Malibu Canyon Road, Malibu, CA 90265, USA.

  • M. A. Bisson

    1. Department of Biological Sciences, State University of New York at Buffalo, Cooke Hall 109, Buffalo NY 14260–1300, USA
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Mary A. Bisson. E-mail: bisson@acsu.buffalo.edu

ABSTRACT

Chara longifolia is a salt-tolerant Charophyte which regulates its turgor inresponse to osmotic stress. Membrane depolarization, in creased membrane conductance, and cessation of cytoplasmic streaming (due to increase in cytoplasmic Ca2+) precede regulation in response to hypotonic stress. Measurements of these three parameters are presented here with simultaneous turgor measurements. Variability in the occurrence, rate and extent of turgor regulation in individual cells was correlated with magnitude of the stress. Hypertonic stress showed the same slow time course as was found previously, requiring several days for complete regulation. Fifty μM nifedipine, a Ca2+ channel blocker, inhibited turgor regulation. In the presence of 5 μM nifedipine, turgor regulation was delayed. An increase in conductance preceded regulation, but membrane depolarization was less and no detectable change in cytoplasmic streaming was observed, requiring modifications to a previously presented model for turgor regulation. There was no significant difference in 45Ca2+ influx under control and stress conditions. However, the control flux was insensitive to nifedipine, whereas under stress the flux is inhibited 54% by nifedipine. We suggest that osmotic stress results in a rapid increase in a nifedipine-sensitive Ca2+ entry mechanism, followed very quickly by a decrease in the control entry mechanism.

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