Abstract

The release of endogenous phosphorus from sediments leads to the eutrophication of water bodies. Bacteria in sediments play a vital role in phosphorus cycling. A high hydrostatic pressure can alter the microecology and affect bacterial functions at the water–sediment interface. The aim of this study was to analyze the expression patterns of functional genes in bacteria associated with phosphorus transformation at the water–sediment interface of a deep reservoir under different hydrostatic pressures. Furthermore, the effects of hydrostatic pressure on phosphorus cycling pathways mediated by bacteria were explored. A device was designed to simulate the microecological environment in sediments from a reservoir in Xi’an, China, at atmospheric pressure, 0.2 MPa, 0.5 MPa, and 0.8 MPa. Phosphorus transformation genes, phoD, ppk, and pqqC, were quantified using real-time PCR. The bacterial community composition and diversity were analyzed using high-throughput sequencing of the ppk gene. The total phosphorus contents in the sediments were 724.72, 646.97, 630.92, and 682.88 mg kg–1 at the four respective hydrostatic pressures, respectively. Of this, inorganic phosphorus accounted for 68.8–79.0%, and Fe/Al-P accounted for 47.4–57.2%. The expression of phoD facilitated the transformation of organic to inorganic phosphorus and of Ca-P to Fe/Al-P, whereas the expression of ppk and pqqC regulated organic phosphorus hydrolysis by affecting phosphatase activity. The abundance and diversity of ppk-harboring bacteria were highest at 0.2 MPa, while the dominant genera did not change at the four pressures. The five most abundant genera were Pseudomonas, Bordetella, Cupriavidus, Achromobacter, and Rhizobium. High hydrostatic pressure facilitates the transformation of Fe/Al-P to Ca-P in, and phosphorus release from, reservoir sediments by regulating phoD, ppk, and pqqC expression in bacteria. Changing the hydrostatic pressure can alter the bacterial community structure at the genus level, but not the dominant populations harboring the ppk gene.

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