Table 1.
Results summary.
Fig 1.
Phage gene expression in early, middle, and late temporal clusters during light and dark infection.
Relative expression of phage mRNA is in units of reads per kbp gene length per million (RPKM) of host and phage reads (see methods). Phage auxiliary metabolic genes (AMGs) are labeled: cp12, Calvin cycle inhibitor CP12; talC, transaldolase; psbA and psbD, photosystem II D1 and D2 proteins; nrdA and nrdB, ribonucleotide reductase alpha and beta subunits; and hli, high-light inducible proteins.
Fig 2.
Heat maps of differentially expressed genes in light and dark infections (infected:uninfected ratio) and in uninfected and infected treatments (dark:light ratio).
Genes are listed in order on the MED4 chromosome. Bold gene labels indicate involvement in photosynthetic electron transport or nucleotide biosynthesis, and asterisks indicate genes found in both heat maps. The color gradient indicates gene transcripts enriched (yellow) or diminished (cyan) as follows: (A) in infected relative to uninfected treatment in one or more light or dark time point or (B) in dark relative to light in one or more uninfected or infected time point (note the different scales).
Fig 3.
Host differentially expressed genes (DEGs) following infection in the light and dark, organized by pathway.
Genes shown were differentially expressed at one or more time point, marked with a black ‘X’ if NOISeq probability q > 0.95, and match those in S3 Table. Line color shading is proportional to relative transcript abundance at 0.5 h post-inoculation. Two-fold changes up and down are indicated by dotted lines, and zero fold change is indicated by a dashed line.
Fig 4.
Schematic of proposed flow of electrons, energy, and carbon in cyanophage-infected cyanobacteria in the light.
In the dark (not pictured), PET and phage replication are stunted because the cell is not receiving light energy. In the light, however, energy (hν) excites electrons in water to travel through the photosynthetic electron chain, with the terminal electron acceptor being NADP+ via ferredoxin–NADP+ reductase (FNR) in uninfected cells (A) and oxygen via plastoquinol terminal oxidase (PTOX) or cytochrome c oxidase (COX) in infected cells (B). Under phage infection, host FNR transcripts are diminished, and therefore the proposed terminal electron acceptor is not NADP+. Rather, cyclic electron flow goes through NAD(P)H dehydrogenase (NDH) or direct to plastoquinone, with PTOX serving as the terminal electron acceptor. Cyanophage P-HM2 genes (filled viruses) are transcribed for high-light inducible proteins (HLIPs), photosystem II (PSII), the pentose phosphate pathway (PPP), and nucleotide biosynthesis; additional cyanophage genes not in P-HM2 (unfilled viruses) exist for modules along this metabolic network. NADPH is proposed to be generated from pre-existing reduced carbon (glucose) via the PPP. Any NADPH produced by FNR would be designated for the Calvin cycle by docking of FNR with GAPDH and therefore unproductive because of Calvin cycle inhibition by phage CP12. In this model of light-driven phage infection, therefore, the main source of energy (ATP) is cyclic photosynthesis and of reducing equivalents (NADPH) is the PPP, with ATP and NADPH consumed in the production of nucleotides to replicate the phage genome. Other abbreviations: PQ/PQH2, plastoquinone/plastoquinol (oxidized/reduced); Cyt b6 f, cytochrome b6 f, PCox/PCred, plastocyanin (oxidized/reduced); PSI, photosystem I; Fd, ferredoxin; ATPase, F1F0-ATP synthase.