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The Biological Bulletin, Vol 184, Issue 1 1-5, Copyright © 1993 by Marine Biological Laboratory
CELL BIOLOGY |
E. Costas, A. Aguilera, S. Gonzalez-Gil and V. Lopez-Rodas
Genetica Produccion Animal, Facultad de Veterinaria, Universidad Complutense, Madrid, Spain
According to traditional views, the proliferation of unicellular algae is controlled primarily by environmental conditions. But as in mammalian cells, other biological mechanisms, such as growth factors, cellular aging, and contact inhibition, might also control algal proliferation. Here we ask whether contact inhibition regulates growth in several species of unicellular algae as it does in mammalian cells. Laboratory cultures of the dinoflagellate Prorocentrum lima (Ehrenberg) Dodge show contact inhibition at low cell density, so this would be an autocontrol mechanism of cell proliferation that could also act in natural populations of P. lima. But, Synechocystis spp., Phaeodactylum tricornutum (Bohlin), Skeletonema costatum (Greville), and Tetraselmis spp. do not exhibit contact inhibition in laboratory cultures because they are able to grow at high cellular density. Apparently their growth is limited by nutrient depletion or catabolite accumulation instead of contact inhibition. Spirogyra insignis (Hassall) Kutz, Prorocentrum triestinum Schiller, and Alexandrium tamarense (Halim) Balech show a complex response, as they are able to grow in both low and high cell density medium. These results suggest that contact inhibition is more adaptative in benthic unicellular algae.
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