Dynamics of alkaline phosphatase activity in relation to phytoplankton and bacteria in a coastal embayment Daya Bay, South China

Previous studies conducted on Daya Bay implied that the bay had been undergoing potential phosphorus limitation. In this context, alkaline phosphatase activity (APA) and the associated microbes were investigated in three different seasons in Daya Bay, South China Sea. Both bulk-community (fractioned into dissolved and particulate) and single-cell assays of APA were used to estimate the P status of phytoplankton at the community and species level. Unexpected high potential APA (Vmax) was observed in Daya Bay. Bulk APA showed that the maximum value in the spring (mean 583.26 nM h−1) corresponded well to low phosphate concentration. Furthermore, particulate APA (P-APA) showed an inverse hyperbolic relationship with phosphate, implying the coexistence of both constitutive and inducible AP; meanwhile, a threshold phosphate concentration for the transition from high to low APA was found around 0.2 μM in our study. P-APA and dissolved APA (D-APA) exhibited a tight link with phytoplankton and bacteria, which indicated that both of them were two main carriers of the enzyme. During the spring cruise, we encountered a small-scaled bloom of Gymnodinium that was probably at a declining phase. Extreme high levels of bulk and D-APA were characterized at this spring bloom event, and we suspected that bacteria especially active bacteria played an important role in APA production and partitioning at the post-bloom phase. In Daya Bay, diatoms were the dominant phytoplankton groups and percentages of ELF (Enzyme Labelled Fluorescence) labelled diatoms followed the same seasonal fluctuation as bulk APA, which suggested that diatoms were responsible for major variations of the bulk AP activity except for the spring bloom. Taken together, we considered that phytoplankton may be experiencing more P stress in spring and that the mineralization of organic P via alkaline phosphatase may help phytoplankton overcome P deficiency.