The green hydra symbiosis and ammonium. II. Ammonium assimilation and release by freshly isolated symbionts and cultured algae

Freshly isolated symbionts from the European strain of green hydra containing native (E/E) or heterologous algae (E/3N8, E/NC), and the Wytham strain of green hydra (W5) assimilated ammonium at pH 7 in light. Both nitrogen-replete and nitrogen-starved cultures of high (3N813A) and low (NC64A) maltose-releasing strains of Chlorella also assimilated ammonium at pH 7 in light. However, at pH 4, freshly isolated symbionts from E/E, E/3N8 and W5, and nitrogen-replete cultures of the high maltose-releasing strain 3N813A released ammonium, and the rate of release was stimulated in darkness. Freshly isolated symbionts from the association E/NC released ammonium at pH 4 when incubated in darkness but assimilated ammonium in light. Nitrogen-starved cultures of both high and low maltose-releasing strains assimilated ammonium at pH 4 in both light and dark. Ammonium-assimilation characteristics of nitrogen-starved cultures were sufficiently different from those of freshly isolated symbionts to indicate that symbionts are not maintained by the host under nitrogen deficiency at high pH. A detailed model of symbiont regulation is proposed that suggests that the ammonium compensation point (defined as the pH at which there is no net release or assimilation of ammonium) is important as a homeostatic mechanism for maintaining high rates of maltose release in light and as a mechanism for controlling both symbiont cell division and changes in algal number per digestive cell with changes in environmental conditions. Experimental evidence consistent with the model is presented. Nitrogen-replete cultures of the high maltose-releasing strain 3N813A decreased medium pH during ammonium assimilation and increased medium pH during ammonium release. Furthermore, dark-grown animals of the association E/E released ammonium when transferred to a 12 h light : 12 h dark régime and release was stimulated by the photosynthetic inhibitor 3-(3, 4-dichlorophenyl)-1, 1-dimethylurea.