Mechanisms controlling virus abundance and partitioning of loss of bacterial production between viral lysis and protozoan predation are discussed within the framework of an idealized Lotka-Volterra-type model. This combines nonselective protozoan predation with host-selective viral lysis of bacteria. The analysis leads to a reciprocal relationship between bacterial diversity and viruses, in which coexistence of competing bacterial species is ensured by the presence of viruses that ''kill the winner,'' whereas the differences in substrate affinity between the coexisting bacterial species determine viral abundance. The ability of the model to reproduce published observations, such as an approximate 1 : 10 ratio between bacterial and viral abundance, and the ability of viral lysis to account for 10-50% of bacterial loss are discussed.
There are probably millions of species in the microorganismal domains Bacteria and Archaea (the prokaryotes), and we are only just beginning to work out the basic principles governing their distribution and abundance in natural environments. One characteristic that has become clear is that prokaryote diversity in aquatic environments is orders of magnitude less than in sediments and soils. Hypotheses and models explaining such differences are under development and are beginning to offer promising insights into the mechanisms governing prokaryote diversity and ecosystem function.
The remarkable diversity of genes within the pool of prokaryotic genomes belonging to the same species or pan-genome is difficult to reconcile with the widely accepted paradigm which asserts that periodic selection within bacterial populations would regularly purge genomic diversity by clonal replacement. Recent evidence from metagenomics indicates that even within a single sample a large diversity of genomes can be present for a single species. We have found that much of the differential gene content affects regions that are potential phage recognition targets. We therefore
Phosphate addition to surface waters of the ultraoligotrophic, phosphorus-starved eastern Mediterranean in a Lagrangian experiment caused unexpected ecosystem responses. The system exhibited a decline in chlorophyll and an increase in bacterial production and copepod egg abundance. Although nitrogen and phosphorus colimitation hindered phytoplankton growth, phosphorous may have been transferred through the microbial food web to copepods via two, not mutually exclusive, pathways: (i) bypass of the phytoplankton compartment by phosphorus uptake in heterotrophic bacteria and (ii) tunnelling, whereby phosphate luxury consumption rapidly shifts the stoichiometric composition of copepod prey. Copepods may thus be coupled to lower trophic levels through interactions not usually considered.
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